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An investigation of the chronic physiological changes due to relaxation training and practice
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An investigation of the chronic physiological changes due to relaxation training and practice
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Content
AN INVESTIGATION OF THE CHRONIC
PHYSIOLOGICAL CHANGES DUE TO
RELAXATION TRAINING AND PRACTICE
by
Robert Thorenz Hopper
A Dissertation Presented to the
FACULTY OF THE GRADUATE SCHOOL
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment of the
Requirements for the Degree
DOCTOR OF PHILOSOPHY
(Physical Education)
April 1976
UNIVERSITY OF SOUTHERN CALIFORNIA
THE GRADUATE SCHOOL
UNIVERSITY PARK
LOS ANGELES, CALIFORNIA 90007
This dissiertation) written by
Robert Thorenz H pper
under the direction of h[:1 ______ Dissertation Com-
mittee) and approved by ail its members) has
been presented to and ar:cepted by The Graduate
School) in partial fulfil -·,ient of requirenzents of
the degree of
DOCTOR OF PHILOSOPHY
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TABLE OF CONTENTS
LIST OF TABLES
LIST OF FIGURES
Chapter
I.
11.
111.
INTRODUCTION
Statement of the Problem
Significance of the Study
Definition of Terms
Delimitations
REVIEW OF THE LITERATURE
Common Health Problems and Relaxation
Definitions of Stress
The Changing Nature of Stress
Physiology of Stress
Role of ascending reticular arousal system
Role of the hypothalamus
Role of the endocrine system
Role of proprioception
Generation of proprioceptive input
The "Relaxation Response"
Measurement of Relaxation
Analys:s of Relaxation Studies
Description of Relaxation Methods
Progressive Relaxation
Yoga
Transcendental Meditation
Autogenic Training
Exercise
METHODS AND PROCEDURES
Subjects
Experimental Design
Instrumentation
EMG measurements
Metabolic measurements
Plethysm ~raphy measurements
Protocol
Pretest and posttest procedures
Relaxation training procedures
. IV
. IV
Page
. 1
. 3
. 4
. 4
. 5
. 6
. 6
. 8
. 9
. 11
. 11
. 13
. 15
. 16
. 18
. 22
. 23
. 28
. 28
. 30
. 37
. 39
. 40
. 42
. 45
. 45
. 46
. 46
. 46
. 49
. 52
. 55
. 55
. 56
..
II
IV. RESULTS
. 58
V. DISCUSSION . 68
VI. SUMMARY AND CONCLUSIONS . 74
Summary
. 74
Con cl us ions . 75
Recommendations . 75
BIBLIOGRAPHY
. 77
APPENDIX
. 87
I. Relaxation Techniques . 87
...
111
LIST OF TABLES
Table Page
1. Physiologic Parameters Supporting the Existence of the "Relaxation
Response" During the Practice of Various Mental Techniques . 24
2. Description of Subjects (Experimentai Group) . 47
3. Description of Subjects (Control Group) . 48
4. t Test Analysis of Pretest Data . 59
5. Mean EMG Scores of Experimental Group (30-Second Intervals) . 60
6. Mean EMG Scores of Control Group (30 Second Intervals) . 61
7. Pretest Posttest Analysis for Experimental Group 64
8. Pretest Posttest Analysis for Control Group . 65
9. t Test Analysis of Mean Difference Scores for Experimental and
Control Groups . 66
10. Analysis of Relaxation Training Duration . 72
LIST OF FIGURES
Figure Page
1. 1 llustration of Subject Seated in Screen Room with All
Instrumentation in Place . 50
2. Block Diagram of EMG Monitoring System . 51
3. Metabolic Circuit and Calculations for Oxygen Consumption . 53
4. Sample Plethysmographic Tracing and Equation for Blood Flow
Computation . 54
5. EMG Time Course Showing Mean MAP Values for Each of the 20
30-Second Collection Periods . 63
IV
CHAPTER I
INTRODUCTION
Relaxation training makes a contribution to the prevention and care of numerous
health problems: functional disorders such as tension headaches and anxiety states
(Whatemore, 1962b); essential hypertension (Aagard, 1970; Jacobson, 1940a, 1940b;
Patel, 1973, 1975), and certain psychological problems such as systematic desensiti
zation treatment of phobias (Wolpe, 1958). Relaxation training, which has also been
termed motor re-education (Whatemore, 1962b), should be of interest to the physical
educator since this teaching of motor re-education might effectively be implemented in
the public schools. Of the numerous methods of relaxation, Progressive Relaxation
(Jacobson, 1938) seems to be best suited for physical education classes. Another form
of motor re-education called abbreviated relaxation training, modeled after Progressive
Relaxation, is widely used in psychological fields, and would be the easiest method to
include in the physical education curriculum.
Progressive Relaxation enables the subject to learn "muscle sense" and may
require from 10 up to 1
1
.JO hours of instruction over several months. Instruction is on
an individual basis, although Steinhaus and Norris ( 1964) have applied the methods to
a group situation. Individual sessions are normally limited to practice with one or two
mu~~le groups. 10-20 hours of instruction are normally necessary to teach relaxation
methods for all the different muscle groups. Abbreviated relaxation, on the other hand,
requires only 1-6 hours of instruction (Wolpe, 1958). An average session consists of 30
minutes of relaxation exercises, which are modeled after Jacobson's concepts. The
same procedure is repeated at all training sessions. Both methods require practice, with
Jacobson suggesting one hour per day, while Wolpe and Lazarus (1906) suggest 2
periods of 15 minutes per day for the abbreviated method. There exists good data
supporting the physiologicui effects brought about by Progressive Relaxation training
(Jacobson, 1938, 1943; Steinhaus & Norris, 1964), but the evidence for abbreviated
1
relaxation training Is not conclusive. Few controlled studies using EMG have been
conducted using abbreviated relaxation training. Grossberg (1965) compared abbrevi ated relaxation with 2 control procedures (instructions to rest, and listening to music),
using the measures of forearm and frontars EMG, heart rate, and skin conductance as
dependent variables. There were two one-hour testing sessions, spaced 5 days apart,
during which the treatments were administered. No significant differences between the
groups w ~re found during the treatments in session 1 or session 2. However, Grossberg
suggested an acute trend (a trend during the treatment) of decreased EMG for the
experimental group. There were no significant differences between the 2 testing
sessions for the experimental or control groups, which indicated no chronic training
effect due to relaxation.
Paul ( 1969) compared abbreviated relaxation training with relaxation induced by
hypnosis, and with a control group, using heart rate, conductance, EMG, and respira tory rate as dependent variables. There were two testing sessions, one week apart, with
the experimental group asked to practice relaxation each day. Both relaxation and
hypnotic suggestion produced significantly greater acute effects (measured during the
relaxation procedures) than the control groups in all measures. In addition, EMG
reduction for the relaxation group was significantly greater than the hypnotic sugges
tion group and the control group. No significant differences were found between the
first testing session and the second testing session for the experimental groups,
indicating no learning effects occurred. Ho\Never, on the basis of trends in the data,
Paul suggested some learning effect may have occurred.
Mathews and Gelder (1969) conducted a controlled 6-week training program using
abbreviated relaxation training and practice, measuring EMG, skin conductance, and
blood flow, before and after training. No significant EMG changes were found, but
experimental group EMG reductions occurred in the hypothesized direction. The
number of subjects per group was 5, and one subject in the control group had very
high prete$ t EMG values, making the control pre-post data difficult to interpret. Had
the study been conducted with a larger number of subjects, a stronger interpretation of
the data would have been possible.
2
Thus there is still an open question whether abbreviated relaxation training and
practice has measurable chronic effects on body tension, as measured by EMG levels.
Statement of Problem
The purpose of this study was to investigate the long term effects of abbreviated
relaxation training on the major physiological parameters characteristic of relaxation.
These physiological changes (due to relaxation) have been termed the "Relaxation
Response" (Benson, Beary, and Carol, 1974), and have been characterized as an
"integrated hypothalmic response which results in generalized decreased sympathetic
nervous system activity and perhaps also increased parasympathetic activity." The
response can result in decreased activity of skeletal musculature, decreased blood
pressure, decreased respiratory rate, decreased pupil constriction, decreased oxygen
consumption, and increased blood flow to skeletal muscle (Benson, Beary & Carol,
1974; Hess, 1957).
Jacobson ( 1943), and Steinhaus and Norris ( 1964) used Progressive Relaxation
metl-o: s for 10 and 8 weeks respectively, and found decreased iesting EMG levels.
Gru~~bc1·g ( 1965) and Paul ( 1969) have investigated abbreviated relaxation training, and
while not achieving significant results, they suggested that physiological trends
indicated possible chronic training effects due to relaxation training. Mathews and
Gelder ( 1969) tested the effectiveness of abbreviated .-elaxation training using physio
logical and physchological measures before and after 6 weeks of training. While not
achieving significant differences,· experimental design problems and possible EMG
trends indicate the need for further investigation of abbreviated relaxation training.
The question of whether there exist a long term or "chronic" decrease in EMG
values with abbreviated relaxation training is therefore still unresolved. This research
was directed to testing the hypothesis thai: abbreviated relaxation training and practice
would bring about a chronic reduction in EMG values and concurrently bring about
the integrated chronic physiological changes which are characteristic of the Relaxation
Response. In particular 5 sub-hypotheses could be stated. With abbreviated relaxation
training and practice, the following physiological changes would occur: 1) decreased
3
resting muscle action potentials (MAP's), 2) decreased resting oxygen consumption, 3)
increased resting forearm blood flow, 4) decreased resting heart rate, and 5) decreased
resting afterial blood pressure.
Significance of the Study
The contribution of relaxation training to prevention and care of numerous health
problems including functional disorders, essential hypertension, and psychological areas
was mentioned in the introduction. The data from those investigations cited suggest
that motor activity plays an important role in these health problems, and that relax
ation (or motor re-education) may serve an important role in decreasing incidence and
severity of these disorders.
This teaching of motor re-education might be effectively implemented in the
public schools in physical education classes. In this fashion, the learning of motor
re-education might serve as a preventive measure, rather than a treatrnent after the
problem has been well developed. Therefore, there is a need to validate methods of
relaxation which may be applicable to physical education classes. Methods of relax
ation used in a clinical situation are not necessarily appropriate for the group
approach. This study will provide additional data toward that goal.
Of the mi '"hods of relaxation, Progressive Relaxation, abbreviated relaxation
training, Yoga, TM, and Autogenic Training seem to be best suited for use in physical
education classes. In physical education the emphasis has been on learning appropriate
methods for "turning on" the musculature in exercise, i.e. improving strength,
endurance and coordination. Emphasis has been on the development of motor skills
used for sports and recreational activities. A natural correlate to this process is learning
to "turn off" the musculature during relaxation. Students could and should receive
instruction on how to decrease as well as increase muscle activity as part of the
physical education background.
Definition of Terms
Diastolic blood pressure (4th and 5th phases) -- The 4th phase diastolic pressure is
4
recorded when the clear tapping sound (Korotkoff sound, 3rd phase) becomes lower
pitched and less intense. The 5th phase diastolic pressure is recorded when the tapping
sound disappears completely.
Muscle action potentials (MAP's) -- Muscle electrical activity occurs in all muscle
fibers with contraction. At the surface of the skin, eiectrodes pick up the sum of this
muscle electrical activity from the numerous contracting muscle fibers, and this sum is
termed Summated Muscle Action Potential (MAP's).
Acute and Chronic Changes -- When physiological measurements are taken during
practice of relaxation, the changes that occur are termed acute. When measurements
are taken before and after a training period (i.e. before and after some weeks of
relaxation training), the changes that occur are termed chronic.
Delimitations
Subjects for the present investigation were chosen from a population that
considered itseH '.-itressed in some fashion. These subjects exhibited one or more of the
following symptoms: 1) difficulty in getting to sleep, 2) general nervous tension, 3)
!')ersistent feeling of tension and strain, 4) irritability, 5) unremitting worry, 6) restless
ness, 7) inability to concentrate, or 8) feeling of panic in everyday situations.
5
CHAPTER II
REVIEW OF THE LITERATURE
This review is divided into seven sections: 1) Common Health Problems and
Relaxation, 2) Definition of Stress, 3) Changing Nature of Stress, 4) Physiology of
Stress, 5) The "Relaxation Response," 6) Measurement of Relaxation, and 7) Analysis
of Relaxation Studies.
Common Health Problems and Relaxation
Relaxation training has been used in the cure and prevention of numerous health
problems including functional disorders, essential hypertension, and some psychological
disorders. Several common health problems of today are considered by some physicians
to be functional in origin and are therefore called functional disorders; such ailments
include tension headaches, migraine headaches, certain types of backache, functional
bowel distress, spastic esophagus, duodenal ulcer, anxiety states, certain depressed
states, many fatigue states, insomnia, phobic states, and obsessive-compulsive states
(Whatemore, 1962b). Whatemore also suggested a functional factor might exist in
essential hypertension, myocardial infarction, asthma, certain skin disorders, and
rheumatoid arthritis. He cited numerous clinical studies, some employing electro
myography, which have demonstrated the presence of hyperponesis (exaggerated
activity in the motor nervous system) in patients with various functional disorders, and
its antecedency to the onset of symptoms. In an attempt to deal \_,vith these health
problems, Whatemore has outlined 4 modes of treatment, one of which is motor
re-education. This system of motor re-education is modeled after Jacobson's Progressive
Relaxation (Jacobson, 1938).
Cardiovascular dif• ~ase, suggested by Whatemore ( 1962b) as a possible functional
diso · er, is the number one cause of death in the United States (Commission for Heart
Disease Resources, 1970). Various degrees of hypertension, which predispose one to
6
the diseases of atherosclerosis, heart attacks, and stroke are present among 15-33% of
the adult population (Benson, 1975). A number of investigators have indicated the
involvement of stressful circumstance in the etiology of essential hypertension
(Gutmann and Benson, 1971; Benson et al, 1969, 1970, & 1973; Henry and Cassel,
1969; Jacobson, 1939a, 1939b, 1940a and 1940b; Friedman and Rosenman, 1974; and
Selye, 1955, 1956, 1970).
Stre~s is a common word found in these investigations. The concept of stress will
be discussed in greater detail in another section of this paper. Gutmann and Benson
(1971) have suggested that stress is created by situations which require behavioral
adjustment. They stated that " ... stressful circumstances are those associated with
rapid cultural change, urbanization and migration, socioeconomic mobility, or
uncercainty of immediate environment" (p. 543). Ostfeld and Shekelle ( 1967) have
reported:
There has been an appreciable increase in uncertainty of human
relations as man has gone from relatively primitive and more rural to
the urban and industrial. Contemporary man ·n much of the world, is
faced everyday with people and with situations about which there is an
uncertai11ty of outcome, wherein appropriate behavior is not prescribed
and validated by tradition, where the possibility of bodily or psycho
logical harm exists, where running or fighting is inappropriate, and
where mental vigilance is called for.(p. 101)
These ideas suggest that stress and the way people react to stressful situations may
play an important role in the development of hypertension, and consequently cardio
vascular disease.
The treatment of hypertension has been approached by numerous methods
(Aagaard, 1973). Aagaard reviewed the methods of hypertension treatment and
suggests relaxation as one of the first general measures for the treatment of mild
hypertension. In particular he suggests Progressive Relaxation, Autogenic Training, and
various Yoga exercises, including Transcendental Meditation (TM). These suggestions
are based on good experimental data. In investigations using hypertensive subjects,
Progressive R~laxation (Jacobson, 1940a, 1940b; Steinhaus and Norris, 1964), Yoga
(Patel, 1973, 1975), Autogenic Training ( Luthe, 1969), and Transcendental Meditation
7
(Benson, Marzetta, and Rosner, 1974) have been effective in causing decreases in blood
pressure. Exercise might also be listed with the above group (Boyer and Kasch, 1970).
A final area, where relaxation training has also been used effectively, is in the
treatment of certain psychologica !)rob I ems. Brief, or abbreviated, relaxation training
comprises one major component of he systematic desensitization treatment of phobias
(Wolpe, 1958). Rachman ( 1967) summarized numerous investigations, which docu
mented the importance of relaxation training in systematic desensitization treatment.
Relaxation training has been used in the cure of numerous health problems
including functional disorders, essential hypertension and certain psychological dis
orders. These facts add considerably to the importance of relaxation as a prophylactic
measure, which could be taught as part of the physical education curriculum.
Definition of Stress
Hans Selye ( 1956) has been a pioneer investigator in the area of stress. He has
defined stress as the state manifested by a specific syndrome which consists of all
non-specifically induced changes in a biologic system. The specific syndrome is called
the General Adaptation Syndrome, and can be due to any number of diverse stressors,
and therefore is non-specifically induced. According to Selye (1956), he could find no
noxious agent that did not elicit the syndrome. The General Adaptation Syndrome is a
triad of physiological effects: enlargement of the adrenal cortex, atrophy of the
thymus and lymphatic structures, and bleeding ulcers of the digestive tract. The
physiology of stress will be discussed in a subsequent section. Basically a stressor (an
agent which causes stress) stimulates {in some unknown fashion) the anterior pituitary
to release adrenal corticoids (glucocorticoids). The glucocorticoids are responsible for
the General Adaptation Syndrome.
The body's response to a stressor (a stressfu I situation or an agent which causes
stress is opposite to the body's response to relaxation (Benson, Beary, and Carol,
1974). Two opposite states exist: the ergotropic (excited) state, and the trophotropic
(relaxed) state { Hess, 1957). The physiologic changes due to stressful situations lead to
an unrelaxed state, which is characteristic of the ergotropic state. According to Hess
8
( 1957) motor excitability is increased in the ergotropic state, and therefore one would
expect increased muscle action potentials (MPAs). Increased MAPs as a result of a
stressful situation, have been demonstrated by von Eiff (1952). It is reasonable to
believe that teaching relaxation may provide prophylaxis against effects of stress.
Therefore it is important to understand what stress is and how it affects the body.
The Changing Nature of Stress
In prehistoric times a stressor was a life-threatening event which resulted in fight ing or running. Stressors in modern society are of a different nature. The types of
situations which create stress are now usually psychosocial. Charvat et al ( 1964)
characterized today's stressors as those which revolve around symbolic challenges to
man's socioeconomic st~tus and other mental factors. The effects of these psychosocial
stressors have been the subject of numerous investigations, especially in the area of
essential hypertension.
Henry and Cassel ( 1969) cite animal and human studies to indicate that repeated
arousal of the defense alarm reaction may be an important mechanism involved in the
etiology of hypertension. These stressful situations, which arouse the defense alarm
reaction, arise when previously socially-sanctioned patterns of behavior, especially those
to which the organism has become adapted during critical learning periods, can no longer
be used to express normal behavioral urges. They cite Donnison (1929, 1938) who
surmised that high blood pressure is due to the failure of older persons to adapt to
revolutionary changes in the mode of living and to transmit appropriate modified social
patterns to the young, and that successful childhood integration of the inborn drives into
socially acceptable patterns is the critical factor in creating a stable, non-hypertensive
society. Scotch ( 1957) noted groups with high blood pressure exhibit increased social
tensions and conflict. Scotch and Geiger ( 1963) suggest that hypertension is due to the
failure of individuals to meet demands of the environment with adaptive behavior.
When someone fails to find his ecological niche, he is put into a stressful position.
Gutmann and Benson ( 1971) suggest that elevated systemic arterial blood pressure
seems to be more consistently related to environmental situations which require
9
continuous behavior adjustments on the part of the individual. Ostfeld and Shekelle
(1967) suggest that prevalence of higher arterial blood pressure was found to be
specifically associated with a) rapid cultural change, urbanization and migration; and b)
socioeconomic mobility. These patterns were consistent with the hypotheses that
elevated systemic arterial blood pressure in western urban environmer ts is related to
the conflict and uncertainty inherent in a rapidly changing social system.
These psychosocial stimuli that are postulated to be stressful and cause increases
in blood pressure can be duplicated with laboratory animals. One investigation by
Henry, Meehan, and Stephens ( 1967) involved creation of 4 psychosocial conditions:
1) combination of male mice from different boxes; 2) aggregation in small boxes; 3)
chronic threat from a predator; and 4) territorial conflict in an inter~onnected box
system. The expei"iments lasted six to twelve months and all methods resulted in
sustained elevation of arterial blood pressure. Folkow and Rubinstein ( 1966)
chronically stimulated the hypothalamic defe, 1se area in the rat and found a significant
increase in the resting mean blood pressure level. They concluded that chronic elicita
tion of the defens~ arousal area (due to environmental situations) may play a signifi
cant role in the development of essential hypertension.
The response to a stressful situation has been illustrated in man by the simple use
of mental arithmetic calculations. Subjects were required to maintain pace with a
metronome, which created a stressful situation for the subjects. The hemodynamic
response was similar in nature to the response of the hypothalamically mediated fight
or flight reaction (Brod et al, 1959). These studies have led Benson (1975) to the
conclusion that daily elicitation of this response in the pressure-oriented business world
can lead to chronic elevation of arterial blood pressure.
Stressors of today are extremely diverse in nature. Holmes and Rahe (1967) have
attempted to quantify stressors and the degrees of their effects. They developed a
social readjustment scale based on interviews with 394 subjects who rated certain
events in their lives on a scale of impact, with death of a spouse being most stressful.
They noted that change, whether "good" or "bad" causes some degree of stress to a
human being, leaving him more susceptible to disease. This concept of good or bad
10
j
stress is in agreement with Selye ( 1956), who also indicates stress as one of the factors
involved in hypertension.
Friedman and Rosen man ( 1974) have described a specific overt behavior pattern
associated with a high prevalance of coronary heart disease. Type A behavior was
characterized by excessive drive, aggressiveness, ambition, involvement in competitive
activities, frequent vocational deadlines, pressure for vocational productivity, an
enhanced sense of time urgency, restless motor mannerisms, and staccato type of
verbal response. The type A personality tends to create his own stressful problems by
trying to do more and more in less and less time. He is constantly creating stressful
deadlines, which require numerous efforts to meet those deadlines. The importance of
these efforts will be discussed in a subsequent section. One could conclude from the
foregoing studies that there are stressful situations over which the person has no
control, and situations which the person has created for himself. One could further
suggest that the types of situations which create stress, whether coming from the
environment or self-made efforts, are normally psychosocial.
Physiology of Stress
This section of the review will discuss several aspects regarding the physiology of
the stress mechanism, and elucidate how relaxation training can intervene in this
mechanism and reduce the effects of stress. The major conceptual areas of this section
are: 1) Role of the ascending reticular arousal system (ARAS); 2) Role of the
hypothalamus; 3) Role of proprioception; 4) Role of the endocrine system; and 5)
Generation of proprioceptive input.
kvle of the ascending reticular arousal system {ARAS). The ARAS is an area of
diffuse neurons, distributed through the central core of the brain stem. It begins in the
lower brain stem and extends upward through the mesencephalon and thalamus to be
distributed through the cerebral cortex. Moruzzi and Magoun ( 1949) defined the role
of the reticular formation m the arousal of an organism. They found that stimulation
of the reticular formation m the brain stem produced diffuse excitation in the cortex
of unanesthetized anin1als, while lesions in the reticular formation of the brain stem
1 1
induce coma and lethargy. The changes in EEG due to ARAS stimulation are the same
as the EEG change from sleep to alertness (low frequency waves of 8-12 c.p.s. to
higher frequency waves of 18-30 c.p.s., with a further change from regular synchro
nized to irregular desynchronized waves.) The ARAS is believed to be responsible for
normal wakefulness of the brain (Magoun, 1958).
On the basis of this work Lindsley ( 1951) proposed the Activation Theory,
suggesting that with activation of an organism came the activation pattern of EEG
(desynchronization of EEG waves). Malmo ( 1959) has summarized the activation
theory as a continuum extending from deep sleep (low activation end) to the excited
state (high activation end). This continuum is a function of cortical bombardment by
the ARAS. With increasing ARAS stimulation, there is increasiilg activation
(desynchronization of E.E.G. waves). The relationship between activation and behavior
efficiency is described by an inverted "U." From low activation up to a point that is
optimal for a given function, the level of performance rises monotonically with
increasing activation. Beyond this optimal point further increases in activation produce
a fall 1,, performance level. That is, when the activation levels are low, moderate, and
high, the respective performance levels are low, optimal, and low (Malmo, 1959).
Hebb (Haugen, Dixon, and Dickel, 1958) postulated that stimulation of the
reticular formation results in cortical activity of a purposeful and appropriate type up
to a certain point; but that stimuli in excess of this produced disorganized activity,
with anxiety and panic. Haugen, Dixon, and Dickel ( 1958) have carried this hypothesis
one step further in suggesting that:
... random and intermittent, constantly changing proprioceptive stimuli
would allow for normal cortical activity; but a persistent bombardment
of excessively strong stimuli from chronic bracing of all striated
musculature would result in overactivity of the arousal area, and
culminate in the generation of apprehension, fear and similar phenomena
in the cortex. (p. 110)
One could hypothesize that this chronic bracing of the musculature could be the result
of a stressful situation (a situation which has led to the alerting reaction or the fight or
flight reaction.)
12
Role of the hypothalamus. The hypothalamus holds a role of extreme importance
1n the functioning of the body, having control over many vegetative functions.
Vegetative functions are involuntary functions necessary for living. The hypothalamus
has an effect in regulation of cardiovascular function, body temperature, osmolality of
body fluid, gastrointestinal and feeding functions, as well as regulation of the anterior
pituitary gland of the endocrine system. The ARAS and the hypothalamus are
conceptually different, although anatomically and physiologically closely integrated.
According to Gellhorn and Loofbourow (1963) the reticular formation is more basic,
but less differentiated than the hypothalamus. Gellhorn and Loofbourow believe that
tonic afferent impulses from the reticular formation keep the hypothalamus in a
reactive state, and in turn the hypothalamus exerts a tonic excitatory influence on the
cortex.
The classic work of Hess ( 1957) has contributed greatly to the knowledge of the
diencephalon, and in particular the hypothalamus. Hess mapped the areas of the brain,
implanted electrodes into the cat brain, and then, using electrical stimulation,
associated the areas of the brain with the respective behaviors and physiological
responses. He demonstrated that stimulation of a portion of the hypothalamus leads to
coordinated activation of the sympathetic nervous system. He called this area the
ergotropic zone, an area in the vicinity of the posterior hypothalamus, wnich extends
from the anterior midbrain toward the hypothalamus. Stimulation resulted in dilatation
of the pupils, increased blood pressure (sometimes accompanied by increased heart
rate), activation of respiration, and heightened motor excitability.
In addition to noting the location of the ergotropic zone in the hypothalamus,
Hess ( 1957) also isolated the trophotropic zone. This area, located in the anterior
hypothalamus, causes the opposite response of the ergotropic zone, with decreased
muscle excitability, decreased blood pressure, decreased respiration, decreased pupil
constriction, and decreased responsiveness to certain nervous structures. This zone is
part of the trophotroµic-endophylactic system of the diencephalon, and its response is
mediated . by the parasympathetic nervous system. This endophylactic system might be
termed an internal protection system. This response is characterized by a typical
13
protective or riddance mechanism. As Hess ( 1957) states, "We are actually dealing with
a protective mechanism against overstress belonging to the trophotropic-endophylactic
system and promoting restorative processes." (p. 35).
Hess noted that there are no foci that correspond to individual isolated responses,
and suggested that:
In the diencephalon we are dealing with a 'collective representa
tion' of a group of responses, which includes responses of the
autonomic system as they made their appearance in the form of
synergically associated mechanism. In the truly physiologic situation,
this is the case under conditions of physical stress. (p. 35)
When the brain receives messages from intero, extero, and telereceptors of a ,
stressful situation, an integrated response is elicited consisting of the somatomotor
system, the visceromotor system, and the endocrine system (Charvat et al, 1964).
According to Hess ( 1957) the physiologic significance of the diencephalon is that the
purely vegetative responses, such as cardiovascular responses and gastrointestinal
function, become associated with complex somatomotor functions to give a physiologi
cally successful and integrated performance.
There exists a reciprocal relationship between the ergotropic and trophotropic
zones. Nauta ( 1946) showed that anterior hypothalamus lesions lead to sleeplessness
and exhaustioa resulting from released or decreased influence of anterior hypothala
mus, with subsequent increased influence by the posterior hypothalamus. Conversely
lesions to the posterior hypothalamus cause somnolence (Ranson, 1934). According to
Gellhorn these two studies suggest dominance of the anterior hypothalamus (Gellhorn,
1957). This reciprocal relation can be demonstrated by heating the anterior hypothala
mus in an animal subjected to cold stress. The shivering decreases and lessened
sympathetic discharges lead to vasodilatation (Hemingway et al, 1940).
The role of sensory input to the hypothalamus is of great importance. Afferents
from exteroceptive sense organs play a decisive role in the activation of the ergotropic
zone. Especially notable are visual and auditory stimuli. The existence of these
connections is easy to establish, due to the strikingly large number of collaterals from
the lemniscus that enter the ergotropic area. According to Hess ( 1957), the assumption
14
seems justified that the afferents which are specific for higher cerebral areas also
induce mesencephalically and diencephalically mediated activity of vegetative effectors
and subcortical motor function.
The opposite reaction occurs with the trophotropic zone. The influence of the
trophotropic-endophylactic system is overcome by the influence of specific exterocep
tive sense organs, which gives a net ergotropic shift in the ergotropic-trophotropic
balance. Prolonged excitation of the proprioceptors may also play a part in this
markedly ergotropic change (Hess, 1957). Thus afferent stimulation from certain
sensory and proprioceptive receptors activates the ergotropic zone, while also inhibiting
the trophotropic zone. Proprioceptive influences seem to play an important role in
these systems. In the next section the role of proprioception wi 11 be discussed.
The hypothalamus has reciprocal connections to the cortex. During periods of
emotional stress the hypothalamus is excited by pathways from the cortex (Gellhorn
and Loofbourow, 1963). In reciprocal fashion, the hypothalamus can excite the cortex.
Stimulation of the posterior hypothalamus leads to profound changes in the resting
EEG from slow alpha type waves to the faster smaller beta type waves, characteristic
of activation (Gellhorn and Loofbourow, 1963). Bernhaut, Gellhorn, and Rasmussen
(1953) found that stimulation of certain receptors leads to excitement of hypothala mus and cortex. Nociceptive, proprioceptive, auditory, and optic stimulation were used
as sensory stimulation in deeply anesthetized cats and monkeys. Proprioceptive and
nociceptive stimulation were found to be most effective in generalized cortex stimula
tion, with acoustic and optic stimulation much less effective. In fact they suggest that
proprioceptive stimulation may be more effective than nociceptive stimulation. Proprio
ception, caused by flexion and extension of a limb of an anesthetized animal leads to
excitement of the hypothalamus and diffuse cortical arousal. There seems to be a
parallelism between the degree of hypothalamic excitation and intensity and duration
of cortical excitation. Increases in hypothalamic excitation lead to enhanced cortical
excitation, while decreases in hypothalamic excitation (lesions) eliminate cortical
excitation.
Role of the endocrine system. The hypothalamus 1s the most important link
15
between the nervous system and the endocrine system, because it is instrumental in
determining the output of the anterior pituitary. In the monkey, prolonged mild
stimulation of the hypothalamus, far below threshold for rage, elicits maximal
secretion of ACTH. This effect can be blocked by lesions in the hypothalamus
(Gellhorn and Loofbourow, 1963). Mason and Brady (1957) demonstrated a sound
which symbolizes a threat is capable of producing a maximal secretion of ACTH.
The endocrine system becomes involved through the following mechanism
( Guyton, 1976): The hypothalamus secretes corticotropin releasing factor upon stress,
physical or neurogenic. These types of stress include trauma of almost any kind, such
as infection, intense heat or cold, injection of norepinephrine and other sympa
thomimetic drugs, surgical operations, restraining animal so it cannot move, and almost
any debilitating disease. Corticotropin releasing factor is secreted into the hypophyseal
portal system, carried to the hypophysis and ACTH is secreted. A few minutes after
ACTH is secreted, corticoids are released by the adrenal cortex. According to Selye's
theories ( 1956) there are two types of corticoids secreted by the adrenal cortex:
glucocorticoids, or anti-inflammatory corticoids, and mineralocorticoids, or pro
inflammatory corticoids. The two most important glucocortiraids are cortisol and
cortisone, responsible for producing the General Adaptation Syndrome (GAS) which
results from a non-specific stressor. Thus as a result of a stressful situation, the
endocrine system is mobilized by the h~
1
pothalamus, and the GAS results.
Role of proprioception. One of the early investigations on the effect of proprio
ceptive input was done by Bernhaut, Gellhorn and Rasmussen (1953). They found that
in lightly anesthetized cats, proprioceptive impulses are powerful activators of the
sympathetic division of the hypothalamus. This supports the idea that relaxation of the
skeletal musculature is accompanied by a diminution in the state of excitability of the
sympathetic division of the hypothalamus and, through a reduction in the hypotha!a
mic-cortical discharges, by a similar reduction in the state of excitability of the
cerebral cortex.
Gell horn ( 1958 a, b) has conducted some important work using the nictitating
membrane of the cat, which is under sympathetic control. Electrodes were inserted
16
into the posterior hypothalamus, the hypothalamus was stimulated, and changes in the
nictitating membrane were observed before and after administration of a curariform
drug, In a second set of experiments, the EEG was taken from the intact skull, and
potentials from the posterior hypothalamus and cortex were recorded before and after
administration of a curariform type drug. The curariform drug lntocostrin was injected
intramuscularly in both experiments. This drug served to block efferent nervous
activity to the motor end plate, which effectively relaxed the muscle and greatly
reduced proprioceptive input from the muscle. With the use of the curariform drug,
and stimulation of the posterior hypothalamus, the nictitating membrane response was
distinctly lessened compared to the control situation. With increased dosage of
intocostrin, sympathetic reactivity decreased further.
Injections of intocostrin resulted in changes in hypothalamic and cortical poten
tials, which were characteristic of decreased sympathetic reactivity. With this drug
there were marked and reversible changes in the intensity of the EEG, with a change
from small, frequent asynchronous waves to synchronoLl:;, grouped potentials. There
were also parallel changes in the hypothalamic activity. Gell horn concluded, on the
basis of alterations of the hypothalamic recordings, that this drug reduces hypothala
mic excitation. In another phase of his experiments, a weak nociceptive stimulus
produced prolonged excitation in the cortex and hypothalamus. After curarization, the
excitatory effect was greatly reduced in duration. He concluded that curarization leads
to a reduction in responsiveness of the sympathetic division of the hypothalamus to
electrical stimulation, and also to a diminished state of excitation of this structure (as
indicated by hypothalamic recordings and its frequency analysis). Gellhorn summarized
the overall conclusions by saying:
The direct and indirect (cortical) effects of the reduced hypothala
mic excitability seem to be the '.'"esult of the elimination of propriocep
tive impulses by curarization. The effects of curare suggest that the
physiological muscle tone contributes to hypothalamic and cortical
excitation. The frequently observed occurrence 9f increased muscle
tension in states of emotion seems to be not only the result of increased
central sympathetic and somatic discharges whose parallelism at the
hypothalamic level was emphasized by Hess ( 1957) but also to the
17
r '
secondary contribution of the increased proprioceptive impulses to the
state of excitation of the sympathetic division of the hypothalamus and
of the cerebral cortex. The value of a therapy of muscular relaxation
(Jacobson 1929) appears, therefore, well founded physiologically in
states of emotional tension, regardless of the mechanism by which this
relaxation is achieved. (p. 701)
Gellhorn and Loofbourow (1963) have postulated a positive feedback mechanism
of proprioceptive impulses. During the exciteq state, the reticular formation, the
cortex, and the hypothalamus all participate in the arousal process. Von Euler and
Soderberg (1956) have shown that with increased arousal (due to ARAS), there is
increased gamma activity. The small efferent gamma fiber system innervates the
contractile portions of the intrafusal muscle fibers within the muscle spindle. Midway
between the ends of the intrafusal fiber is a short non-contractile area with the
annulospiral endings. With gamma fiber stimulation, the polar regions of the intrafusal
fibers contract. If the muscle as a whole does not shorten, the central annulosphiral
regions are stretched and afferent impulses are generated. These afferent impulses serve
as a positive feedback augmenting the reticular activity, which was responsible for
initiating gamma fiber activity in the first place. Therefore, increased proprioception
(via increased muscle activity during visual and spoken imagination (Jacobson, 1955),
via the bracing reaction to stressfu I situations, or via an emotional response) may have
an effect on sensitizing the hypothalamus. Connections to the cortex, and back to the
muscle spindle may perpetuate and/or potentiate this vicious cycle. The generation of
proprioceptive input will be discussed in greater detail in the next section.
Generation of proprioceptive input. In the late 1920's and early 1930's Jacobson
provided considerable evidence regarding thought processes and muscle tension. His
view was that thought processes had a neuromuscular component, and that without
muscular contractions there could not be thought processes. In one inveistigation
{Jacobson, 1927), subjects were first trained to relax using techniques developed by
Jacobson (1938). After achieving a relaxed state, the subjects noted diminution or
disappearance of conscious processes. When asked to relax completely, and engage in
conscious activity, relaxation was found to be incompatible with the simultaneous
presence of conscious activities.
18
Jacobson ( 1930a) using sensitive E MG equipment, demonstrated that when a
subject steadily imagines bending an arm, electrical phenomena occur in that arm. In
this study 11 subjects, trained in relaxation, were monitored for electrical activity of
their arm muscles while they imagined lifting a ten-pound weight. During the imagina
tion there were electrical fluctuations, but no fluctuations occurred before or after
imagination. 93% of the tests were positive and yielded fluctuations, while controls
showed no fluctuations. The deflections averaged 300% larger than the controls. Subjec
tive results indicated that imagination ceased after they were told to relax. Reaction times
were also examined. Subjects were asked to begin imagination, and electrical activity
commenced within 0.6 seconds. On signal to relax, diminution of large deflections
occured in approximately 0.4 seconds, with complete disappearance in two seconds.
Imagination of various activities commonly performed with the right arm, such as 1)
lifting a cigarette to your mouth, 2) climbing a rope, 3) throwing a ball, 4) and turning
an ice cream freezer, resulted in clear records of increased electrical activity.
Jacobson (1930b) examined electrical activity of eye muscles which resulted from
looking to the right, left, up, and down. Subjects were then asked to use visual
imagination and recollection, and similar electrical patterns were produced.
Another study (Jacobson, 1930c) has provided evidence that with visual imagina
tion and electrical activity, there is also movement. An apparatus was constructed to
det~ct sn,all amounts of movement in the arm. Following a signal to imagine lifting
steadily a ten-pound weight, the lever records flexion of the arm, generally of
microscopic extent. This occured in all 59 tests. Microscopic flexion ceased with the
discontinuation of imagination. A control test, involving imagination with the opposite
arm, indicated no microscopic flexion.
Jacobson ( 1931 a) demonstrated that th inking about activity of the right arm is
characterized by contraction of muscle fibers in that part, or in the ocular region, or in
both. In a subsequent study (1931 b) he trained a group of subjects to achieve virtual
absence of electrical activity in the tongue. When asked to engage in mental activity
involving words or numbers, marked electrical activity occurred. On signal to relax,
electrical activity ceased.
19
The evidence presented by Jacobson substantiates the view that mental processes
contain a neuromuscular factor, or that mental activity is not confined to closed
circuits within the brain, but that neuromuscular regions participate (Jacobson, 1931 a).
In subjects who exhibit neuromuscular hypertension (elevated levels of EMG)
there is a common tendency toward excessive or persistent thinking, whether about
self, business, social affairs, or other matters (Jacobson, 1940a). According to
Jacobson:
From a physiologic standpoint, we can no longer look upon
'thinking' or mental operations in general whether devoid of emotion or
not, as processes which take place in closed circuits exclusively within
the b:ain. All the evidence has pointed to the conclusion that mental
operations include a neuromuscular component quite as essential as the
cerebral component. (p. 646)
Jacobson sugge:;ts that persistent and excessive thinking cause musculature to contract
in amounts greater than normal (elevated EMG levels) causing increased proprioceptive
input into the hypothalamic area, exciting the ergotropic zone, resulting in increased
sympathetic stimulation. This sympathetic stimulation leads in turn to increased motor
excitability and then to increased muscle tension.
Jacobson ( 1940a, 1940b) has cited evidence that this neuromuscular hypertension,
when reduced, gives rise to a corresponding reduction in both systolic and diastolic
arterial blood pressures. This would be reasonable if decreased proprioceptive input
gives rise to decreased sympathetic output.
Another line of reasoning that Jacobson employs is that throughout the day, one
is confronted by times when he must exert effort to get something completed
(Jacobson, 1955). During these efforts there is an increase in muscle tension and
therefore proprioceptive input into the hypothalamus.
Benson, Beary, and Carol (1974) put forth a possible reason for increased neuro
muscular tension as a result of the fight or flight response elicitation, with hypothala
mic stimulation, its subsequent heightened motor excitability, and subsequent
neuromuscular tension. They suggest that throughout the day the ergotropic response
is elicited a number of times in varying degrees. Situations vvhich lead to elicitation of
ergotropic responses revolve around constant insecurity in a job, inability to make
20
deadlines because of sheer weight of obligations, and situations which involve changes
in behavior (Benson, 1975). When a stressful situation occurs in civilized man, the
defense alarm reactions are produced, but the somatomotor component is usually more
or less effectively suppressed, while the visceromotor and endocrine changes occur
normally. In other words the originally well coordinated somatomotor, visceromotor,
and hormonal discharge pattern becomes dissociated (Charvat et al, 1964). They
suggest that mobilization of the cardiovascular and metabolic resources, which were to
be used for physical exertion, will not be used in a natural way; for such reasons
physiological changes can be expected to be more long-lasting than when a violent
muscular exertion ensues. One of these changes that is increased is muscle tone, with
its associated proprioceptive input into the hypothalamus, which contributes to the
positive feedback mechanism for muscle tension.
Gell horn ( 1964) presents another view for the generation of proprioceptive input,
suggesting emotions and their characteristic postures play an important role. According
to Klaesi (1953), there is loss of muscle tone in sadness and similar moods. The low
intensity of proprioceptive input in sadness gives rise to a shift in hypothalamic
balance to the parasympathetic side, which aids in the maintenance of the mood
(Gell horn, 1964). The reverse is true for happy states. Gellhorn further proposes that the
direct cause of mood appears to be a specific stimulus, mostly in the form of symbols
(words seen or heard). The posture and muscle activity play an important role in the
setting of the hypothalamic balance. He suggests tha.,t: the total quantity of proprioceptive
input impinging on the hypothalamus per unit time is of considerable importance-.
Pasquarelli and Bull (1951 ), using hypnosis, told a subject to assume a posture of
triumph, and found a depressive mood cannot be brought about unless the postural
setting is changed. In addition to posture, Gellhorn (1964) includes the effect of facial
muscles and expressions, as an important factor in proprioceptive input generation.
The "Relaxation Response"
Two conceptually different approaches for induction of the relaxation state can
be hypothesized, which are characterized by two different points of intervention into
21
the positive feedback system for muscle tension: 1) cortical intervention through
mental processes, and 2) neuromuscular intervention through muscular relaxation.
Examples of cortical intervention include Transcendental Meditation and Autogenic
Training, while Progressive Relaxation and Yoga would be examples of neuromuscular
intervention.
One might postulate the following cortical mechanism: repetition of a mantra, or
some mental device, leads to a halting of mental thinking or distracting thoughts. On the
basis of Jacobson's research (1930a, 1930b, 1930c, 1931a, 1931b), decreased mental
processes, which contain a neuromuscular component, lead to decreased muscle activity,
and therefore decreased proprioceptive input into the reticular formation and the hypo
thalamus. Concurrently, by virtue of reciprocal connections between the cortex and
hypothalamus, there would be a theoretical decrease in cortico-hypothalamic input.
One might postulate the following mechanism for neuromuscular mechanism: the
point of intervention would be at the source of the proprioceptive input, or at the
muscle. Throughout practice of muscle relaxation, decreased muscle activity leads to
decreased proprioceptive input, and therefore intervention into the positive feedback
system.
Exercise might also be considered a neuromuscular method for intervention.
Several hyptheses of intervention can be suggested. Haugen, Dixon, and Dickel (1958)
suggest that random and intermittant proprioceptive input contribute to normal
cortical activity. deVries (1975) has carried this reasoning one step further, by
suggesting that light, rhythmic exercise would provide this random and intermittant
input necessary for normal cortical activity. Additionally, Gellhorn (1958a) has shown
that increased carotid blood pressure (which would occur during exercise) gives rise to
a relaxation effect. The sympathetic division of the hypothalamus was electrically
stimulated, and the measure of sympathetic excitability of the hypothalamus was
obtained by recording the nictitating membrane, blood pressure, and heart rate.
Stimulation of hypothalamus normally causes a marked pressor effect, a distinct
contraction of the nictitating membrane, and an acceleration of the heart rate. When
carotid blood pressure increases are induced by epinephrine, the changes in the
22
nictitating membrane and heart rate are minimal, and the presser effect is converted
into a depressor action. When the sinoaortic area was denervated, there was no
reduction in sympathetic activity. This is in agreement with Koch ( 1932), who showed
that an increase in the pressure of the isolated carotid sinus induced muscular relaxa tion (as measured by decreased knee jerk) in the unanesthetized dog. Reduction of this
pressure was accompanied by an increase in neuromuscular excitement.
Benson, Beary, and Carol ( 1974) have investigated the physiological changes due
to relaxation (TM) and have designated Hess' trophotropic response the "Relaxation
Response." Numerous methods give rise to this response, such as TM, Progressive
Relaxation, Yoga, and Autogenic Training. According to Benson, Beary, and Carol
( 197 4), four elements underly all these methods: 1) a quiet environment, 2) "an object
to draw on," 3) a passive attitude, and 4) a comfortable position. Whether they are
essential and necessary for relaxation has not been determined. A quiet environment
and a comfortable position lead to decreased muscular activity and decreased proprio ceptive input. "An object to draw on" might be a mantra, concentration on relaxing a
body part, or concentration on a warm or heavy feeling in a body part, which would
lead to decreased mental thinking, and decreased muscle activity. A passive attitude
would also discourage active mental processes. The net results would be decreased
mental processes, leading to decreased muscular activity, leading to decreased proprio
ceptive input, and therefore intervention of the positive feedback system.
Measurement of Relaxation
Benson, Beary, and Carol ( 1974) have reviewed some of the physiological changes
which occur with different methods of relaxation. These results are presented in table 1.
A review of the results of Hess' experiments on cats and hypothalamic stimulation
provides the basis for choices of physiologic parameters to examine.
Hess (1957) found that stimulation of the ergotropic zone resulted in dilatation
of the pupils, increased blood pressure, increased heart rate, activation of respiration,
and heightening of motor excitability. Conversely stimulation of the trophotropic area
resulted in constriction of pupils, decreased respiration rate, decreased blood pressure
23
I\,)
~
TABLE 1
Physiologic Parameters Supporting the Existence of the "Relaxation Response"
During the Practice of Various Mental Techniques
(Adapted from Benson, Beary & Carol, 1974)
Parameter
Oxygen consumption
Respiratory rate
Heart rate
Alpha waves
Skin resistance
Blood pressure
Muscle tension
? = Inconclusive results
N.M. = Not measured
Transcendental
Meditation
decreases
decreases
decreases
increases
increases
No change
N.M.
* = Hypertensive subjects
Autogenic
Training
N.M.
decreases
decreases
increases
increases
?
decreases
Zen and
Yoga
increases
decreases
decreases
increases
increases
No change
N.M.
Progressive
Relaxation
N.M.
N.M.
No change
N.M.
N.M.
decreases*
decreases
and heart rate, and decreased motor excitability. Since relaxation brings about the
trophotropic response, these physiological changes associated with the trophotropic
state would be expected to occur as a result of relaxation training.
One might postulate measurement of muscle activity as the most important
parameter, due to the demonstrated importance of proprioceptive input. Measurement
of resting muscle electrica:--activity would be accomplished by using sensitive electro
myography (EMG) apparatus.
The EMG apparatus must be very sensitive in order to discern low level electrical
activity of the muscles during resting state. Several investigators have reported that
electrical silence is attained when the subject is told to relax completely (Basmajian,
1957; Hoefer, 1941; Hoefer and Putnam, 1939; Basmajian and Latif, 1957). However,
in several reports, Jacobson (1939c, 1940c, and 1940d) has described integrating EMG
equipment, combining very high sensitivity with a very low level of internal noise
(0.1 uV RMS). Others (deVries, 1965; Whatemore, 1962a) have developed instruments
of similar sensitivity and noise levels. Using these sensitive instruments muscle action
potentials (MAPs) have been found in muscles giving every outward· indication of being
in a state of complete rest. The difference in the results stem from measurement of
resting muscle with equipment of insufficient sensitivity.
Some question regarding the validity of low level EMG (0-10 uV), as a measure of
motor unit activity, has been raised (Joseph et al, 1955, and Hayes, 1960), and
convincing evidence has been presented that gives strong indications that even the lowest
EMG measurement reflects motor unit activity. Lippold (1952) demonstrated a linear
relationship between magnitude of muscle tension and electrical activity for voluntary
isometric contractions. de Vries ( 1965) has demonstrated a high degree of linearity
between force of contraction and integrated muscle action potentials at very low levels
(1-10 uV RMS) suggesting that even the smallest potentials recorded from the muscle
tissue with surface electrodes are probably attenuated MAPs. Jacobson ( 1943) has
demonstrated that, with relaxion training, these MAPs can be decreased, or they dis
appear. deVries et al (1976) showed highly significant correlations to exist between
integrated MAP level and concurrently measured oxygen consumption. It would seem
25
that evidence supports the concept that resting EMG measures degree of muscular
activity.
In the study of relaxation it is not possible to monitor the entire skeletal system,
nor is it practical to monitor numerous muscles. Experimental evidence has been
presented to support the concept that a general factor of resting muscle tension exists.
This means that at rest when one muscle becomes more tense, the other muscles of the
body tend to also increase in tension. In one investigation muscle tension sco es from
15 subjects, instructed to relax, were obtained concurrently from the frontalis, left
forearm extensors, extensors of the left foot, and posterior cervical muscles, and a
significant coefficient of concordance was found (Sainsbury and Gibson, 1954). This
suggests that an increase in tension in one area of the body is reliably associated with
an increase in other areas, and that a general factor of muscle tension exists.
Nidever ( 1959), in a factor analytic study, using 80 subjects, and sensitive EMG,
found a factor of general muscular tension including 19 out of 23 muscle groups. The
right biceps had the highest loading (or correlation) with this factor. Balshan (1962)
conducted an investigation similar to Nidever, using female subjects, and found a
similar factor of general muscle tension. These findings agree with the clinical findings
of Jacobson who uses the biceps as the representative muscle. Results from Nidever
(1959) plus Balshan ( 1962) showed that the frontal is muscle had insignificant correla
tions with the factor, while the limb muscles account for the highest loadings. Balshan
suggests that those muscles which are most difficult to relax (such as frontalis) are the
ones which show very little relationship with a general muscle factor.
In the measurement of muscle electrical activity one can use integrated, or non
integrated EMG measurements. Integrated EMG gives a quantified view of muscle
activity. In order to assess the total activity of a resting muscle, the integrated
approach would be more informative.
Resting oxygen consumption measurements would be a further indication of the
degree of muscle activity. Von Eiff (1952), using a math problem to create increases in
EMG, found a corresponding increase of 36% in resting oxygen consumption. In a
control situation of contempl'3tion, there was no increase in EMG, and a 1 % decrease
26
in resting oxygen consumption. de Vries et al ( 1976) found highly significant correla
tions (r = 0.58) between resting integrated muscle activity in one muscle (elbow
flexors) and total body oxygen consumption.
The hemodynamic responses due to stress include changes in heart rate, blood
pressure, and blood flow. Brod et al ( 1959) conducted a classic study involving stress
and hemodynamic changes. Using mental arithmetic and time stress created by a
metronome, they found increases in blood pressure (systolic and diastolic}, blood flow,
and heart rate. Studies involving relaxation (Wallace, 1970; Wallace and Benson, 1971;
Levander et al, 1972) found decreased heart rate and increased blood flow. There
seems to be a paradoxical situation of increased blood flow during stress and also
during relaxation. Wallace and Benson ( 1971) interpret the increased blood flow during
relaxation to be due to decreased sympathetic adrenergic activity, so that constriction
of blood vessels is decreased. More blood would flow through the capillary bed,
accounting for the decreased lactate concentration with relaxation which they found.
Brod et al ( 1959) suggest that under conditions of stress that the blood flow shifts
from the viscera to the muscles, and that this type of response closely resembles the
circulatory changes that accompany strenuous muscular exercise. They further propose
that the similarit'; of hemodynamic changes for emotion and strenuous exercise
suggests a common circulatory reaction, where muscular action might be necessary for
self preservation. Active vasodilatation results in increased blood flow through the
arterio-venous anastomoses, but not true capillaries.
Forearm blood flow is commonly measured by venous occlusion plethysmography.
Several studies suggest that blood flow is affected by anxiety. Spielberger's \ 1966)
state-trait anxiety theory postulates 2 distinct anxiety constructs. State anxiety
(anxiety state) is characterized by subjective, consciously felt periods of apprehension,
tension, and autonomic nervous system activity. Trait anxiety (anxiety trait) is seen as
the individual persons predisposition to manifest anxiety under any given stress
situation. Kelly ( 1967) has found resting forearm blood flow to be a valid and reliable
physiological index for anxiety. Blood flow correlated highly with Taylor Scale of
Manifest Anxiety in the study of 200 psychiatric patients, and 60 normal controls.
27
Gelder and Mathews ( 1968) found that forearm plethysmography can be a sensitive
indicator capable of reflecting transient increases in arousal, and suggest that forearm
blood flow measurements will be sensitive to the state-anxiety of the subject.
Analysis of Relaxation Studies
In this section of the paper the physiological effects of relaxation training will be
examined with respect to both acute and chronic effects. This section will be divided
into 6 areas: 1) Description of Relaxation Methods, 2) Progressive Relaxation, 3) Yoga,
4) Transcendental Meditation, 5) Exercise, and 6) Autogenic Training.
Description of Relaxation Methods. Numerous methods for inducing relaxation
exist, a number of which have been scientifically investigated. The most prominent of
these methods are the following: Progressive Relaxation (Jacobson, 1938), Transcen
dental Meditation (Maharishi Mahesh Yogi, 1966), Autogenic Training (Luthe, 1969),
and Yoga (Hoenig, 1968).
Progressive relaxation is a method developed by Edmund Jacobson (1938). He
suggests that anxiety and muscular relaxation produce opposite physiological states,
and therefore cannot co-exist. When a subject is asked to relax, he may still have
measurable tension in the muscle called residual tension. Progressive relaxation involves
teaching kinesthetic proprioception, which enables the subject to recognize such
residual tension, and to relieve this tension, through attaining complete electrical
silence. The subject is taught discriminative control over skeletal muscle, to recognize
and avoid the smallest contraction. The method is usually taught in a supine position,
in a quiet room, with a passive attitude. A passive attitude is important because mental
images, due to active thought processes, induce slight measurable tensions in muscles,
especially eyes and face (Jacobson, 1931a, 1931b) and prevent complete relaxation.
Throughout this method there is no hypnotic suggestion of neuromuscular relaxation.
Abbreviated relaxation training is modeled after Jacobson's concepts of Progres
sive Relaxation. The basic methods of tensing and then relaxing the muscles, in order
to learn how to recognize muscle tension, have been condensed into a 20-30 minute·
format. Instruction normally requires 1-6 sessions of instruction, with the same format
28
repeated at each session. Suggested practice is 2 periods/day, 15 minutes/period.
Transcendental Meditation is a form of Yoga developed by Maharishi Mahesh
Yogi, and is defined as: "Turning the attention inwards towards the subtler levels of a
thought until the mind transcends the experience of the subtlest state of the thought
and arrives at the source of the thought" (Maharishi Mahesh Yogi, 1966, p. 10).
Instruction is given individually by a teacher qua I ified by Maharishi Mahesh Yogi, and
can be learned in the first session, without physical or mental control. The technique is
simple, and is based on systematic method of repeating a word or sound called "the
mantra," without concentrating on it. The student practices from 15 to 20 minutes
twice a day, while sitting comfortably with eyes closed. It is claimed by proponents
(Maharishi Mahesh Yogi, 1966) that subjects experience immediately beneficial
physiologic changes.
Autogenic training 1s a method of relaxation developed by a German neurologist
H. H. Shultz, and is defined as: "A self-induced modification of corticodiencephalic
interrelationships which enables the lower brain centers to activate trophotropic
activity" ( Luthe, 1969, p. 117). Autogenic training consists of six psychophysiologic
exercises which are practiced several times a day. The goal is to shift voluntarily from
a high arousal state to a wakeful low arousal state (trophotropic state). This can be
accomplished by a group of exercises cal led the "Standard Exercises" ( Luthe, 1969).
Necessary requirements for Autogenic Training include a quiet environment, horizontal
position, eyes closed and a passive concentration on the exercises: a sort of "let it
happen" nature (Luthe, 1972). These exercises include a focusing on different feelings
and sensations in the body: 1) feeling of heaviness in the limbs; 2) sensation of
warmth in limbs; 3) heart rate regulation; 4) passive concentration of breathing; 5)
sensation of warmth in upper abdomen; and 6) feeling of coolness of forehead.
Yoga is based on the Indian culture of ancient Hindu thinkers, and involves
meditation practices and physical techniques with many variations. Hatha Yoga
involves appropriate postures and the control of respiration. Shavasana (the corpse
pose) is the yogic technique for teaching relaxation. The person practicing this method
assumes a characteristic corpse-iike supine position which promotes relaxation of the
29
musculature. The feet are apart about 9 inches, toes directed outward, hand close to
body with palms upward. The facial muscles are relaxed with the jaw slightly open.
Breathing pattern consists of a short inspiratory effort followed by a prolonged
expiratory period. Muscle groups are relaxed one group at a time with the order of
lower extremities, then the upper extremities, neck and face, and lastly the trunk.
Then the muscles of the whole body are relaxed at the same time. This is the true aim
of Shavasana. This pose is retained for 3-6 minutes.
Progressive Relaxation. Most of the earliest research m the United States on
neuromuscular tension came from Jacobson. He began his research looking for the
cause oof the "nervous start." Subjects who exhibited muscle tension, were found to
jerk more violently when they heard a sudden, loud noise. With relaxation there was
decreased jerking or no jerk at all (Jacobson, 1938).
Jacobson and Carlson (1925) used 7 subjects, trained to relax using Jacobson's
methods of Progressive Relaxation, in a test of the knee jerk response to tapping the
patellar tflndon. With extreme relaxation the knee jerk was usually absent or greatly
diminished in magnitude. After the experiment, when the subject was no longer trying
to relax, the knee jerk response was slightly increased, but still less than prior to the
relaxation. There seemed to be a "hang over" effect due to the relaxation. The fact
that the relaxation effect remained, even after the subject stopped relaxing, is one of
the bases for Jacobson formulating his ideas on Progressive Relaxation.
Miller ( 1926) trained 7 subjects to relax for 3 months, 3 times per week, 1 ½
hours per session. The subjects held their hands in salt solution, and a painful stimula
tion current was used to cause a flexion reflex. The results showed a marked decrease
in the magnitude of the flexion reflex (withdrawing the hand from the solution) due
to relaxation, and in some cases there was no movement, indicating a significant
decrease in the excitability of the musculature due to relaxation.
Jacobson ( 1928) conducted further studies on the knee jerk and relaxation. Using
21 untrained subjects who read, copied from magazines, or wrote numbers, the knee
jerk decreased over the 25 minute period. Jacobson concluded that while seated, with
no activity to legs and no emotional excitement, normal individuals become relaxed.
30
Using neurotic subjects, who were much tenser, he failed to get the same results. Then
using 14 subjects trained in relaxation, he tested them during a control period, a
relaxation period, and a post relaxation period. Jacobson found decreased knee jerk
responses during the relaxation period. After the relaxation period, the subjects were
requested to clench their fists, or to rotate their arms or to do some form of general
exercise. This activity failed to restore the knee jerk response to pre-relaxation levels.
However, stiffening the leg, which would promote strong proprioceptive input from that
leg, did restore the knee jerk.
Jacobson has done considerable amounts of clinical work using sensitive
instrumentation to measure muscle activity. As of 1937 he maintained that:
... thousands of records have been taken to date. They fail to confirm
the traditional view that healthy muscles, even in the resting state, are
always in a state of slight sustained contraction, commonly called "tonus."
They show clearly that rest in healthy man and in healthy animals may be
complete in a muscle or a nerve. (Jacobson, 1938, p. 314)
Thus complete relaxation can occur in the muscles, but although it is possible, it does
not appear to be typical except in those trained to relax.
Jacobson ( 1934a), testing students not trained to relax, found that none of the
group could maintain relaxation for the entire 30 minutes. The highest occurance of
relaxation was in one subject who could remain relaxed 79% of the time. The range in
this group was from 20% to 79% of the time.
The methodology that Jacobson used involved photograp:,ing the shadow
movement of a string galvanometer, which was recording amplified electrical activity
from wire electrodes inserted into skeletal muscle. This EMG apparatus was of very
high sensitivity and low noise level. It was not, however, an integrating EMG apparatus,
which was developed later. The critical measurements from this method of EMG
described the amplitude of the MAP, from the zero potential line to its highest point.
An adjustment was made to take into account the noise level of the system. Thus peak
microvoltages indicate the maximum microvoltages impressed during muscular
contraction upon the electrodes. These measurements were taken every centimeter
from the recording film, and only the single highest MAP per cm was recorded. When
31
the entire record was examined, and the peak microvoltages (uV) averaged, the result
was the mean peak microvoltage.
In the second part of this study (Jacobson 1934a) patients who had difficulty in
relaxing learned how to relax using Progressive Relaxation methods. In this group of 6
patients peak microvoltages ranged from 1.46 uV to 8.00 uV, with an average of
3.63 uV. In this group none could relax more than 30% of the 30 minute period. After
training the mean value decreased from 3.63 uV to 0.26 uV, after 4-9 months of
training. After training they were able to relax 81 to 98.8% of the 30 minute period,
and the variability of their microvoltages was considerably decreased.
In another study Jacobson ( 1934b) looked at the relaxation times of individuals,
and of fourteen students not trained to relax, 13 failed to relax forearm flexors within
1 second. At this interval, on the average, the mean peak microvoltage had fallen to
about 3 uV. In some instances failure to relax is prolonged for several minutes or
more. Then Jacobson selected tense patients who exhibited failure to relax upon signal
much more striking than any of the students tested. After relaxation training, the
patients all relaxed while awaiting the sig~al and they relaxed more promptly and
completely as a rule than did the untrained students at the end of one second.
Jacobson ( 1943) studied the long term effects of relaxation training on the right
quadriceps femoris. 10 one-hour periods of instruction, along with daily practice of
30-50 minutes, comprised the training periods. 10 subjects served as controls. While the
control group showed a slight increase in average microvoltages, the experimental group
showed a significant decrease from 0.83 to 0.15 uV average. The terminology in this
study had changed from mean peak microvoltage to average microvoltage, indicating a
change in the EMG apparatus to an Integrating Myovoltmeter (or Neurovoltmeter),
(Jacobson 1939c, 1940c, 1940d). Jacobson developed an integrating myovoltmeter
which was capable of measuring MAPs without photography. The MAPs were
amplified, rectified, and averaged over the 2 minute collection period. These values
(average microvoltage) were plotted against time.
Steinhaus and Norris ( 1964), in an extensive long tern1 study on the effects of
Progressive Relaxation, provided further evidence for the long terrn, chronic effects of
32
relaxation training. They conducted pre-post tests, following 8 weeks of instruction (2
times per week) using a student group (experimental group N=120, control group
N=80) and a general population group (experimental group N=81, control group
N=28). The students were members of a class on relaxation. Significant chronic
reductions in integrated EMG recordings were found. Using forehead tension measure
ments, the student group decreased some 40% from 2.27 uV to 1.36 uV, significant at
the .001 level, while no change occurred in the control group. In the general
population group there was a 26% decrease from 3.23 uV to 2.38 uV, significant at the
.001 level, with no concurrent decrease in the controls. Using arm tensions, the student
group again showed a significant decrease fr· om .57 uV to .45 uV, significant at the .05
level. There was no significant change in the control group. In the general population
there was a significant decrease from .87 uV to .60 uV, significant at the .001 level,
with no significant decrease in the controls.
The arm tension analysis for the student group 1s somewhat misleading. The
experimental group arm tensions changed from .57 uV to .45 uV, while the control
group changed from .50 uV to .38 uV. Both groups changed .12 uV in the downward
direction, with only the experimental group changes reaching significance, and the
control group changes being nearly significant. The general population arm tension
scores did exhibit greater differences between the experimental and control groups.
The experimental group changed from .87 uV to .60 uV (total change .27 uV) while
the control group changed from .39 uV to .36 uV (total change .03 uV). With the
student group, there were low levels of tension initially, and the data were therefore
not free to vary downward to any great degree. The general population experimental
group tension levels were initially higher than the control group, and therefore greater
differences between experimental and control groups could be discerned. In general,
both student and general population groups had reasonably low initial levels of muscle
tension, therefore expected changes would be small. On the basis of the foregoing
experiments there seems to be some limited evidence to support the contention that
relaxation training can enable subjects to achieve lowered chronic levels of neuro
muscular tension.
33
Steinhaus and Norris also examined changes in heart rate, respiration and arterial
blood pressure. They found no significant long term changes in heart rate and
respiratory rate. With blood pressure there was no significant change in the student
group. But with the general population, for the group with systolic blood pressure in
excess of 130 mm Hg, there was an 8 mm Hg reduction, significant at the .05 level. For
the same subjects there was a 5 mm Hg reduction in diastolic pressure, significant at
the .01 level. Blood pressure reductions seem to occur when blood pressure was in
excess of normal.
Jacobson has long maintained that Progressive Relaxation can reduce high blood
pressure (Jacobson, 1939a, b; 1940a, b; and 1947). He has many clinical examples of
blood pressure decreasing with relaxation, and has published a detailed account of one
of his subjects who showed decreased muscle tension as well as decreased blood
pressure (Jacobson, 1940a).
Steinhaus and Norris also conducted an interesting sub-experiment on the time
course of relaxation, using 31 experimental subjects, and 24 control subjects. They
tested forehead muscle tensions at 2, 4, 6, and 8 weeks, and found no significant
decreases at 2, 4, and 6 weeks, although the reductions approached significance
(change at 4 weeks was .48 uV, with a .50 uV change necessary for significance at the
.05 level). After 8 weeks there were significant changes at the .01 level. From this
Steinhaus and Norris concluded that it takes a period of time greater than 8 weeks to
achieve significant changes in physiological parameters.
This interpretation might be questioned. The muscle used for measurement was
the frontalis muscle, which has been suggested to be more difficult to relax, due to its
relation to eye and facial movements (Mathews and Gelder 1969; Balshan, 1962).
There were decreased frontalis EMG levels after 2, 4, 6, and 8 weeks, while instruction
for the frontalis muscle occurred during the 5th through 8th weeks. The EMG changes
at 2 and 4 weeks may have been due to generalized decreased muscle tension resulting
from relaxation of the rest of the body. Three weeks of practice with the frontalis
muscle relaxation might have provided a learning effect, specific for that muscle, which
accounted for the dramatic frontalis EMG reduction from the 6th week to the 8th
34
week. It might be suggested that there was some general physiological effect (due to
the relaxation training) in the first 2 to 4 weeks. This evidence may provide some
indication that a relaxation effect may occur after a relatively short amount of time,
and also provide some justification for the investigation of abbreviated muscle
relaxation training.
Grossberg ( 1965) compared abbreviated relaxation training with 2 control
procedures (instructions to rest, and listening to music), using the measures of forearm
and frontalis EMG, heart rate, and skin conductance as dependent variables. 30 male
subjects were divided into 3 groups (10 per group). There were 2 one-hour testing
sessions, spaced 5 days apart, during which the treatments were administered. Subjects
were not asked to practice relaxation exercises during the 5 days. The results indicated
no significant differences occurred among groups attributable to treatment, sessions
(first session vs. second session), or trials within sessions. According to Grossberg,
"Although analysis of variance generally indicated no overall differences among the
groups, there were some suggestions of a differential effect of relaxation exercises on
skin resistance, and a systematic decrease in forehead muscle activity of the exercise
group. These findings seem conclusive enough to warrant an expanded and improved
test of the hypothesis." Greater reductions in MAPs occurred in the relaxation group
than in the two control groups. The analysis of variance approached significance
suggesting an acute effect due to relaxation training. Son1e question regarding the
validity of EMG measurements and the sensitivity of EMG instruments was raised by
Grossberg. The forearm EMG failed to yield measurable amounts of muscular activity.
This muscle is fairly representative of body tension (Balshan, 1962; Nidever, 1959),
and consistent readings should have been recorded. This fact might indicate insufficient
sensitivity of the instrument. Grossberg did not detail specifications regarding
sensitivity and noise level for his instruments, and therefore no conclusion about these
results can be drawn.
Paul ( 1969) compared abbreviated relaxation training with relaxation induced by
hypnosis, and with a control procedure, using heart rate, skin conductance, EMG, and
respiratory rate as dependent variables. 60 female subjects were divided into 3
35
experimental conditions, and tested on 2 one-hour sessions, 7 days apart. The
relaxation group was asked to practice relaxation exercises each day during the week.
Measurements were taken during the experimental treatments. Both relaxation and
hypnotic suggestion produced significantly greater acute effects than the control group
methods in all measures (EMG reduction for the relaxation group was also significantly
greater than the hypnotic suggestion group). While Grossberg (1965) found only a trend
toward decreased EMG, Paul did find significant differences. Two major differences
between the investigations of Paul and Grossberg were evident: 1) Paul's relaxation group
practiced relaxation exercises each day, while Grossberg's relaxation group did not
practice daily, and 2) Paul used forearm extensors for EMG measurements while
Grossberg was unable to obtain readings for this muscle. Paul's EMG apparatus seems to
be more sensitive, although he does not specify sensitivity or noise levels for his
instruments. No signif_ icant chronic changes were found between first and second testing
sessions for the experimental groups, which indicated that no learning effects occurred.
However, on the basis of trends in the data, Paul suggested some chronic effect may have
occurred. The net results of Paul's investigations suggest that abbreviated relaxation
training does have an acute effect on decreased EMG during the relaxation exercises, and
that possibly there may be some chronic effect due to relaxation exercises.
Mathews and Gelder (1969), in a study using 10 phobic patients, trained subjects
to relax using 6 weekly sessions of relaxation training or control procedure. Patients were
instructed to practice a short time each day. EMG from the forearm extensor muscles,
forearm blood flow, and skin conductance were the physiological dependent variables.
Two psychological tests were also used. The results showed no significant treatment
effects. However, experimental group EMG reductions occurred in the hypothesized
direction. The number of subjects per group was 5, and one subject in the control
group had very high EMG values, which made the control data difficult to interpret.
In the second part of this study, using 14 phobic patients and brief relaxation
training for 2 weeks, a~ute physiological changes were assessed during a testing
situation. The 14 subjects were divided into two groups: 7 subjects participated in a
testing period which consisted of listening to a relaxation recording followed by a
36
control recording. The other 7 subjects reversed the order, listening first to the control
recording followed by the relaxation recording. EMG valt.:es were decreased during the
relaxation portion as compared to the control portion, which indicated that an acute
effect (during relaxation practice) occurred.
Shoemaker and Tasto ( 1975) used cassette tapes with abbreviated relaxation
instructions and found significant changes in systolic and diastolic blood pressures. 15
hypertensive subjects were instructed for 2 weeks (six sessions) on relaxation methods,
and their blood pressures compared to a control group. They showed a mean systolic
reduction of 6.8 mm Hg, and a diastolic reduction of 7.6 mm Hg., both significant values,
with no significant changes in the control group. Through the use of biofeedback in
which the subjects concentrated on decreasing the diastolic pressures, there was also a
significant decrease in diastolic pressures. One interesting subjective observation was that
when the subjects used biofeedback, their method of achieving the lowered blood
pressure had a common denominator of relaxation in the succe sful attempts.
Yoga. There have been numerous studies on Yoga. Hoenig (1968) has reviewed
the medical literature on studies concerned with physiological changes in Yoga. Anand et
al (1961) conducted the most rigorous study, having Shri Ramanand Yogi stay in a sealed
metalic box for scientific observation for 10 hours. Various physiological parameters were
monitored including oxygen consumption, heart rate, respiration, and EEG. There have
been other experiments which involved burying a subject in a pit, but it was found that
seepage of oxygen and CO
2
occurred. With Anand's study, an air tight metal container
avoided this problem. Before the experiment his basal metabolic rate was 19.5 liters of
oxygen/hour. During the first hour oxygen consumption rose to 21.3 liters/hour, and
then began to decrease, reaching the lowest level of 10 liters/hour, at the fifth hour.
Mean oxygen consumption was 13.3 liters/hour. This change in oxygen consumption is
much more than expected on the basis of sleep experiments (Anand, et al 1961 ).
The heart rate upon entry into the box was 85 beats/minute. This dropped to
60-72 beats/minute in the box. During the last hour the heart rate rose to approxi
mately 80 beats/minute due to decreased oxygen concentration and increased CO
2
concentration (15% and 5% respectively). Hoenig (1968) found a different heart rate
37
response than did Anand. There was marked variation in rate, which tended to show a
certain regularity. The rate gradually changed from 100 to 40 beats/minute, and this
change, which was gradual, repeated itself every 20 to 25 minutes.
The respiration rate was about 20/minute at entry into the box, and did not vary
significantly during the experiment until the last 2 hours. At this time it rose due to
the increased CO
2
level (5%), which has an effect on regulation of respiration. The
breathing is mostly thoracic and consists of a number of techniques called Pranayama.
The breathing pattern is irregular. Miles ( 1940), in a study analyzing different
breathing patterns, has suggested that metabolic rates during relaxed breathing were
probably near normal and that all these Yoga breathing patterns examined were found
to demand an increased oxygen consumption.
In the study by Anand et al (1961 ), 2 normal control subjects duplicated the
conditions of the experiment and there was an increase in respiration and heart rate,
with no change in oxygen consumption.
The EEG was also examined periodically and showed a dominant alpha rhythm
upon entry and at beginning of experiment. Soon after there was a change to low
voltage fast activity. This remained throughout the experiment. There were periodic
runs of prominant alpha activity and wave patterns associated with the drowsy state of
sleep. There was no typical delta rhythm associated with sleep.
Bagchi and Wenger ( 1957) suggested that one of the most striking observations of
Yogis during experiments was the almost complete immobility of a fixed posture for
such a long time. That is almost a "feat in itself." Hoenig (1968) confirmed that there
were basically no muscle artifacts during the 9 hours of EEG on some of their
experiments. This may serve as further evidence for the role of the proprioceptive
input as an important factor in relaxation, and a possible explanation for decreases in
oxygen consumption.
The effects of Yoga and blood pressure have been documented in several studies.
Datey (1969) used Shavasana as a method of blood pressure reduction. In one group,
without drugs, · the mean blood pressure was decreased from 134 to 107 mm Hg,
significant at the .05 level. In another group, who were on hypertensive drugs, the drug
38
requirement was reduced to 32% in 13 or 22 patients, which was significant at the .05
level. Other subjects in the group were not considered reliable in their daily practice
and had difficulty spending the practice time each day. The investigators theorized that
the shavasana effect was due to the slow rhythmic diaphramatic breathing, thereby
reducing the frequency and intensity of the proprioceptive and interoceptive impulses.
Patel (1973) used Yoga and biofeedback with 20 hypertensive subjects, where the
subjects acted as their own controls. Mean blood pressure drops occurred from
121 mm Hg to 101 mm Hg, despite a 41 % decrease in hypertension treatment drugs. 5
subjects stopped treatment altogether, while 7 reduced drug requirement 30-60%. 4
were not able to control blood pressure. Mean systolic drops were from 160 to
134 mm Hg, and mean diastolic drops were from 102 to 86 mm Hg.
Patel (1975) in a follow up study matched 20 subjects treated with Yoga with 20
control subjects and had them go through a similar program, with resting on a couch
replacing training in shavasana. The treatment group showed a mean systolic drop of
20.4 mm Hg, diastolic drop of 14.2 mm Hg, and the drug requirement in 12 patients
fell an average of 41 .9%. The control group showed only drops of systolic pressure of
0.5 mm Hg and diastolic pressure 2.1 mm Hg.
Transcendental Meditation. Excellent research papers (Wallace, 1970; Wallace,
Benson and Wilson, 1971; Levander et al, 1972) have recently been presented on the
acute physiological changes due to Transcendental Meditation. Wallace ( 1970) using 15
college students, who had practiced TM from 6 months to 3 years, conducted a study
measuring oxygen consumption, respiratory rate, heart rate, alpha waves, and skin
resistance. Oxygen consumption was measured, and decreased within 5 minutes after
the onset of meditation, with a mean decrease of about 20%, or 45 cm3 /minute.
Oxygen consumption remained low during meditation, and then rose toward resting
level after meditation. There was no change in respiratory quotient, with mean R of
0.85. There was a slight decrease in total ventilation, due to either decreased frequency
of breathing or decreased tidal volume. The heart rate of each of the subjects
decreased during meditation, with a mean decrease ·of 5 beats per minute.
Before meditation, with eyes closed, all subjects showed alpha activity~ During the
39
meditation the regularity and amplitude of alpha waves increased in all subjects. In
almost all subjects, alpha blocking caused by repeated sound or light showed no
habituation. After meditation regular alpha activity ccntinued when eyes were closed,
and irregular alpha activity developed when eyes were open. The EEG pattern during
meditation is different than in sleep, where slow delta waves dominate. With TM there
was also an increase in skin resistance, which decreased to resting value fol lowing
meditation. Wallace, Benson, and Wilson ( 1971) conducted another study using 36
subjects, each serving as his own control. Meditators had experience ranging from
25-108 months. There was a 17% decrease in oxygen consumption from 251 ml/
minute down to 211.4 ml/minute, rising to 242.1 ml/n1inute after meditation. There
was no change in R which remained in the normal basal range.
Minute ventilation decreased approximately 1 liter/minute and respiration
decreased m rate approximately 3 breaths/minute during meditation. Blood lactic acid
decreased 11.4 to 8.0 mg per 100 ml blood during the meditation period. The lactate
level continued to drop to 6.85 mg/100 ml during the 10 minutes after meditation,
and during the next 10 minutes rose back up to 8.16 mg/100 ml blood. This change in
lactic acid was explained on the basis of an increase in blood flow. They suggested that
meditation reduces the activity of the major part of the sympathetic nerve network, so
that its constriction of the blood vessels is absent. This allows more blood, and
therefore oxygen to reach the muscles, and therefore less anaerobic metabolism.
Riechert (1967) conducted studies using TM and showed a 300% increase 1n
forearm blood flow. Levander et al (1972) showed a much smaller, but still significant
increase in blood flow which supports the above explanation that rather small, but
consistent increases of blood flow in the resting forearm during TM are consistent with
decreased arteriolar sympathetic adrenergic activity. Wallace, Benson, and Wilson
(1971) also looked at arterial blood pressure, using an indwelling catheter, but found
no significant changes with TM. This may be explained on the basis of already low
blood pressures, averaging 106/57.
Autogenic Training. There have been numerous investigations concerned with the
physiological changes accompanying Autogenic Training. Most studies examined trained
40
subjects during practice of the first and second standard exercises, which are 1) feeling
of heaviness in limbs, and 2) sensation of warmth in limbs. However, no controlled,
long term studies, examining the chronic changes due to Autogenic training were found
in the literature. Luthe (1969) has reviewed the literature for investigations concerned
with the physiological changes due to Autogenic training.
There have been numerous studies looking at EMG changes with Autogenic
Training. von Siebenthal ( 1952) had subjects passively concentrate on the following
suggestions: 1) my left arm is heavy, 2) my right arm is heavy, or 3) both arms are
heavy. He found simultaneous decreases in muscle action potentials and an increase in
the weight of the arms in the majority of the subjects. Wittstock ( 1956) showed that
with passive concentration on heaviness, potentials of 5 uV were recorded. With
imagination the potentials increased to 20-30 uVs, and with slight movements, 50-100
uVs. Polzien ( 1955) demonstrated decreased MAPs on the m. levator ani, with passive
concentration on topographically non-specific heaviness formulae. Schultz ( 1966)
demonstrated decreased patellar reflex an1plitude during autogenic training.
Several investigators (Von Eiff and Jorgens, 1963; Kaneko, 1967; and Wallnoefer,
1968) used 4 different psychophysiologically different situations of simple rest,
listening to a cultural travel report, arithmetic calculations speed test, and Autogenic
Training to test for the effects of intermittant mechanical stimulation on MAPs. They
found no significant change in MAPs with simple rest or listening to a travel report,
while increased reflex ar.plitudes and MAPs during arithmetic calculations occurred.
With the passive concentration stage of Autogenic Training, there were decreased reflex
amplitudes and decreased MAPs.
Several blood flow experiments have been conducted with Autogenic Training in
conjunction with body temperature changes. Schultz (1926) found increased limb
temperature with Autogenic training. Benswanger (1929) demonstrated a progressive
increase in warmth as the Autogenic exercises are prolonged. Dobeta, Sugano, and
Ohno (1966) suggested that increased warmth was due to a demonstrable increase in
peripheral blood flow in arms during passive concentration on warmth in arms. Vogel
and Langen ( 1966) observed an increased blood flow in all standard exercises, when
41
done separately. However, when done in sequence, the blood flow tended to reach a
plateau and remained constant after the first two exercises.
Heart rate and blood pressure tend to decrease with Autogenic Training (Polzien,
1953, 1959). Polzien (1959), on the basis of numerous clinical observations, found an
average 5 to 25% decrease in systolic and diastolic blood pressures in most
hypertensive subjects during practice in the first 3 standard exercises. Luthe ( 1958)
found no significant changes with normotensive individuals.
Exercise. In the study of relaxation one should make mention of the
neuromuscular relaxation effects of exercise. This neuromuscular relaxation effect of
exercise has been substantiated by deVries, in a number of investigations (deVries,
1968; deVries and Adams 1972). He has adapted the hypothesis of Haugen, Dixon,
and Dickel (1958) to suggest that light to moderate physical exercise promotes random
and intermittant proprioceptive input necessary for normal cortical activity, and
therefore normal neuromuscular activity.
deVries conducted a pilot study using 8 subjects, working at 550 KgM per minute
for 30 minutes, and found small decreases in neuromuscular activity, which
approached, but did not reach significance, presumably due to the small number of
subjects.
In a subsequent study, deVries (1968) conducted a two-pronged study looking at
the short and long termed relaxation effects of exercise. 29 subjects were tested for
electrical activity in the quadriceps femoris and elbow flexors immediately before and
after exercise, and also one hour after exercise. Each subject visited the lab on 2
consecutive days, once as an exercise subject, and once as a control subject. There was
a mean decrease of 58% on the exercise day compared to the 1.5% decrease on the
control day. The change in the exercise day was significant at the .05 level of
confidence. The leg measurements showed a mean decrease of 32% for the exercise
day, and a 6% increase on the control day. These changes did not reach significance.
In the second part of the experiment, 18 subjects were instructed in a physical
fitness program consisting of barbell exercises and cardiovascular conditioning, one
hour per day, 2-3 times per week, until 17 sessions had been achieved. The groups of
42
muscles measured were the left elbow flexors, the right elbow flexors, and the right
quadriceps · femoris. The conditioning group showed a significant increase in their
maximum oxygen consumption, due to the training. The experimental group also
showed a 38% decrease in MAP levels in the right elbow flexors, significant at the .05
level. The quadriceps femoris, which showed a 50% decrease did not reach significance.
The left elbow flexor showed no change. Using the sum of the 3 muscle tensions, and
comparing the algebraic differences in the mean changes between experimental and
control groups, the control groups showed a rise in total electrical activity of 24%,
while the experimental group decreased by 24%. Difference in these changes was
significant at the .02 level of confidence. It is interesting to note that at the beginning
of the study, 6 of 11 subjects in the experimental group voiced complaints of
symptoms of neuromuscular hyperactivity, such as feelings of tenseness in muscles.
These six nervous subjects decreased by a mean percentage of 30.3, while the 5
non-nervous decreased an average of 2.3%.
de Vries ( 1970), using 112 older subjects, trained these subjects one hour per day,
3 times per week for varying lengths of time. Resting neuromuscular activity showed a
downward trend, but did not reach significance. This failure may be due to the fact
that subjects started with low scores (less than half the values found in an earlier
middle age group), and obviously data which approach electrical silence are not free to
vary downward.
de Vries and Adams ( 1972) conducted an interesting study involving the use of
meprobamate (a tranquilizing drug), and compared meprobamate to exercise as a
relaxant. Using 20 older subjects, with complaints of nervous tension, EMG readings
were taken before, immediately after, 30 minutes after, and 60 minutes after each
treatment. The treatments were as follows: 1) meprobamate 400 mg, 2) placebo
(400 mg lactose), 3) 15 minutes "walking" at heart rate of 100, 4) 15 minutes
"walking" at heart rate 120, 5) resting control. At heart rate of 100, electrical activity
decreased 20, 23, and 20% for the first, second, and third posttest respectively. These
values were significantly different from the controls at the .01 level of confidence. The
meprobamate or placebo gave no significant change. At the heart rate of 120, data
43
were more variable, and approached, but did not reach significance.
One of the therapeutic aspects of exercise has been thought to be its effect on
lowering elevated blood pressure. Boyer and Kasch ( 1970) using 23 hypertensive
subjects (diastolic pressure greater than 95 mm Hg) and 22 normotensive subjects
(blood pressure less than 140/90). Using a training program of 2 times/week for 24
weeks, there was a drop in mean diastolic pressure of 11.8 mm Hg, which was
significant at the .01 level. The mean pre value was 105, while the mean post value
was 93. The mean systolic pressure decreased 13.4 mm Hg, which was significant at
the .01 level. In the normotensive group, the mean decrease of 1 mm Hg did not reach
significance.
44
CHAPTER Ill
METHODS AND PROCEDURES
The purpose of this study was to investigate the long term effects of abbreviated
relaxation training on various physiological parameters. This chapter describes the
instrumentation and procedures used. It is divided into 4 sections: 1) subjects, 2)
experimental design, 3) instrumentation, and 4) protocol.
Subjects
Subjects for this study were solicited from the faculty, staff, and graduate school
population of the University of Southern California by means of a university newspaper
article and flyers. They were invited to an open meeting to learn more about the project.
The investigation was aimed at those who exhibited the following symptoms: 1)
difficulty in getting to sleep, 2) general nervous tension, 3) persistent feeling of tension or
strain, 4) irritability, 5) unremitting worry, 6) restlessness, 7) inability to concentrate,
and 8) feeling of panic in everyday situations. The purpose of choosing such subjects
was to provide a sample which might exhibit increased levels of electrical activity in
their muscles. Jacobson ( 1938) showed that well relaxed subjects approach EMG values
less than 1 uV at rest. Whatemore ( 1962a) reports increased neuromuscular tension for
subjects with anxiety-tension problems. He also suggested that neuromuscular relaxa
tion will relieve the tension and its associated problems. Selection of subjects with
elevated EMG scores provided a more powerful test of the experimental hypotheses.
The screening test (a 15-minute resting EMG test for the right elbow flexor
group) was used because resting EMG is one of the most important parameters investi
gated, and representative of the state of neuromuscular relaxation (Sainsbury and
Gibson, 1954; Nidever, 1959). It was also easy and quick to administer to a large
number of subjects.
From the 103 volunteers who were screened, 40 were chosen ranging in age from
45
20 to 71, with a mean age of 37. Subjects who were taking medication, tranquilizers,
sedatives, or drugs for hypertension, or who were already in relaxation programs were
screened from the program. Tables 2 and 3 give the vital data for the subjects
including EMG screening scores.
Experimental Design
Two groups of subjects (20 per group) served as control and experimental groups.
This assignment of subjects to groups was based on ranked EMG screening scores. The
40 highest EMG scores were ranked and numbered from highest (subject number 1) to
lowest (subject number 40), and divided into 2 groups. The groups were matched with
respect to EMG screening values, with the even-numbered subjects serving as the
control group and the odd-numbered subjects serving as the experimental group. This
choice of odd or even was decided on basis of chance.
Two tests were administered, before (pretest) and after (posttest) 6 weeks of
relaxation training. The experimental group participated in relaxation training 2 days
per week, with daily practice, while the control group remained on its normal
schedules. After 6 weeks both groups were given the posttest. Pre-post data for
experimental and control groups were compared for 5 parameters: right elbow flexor
group electrical activity, resting oxygen consumption, forearm blood flow, resting heart
rate, and blood pressure (heart rate and blood pressure were measured before and after
the other testing procedures).
Instrumentation
This section of the chapter discusses the instrumentation used in this study. It is
divided into 3 sections which include: 1) EMG measurements, 2) metabolic measures,
and 3) plethysmography measurements.
EMG measurements. Instruments with high sensitivity and low noise levels are
required to monitor resting EMG signals. The instrumentation for this study was
developed for these purposes and modeled after the concepts of Jacobson ( 1939c,
1940c, and 1940d).
46
Subject
1. D.A.
2. A.B.
3. J.B.
4. R.D.
5. J.E.
6. C.F.
7. G.F.
8. E.K.
9. M.L.
10. A.L.
11. J.M.
12. R.M.
13. B.M.
14. K.M.
15. s.o.
16. E.S.
17. M.T.
18. C.T.
19. c.v.
20. o.v.
Mean
S.D.
Range
TABLE 2
Description of Subjects
Experimental Group
Height
(inches)
65.00
64.00
65.00
69.25
73.00
63.50
61.00
71.00
64.50
64.00
68.75
64.50
65.00
62.00
65.75
73.50
56.00
67.00
72.50
64.00
65.96
4.34
62-73.5
\Neight
(lbs.)
151
139
145
134
173
136
96
140
187
109
185
237
155
110
138
199
106
153
185
109
149.4
36.3
96-237
Age
(years)
28
33
35
35
28
52
31
55
64
30
48
33
46
34
25
47
54
30
23
25
37.80
11.89
23-64
EMG Screening
Score (uV)
0.98
0.96
1.59
2.15
0.53
0.47
0.79
0.45
0.70
3.00
0.78
1.62
3.13
15.49
1.62
0.69
0.51
1.19
0.46
0.88
1.90
3.31
.45-15.49
47
Subject
1. L.B.
2. 8.8.
3. K.C.
4. J.H.
5. A.M.
6. B.M.
7. M.M.
8. G.P.
9. R.P.
10. D.P.
11. D.P.
12. J.R.
13. J.S.
14. G.S.
15. H.S.
16. T.T.
17. I.T.
18. A.W.
19. R.W.
20. c.z.
Mean
S.D.
Range
TABLE 3
Description of Subjects
Control Group
Height
(inches)
62.00
72.00
63.50
70.50
59.00
66.00
56.50
71.50
67.00
69.50
61.00
65.00
65.00
62.50
64.50
60.50
62.50
64.00
67.50
65.50
64.7
4.1
56.5-72
Weight
(lbs.)
104
177
118
162
116
155
118
163
171
174
102
118
118
124
130
109
100
142
i59
114
133.7
26.3
100-177
Age
(years)
25
57
33
32
20
53
71
30
32
27
54
26
21
24
46
56
27
28
31
27
36.0
14.6
20-71
EMG Screening
Score (uV)
1.62
0.51
1. 75
0.49
0.51
2.12
3.03
0.79
0.69
0.53
0.76
0.43
0.67
0.97
2.34
1.22
0.45
0.88
0.53
4.59
1.24
1.08
.43-4.59
48
The amplifier is a solid state differential voltage amplifier, that drives a voltage
controlled oscillator (VCO). The VCO converts EMG signal (summated MAPs) to a
frequency. It was designed such that 1 uV average input, at the open range of
frequency response, yields 1 pulse/second output (frequency range 1-10,000 cps).
Counting pulses gives a direct integral of EMG voltage over time, and dividing the
integral of EMG voltage by the time base gives the mean level of activity in uVs. The
range of the amplifier used in the experiment was 10-250 cps at the 3 db point.
According to Hayes ( 1960), most EMG frequency lies in this range, and little data is
lost by restricting the range. The benefit of this low range is a decreased noise level of
the amplifier. Calibration was performed using a low frequency oscillator whose signal
was attenuated by known amounts with a voltage divider system.
Electrodes were bi-polar surface electrodes, consisting of 2 vacuum cup electrodes,
mounted in lucite, with a 2 inch span between centers. Electrodes were placed on the
right arm over the belly of the biceps brachii, so that the electrodes were equidistant
about a point, midway between the antecubital space and the anterior axillary fold,
according to the methods of Davis (1959). A ground electrode was placed over the
volar aspect of the wrist. The basic noise level of the system is a function of the
source resistance. Electrode sites were abraded to reduce the source resistance to less
than 5000 ohms, which accounted for a noise level of approximately 0.3 uV. Lack of
abrasion results in increased electrical source impedance, which results in increased noise.
Figures 1 and 2 show a subject in the screen room with electrodes on the right arm, and a
basic block diagram of the EMG system respectively.
Metabolic measurements. The metabolic station consisted of three instruments: the
Beckman E2 oxygen analyzer, the Godart Capnograph, and the Parkinson-Cowan
gasometer. The subject breathed through a Daniels valve and the expired air was
collected in a 200 liter Douglas bag, and analyzed for oxygen and carbon dioxide
concentrations in the following manner. A continuous, timed sample (50 ml/minute
was drawn from the Douglas bag by a small pump and flowmeter, and passed through
a drying agent (molecular sieve). The sample was then passed into the Beckman E2
oxygen analyzer, in series with a Godart Capnograph for oxygen and carbon dioxide
49
Fig. 1. Illustration of Subject Seated 1n Screen Room with All
Instrumentation in Place.
50
(!f
EMG MONITOR
r
-------
----7
I I I
PRE H VOLTAGE I I I I
----------· AMPLIFIER CONTROLLED .,_.--.. SPEAKER I
OSCILLATOR I
I
L-----,.--
----- , ____ J
BIPOLAR
ELECTRODES
(J1
-
OSCILLOSCOPE
Fig. 2. Block Diagram of EMG Monitoring System
PULSE
COUNTER
analysis respectively. Both gas analyzers were calibrated daily, the CO
2
analyzer with a
CO
2
mixing pump, and the 0
2
analyzer using manometric techniques. Gas volume was
measured by Parkinson-Cowan gasometer. The total volume of expired air was the sum
of the volume taken for gas analysis plus the volume of gas measured by the
gasometer. All gas volumes are expressed STPD. Computations of oxygen consumption
and other derived terms were performed on a Hewlett-Packard 65 programmable
calculator. A diagram of the metabolic circuit Is shown in Figure 3, along with the
equation used for the calculation of oxygen consumption.
Plethysmography measurements. Venous occlusion plethysmography was
employed in this investigation to measure forearm blood flow, using the methods of
Graf (1964a, 1964b). A capacitive plethysmograph (Kenelco), developed by Hyman,
Burnap, and Figar ( 1963) was used. The entire system consisted of 2 occlusion cuffs, 1
capacitance cuff, a compressed air reservoir to fill the occlusion cuffs, the
plethysmography unit to transform capacitance changes into voltage changes, and a
Heathkit recorder.
The electro-capacitance cuff consisted of insulated copper wire woven into a
screen-like cuff, conical in shape, which measures changes in volume of the forearm,
when the venous retun is occluded. This cuff is placed around the largest portion of
the arm, and the circumference at the middle of the cuff is used to calculate tissue
volume. As the arm changes volume, there are concurrent changes in the screen
capacitance, which , a re converted into voltage changes and recorded on a
potentiometric recorder (Heathkit). The cuff constant was derived by calibration
procedures using a special apparatus, consisting of a mechanically expanding truncated
cone. This constant is used in the blood flow equation ( Figure 4).
Two occlusion cuffs are placed above and below the electrocapacitance cuff, and
rapidly inflated to 85 mm Hg pressure to occlude venous return (Graf, 1964a, 1964b).
The arm is placed on an arm rest, such that the elbow is at the level of the right
atrium. Prior to each measurement, a known capacitance change is induced into the
system, and this serves as a calibration of the sensitivity of the instrument and is used
in t he blood flow equation. Cuffs are inflated for 10 seconds, and voltage changes
52
(#I) Volume of expired
air in Douglas bag • 1
Return to
atmosphere
Godart
capnograph
% CO
2
(#4)
RECORDED MEASUREMENTS
Beckman E2
oxygen
analyzer
%02
(#3)
Flow
meter
50ml/min
# I volume of gas left in Douglas Bag aft er
# 2 number of minutes for gas sampling
# 3 % 02
sampling
# 4 % CO
2
PARKINSON -COWAN
GASOMETER
Pum
~
Timer
♦
Drying
tube
Minutes of
gas sampling
(#2)
CA LC ULA TIO NS : , # 2 (min.) x 5 0 m I/min. = v o I. of gas s amp I e d
Thermo meter
for gas
temperature
Douglas
bog
•
vol. of gas sampled +#I (vol. of gas left in bag)= total volume of gos in bag ( VE)
gas volumes were converted to STPD. assume F,N
2
=79.04
CJ1
w
equation for \/0
2
given: VE, % 0
2
+ %CO
2
; V0
2
(STPD)=VE(STPD)[F
1
(FE /F
1
)-FE ]
02 N2 N2 02
Fig. 3. Metabolic Circuit and Calculations for Oxygen Consumption
Volume
time
STEPS:
I. A sample blood flow tracing is shown above.
2. A line of best fit is drawn for the curve.
3, The slope of the line is determined.
4. The equation for blood flow (ml/lOOml tissue/
minute) is:
(SI ope ) (Cuff Constant)
Blood Flow=----------
(Ca libration) ( .63 c
2
)
Where :
Slope = slope of line of best fit
(volume per unit time)
.63 C - circumference coefficient using
circumference of forearm
Calibration = value for calibration test of
sensitivity of instrument ( inches
deflection per unit volume change)
Cuff Constant =value for calibration of Cuff
Fig. 4. Sample Plethysmographic Tracing and Equation for Blood Flow
Computation
54
representing volume changes are recorded on the recorder. Cuffs are then deflated and
the process repeated. Calculations are performed on the HP-65 calculator. Figure 1
shows a subject's left arm with two occlusion cuffs and one capacitance cuff.
Protocol
This section of the text wil I be subdivided into 2 sections: 1) pretest and posttest
procedures, and 2) relaxation training procedures. It will be noted that procedures for
the 15 minute screening test involved only the EMG apparatus, and only 5 one-minute
EMG integral recordings were taken, instead of the 20 30-second measurements used in
the pretest procedures. Otherwise the EMG procedures were the same as in the pretest.
Pretest and posttest procedures. All tests for this study were performed in the
exercise physiology laboratory in the Andrus Gerontology Center. Appointments were
made for the subjects to come for their pretests, and that same time was used for their
posttests. All tests were conducted between the hours of 10 a.m. and 5 p.m. and lasted
approximately 45 minutes. The subjects were requested to be post-absorptive for at
least 3 hours.
When the subject arrived at the laboratory, he filled out a general questionnaire,
and had height, weight, and age recorded. The subject then was taken into the main
lab and seated in an arm chair near the EMG station, where resting heart rate and
blood pressure were recorded. Heart rate and blood pressure were measured before and
after the testing procedures in the screen room in the effort to detect any response to
the testing procedures per se, as well as for training responses. Heart rate was recorded
using a stopwatch, which reads heart rate on basis of time for 10 beats (Lustro). Blood
pressure was recorded using an anaeroid sphygmomanometer. Systolic blood pressures
and fourth and fifth phases of diastolic pressures were recorded. At that time the right
arm EMG electrode sites vvere measured and prepared, while the left arm was measured
and prepared for placement of the plethysmograph cuffs. Measurements were taken so
that the posttest placement of the cuffs and electrodes would be identical to the
pretest placement.
The subject was then seated in a tablet arm chair in the Faraday cage, and all
55
apparatus put in place. The source impedence was checked to be sure it was less than
5000 ohms. Taped instructions were then provided and the subject was shown how
slight tensions caused an increase in sound from an audible electronic counter. The
subject was then checked for obvious tension, and allowed a short amount of time to
relax. At this time the collection of expired air began, during which 20 30-second
integrals of summated MAPs were recorded.
The left arm was then placed on the plethysmograph arm rest, and the subject
was given instructions about the forearm blood flow testing. Blood flow measurements
were taken until 12 technically acceptable measurements were recorded (Graf, 1964a,
1964b). Then the cuffs were removed, acid mantle cream applied to all abraded areas,
and the subject left the screen room. The resting heart rate and blood pressure were
recorded. At this time he was given any further instructions about what was to happen
next in the study.
The posttest procedures were identical to the pretest procedures, except that they
were conducted six weeks after the pretests.
Relaxation training procedures. The experimental group went through 6 weeks of
abbreviated relaxation training, while the control group maintained its normal schedule.
The training was led by the investigator in a room centrally located on campus.
Sessions were held daily and subjects chose 2 sessions per week, which lasted
approximately 30 minutes per session. The method used was that of Wolpe and
Lazarus ( 1966), and was modified from the work of Jacobson's Progressive Relaxation
( 1938). The instruction involved on the most part reading from a prepared script
(appendix). In the first two to three sessions, only a portion of the script was used,
and progressively more of the script was included until the whole sequence was learned
by the subjects.
The subjects lay in the supine position on plastic covered foam rubber mats.
During each session the first 5 minutes "were used to just relax the muscles, without
any contraction preceding the relaxation. Then 20 minutes involved going through the
relaxation script, including contraction, followed by relaxation. The last 5 minutes was
again used to practice relaxing the muscles.
56
After the subjects learned the techniques, differential relaxation was explained to
them, and they were requested to practice relaxation in numerous situations at work
or at home. They were also asked to practice relaxation at least once a day for 15-20
minutes, not counting the class meetings and preferably 2 times per day. The number
of practice sessions was recorded on index cards by the subjects, while attendance at
sessions was kept by the investigator.
57
CHAPTER IV
RESULTS
It was the purpose of this investigation to test the hypothesis that abbreviated
relaxation training and practice would bring about chronic reductions in EMG values,
and concurrently bring about the integrated chronic physiological changes characteristic
of the Relaxation Response. In particular, 5 sub-hypotheses could be stated. With
abbreviated relaxation training and practice the following physiological changes would
occur: 1) decreased resting muscle action potentials (MAPs), 2) decreased resting
oxygen consumption, 3) increased resting forearm blood flow, 4) decreased resting
heart rate, and 5) decreased resting arterial blood pressure.
In order to test for treatment effects due to relaxation training and practice, t
test analyses were conducted for all physiological parameters to test for significance of
differences between within group change scores (pretest minus posttest). The level of
confidence for significant differences was set at p < .05.
To test the hypothesis that experimental and control groups were drawn from the
same population with respect to dependent variables, t tests on pretest data were used
to test for the significance of differences between the control group and experimental
group for all of the dependerit variables. The only significant difference which was
found was for oxygen consumption (ml/kg). Oxygen consumption for the subjects of
the control group was greater than oxygen consumption for the experimental group
(3.38 to 3.01 ml/kg, Table 4). For this difference t = 2.48, p < .02. Of the 15
variables, only one was significantly different, and it is conceivable that this one
significant difference was due to chance.
Tables 5 and 6 present EMG data for experimental and control groups showing
mean muscle electrical activity (uVs) and standard deviation for each 30-second
interval during the EMG monitoring period. Both experimental and control groups
exhibited decreased EMG with time within each test period. The time course in EMG
58
c.n
co
Variable
HR before testing (bpm)
HR after testing (bpm)
Systolic BP before testing (mm Hg)
Diastolic BP (4th) before testing (mm Hg)
Diastolic BP (5th) before testing (mm Hg)
Systolic BP after testing (mm Hg)
Diastolic BP (4th) after testing (mm Hg)
Diastolic BP (5th after testing (mm Hg)
MAP X 1-10 (uV)
MAP X 11-20 (uV)
\/02 ( Uminute)
R
VO
2
(ml/kg)
VO2 (UM
2
)
Blood flow (ml/100 ml/minute)
TABLE 4
t Test Analysis of Pretest Data
Experimental Group
-
X SD
74.2 13.0
68.5 11.7
118.1 11.1
74.5 8.9
68.1 10.2
116.1 10.1
74.2 8.2
69.5 10.9
2.69 4.19
1.23 0.74
0.200 0.050
0.826 0.127
3.01 0.53
0.113 0.018
2.48 0.99
Control Group t
p
-
- -
X SD
74.4 13.0 -0.04 0.971
71.0 11.2 -0.69 0.495
118.9 15.7 -0.19 0.854
75.7 9.6 -0.41 0.685
70.7 9.3 -0.84 0.404
115.0 14.2 0.28 0.779
75.4 9.1 -0.42 0.676
70.2 9.4 -0.22 0.828
1.61 1.06 1.12 0.280
1.43 1.74 -0.46 0.652
0.202 0.034 -0.210 0.839
0.778 0.072 1.48 0.147
3.38 0.41 -2.48 0.018
0.122 0.015 -1.81 0.079
2.65 0.84 -0.60 0.560
TABLE 5
Mean EMG Scores of Experimental Group (30-Second Intervals)
Pretesf-· ---•-··.
Posttest
X(uV) SD(uV) X(uV) SD(uV) % change
2.69 4.19 1.57 1.34 -41.5
2.67 4.20 1.90 1.19 -47.6
2.66 4.25 1.39 1.11 -47.9
2.63 4.28 1.35 1.05 -48.7
2.51 4.25 1.28 1.01 -49.1
2.41 4.26 1.19 0.83 -50.6
2.33 4.57 1.22 0.85 -47.6
2.30 4.70 1.06 0.78 -53.8
2.21 4.56 0.98 0.74 -55.7
2.04 3.96 0.96 0.70 -52.8
1.88 3.46 0.96 0.70 -48.6
1.61 2.27 1.00 0.72 -38.0
1.52 2.38 1.00 0.72 -34.2
1.13 0.81 1.04 0.73 - 8.0
1.06 0.66 1.07 0.72 +0.9
1.11 0.73 1.07 0.70 - 3.6
1.14 0.76 1.08 0.72 - 5.8
1.18 0.78 1.10 0.73 - 6.5
1.18 0.73 1.00 0.59 -15.2
1.23 0.87 0.94 0.53 -23.3
60
TABLE 6
Mean EMG Scores of Control Group (30-Second Intervals)
Pretest Posttest
X(uV) SD(uV) X(uV) SD(uV) % change
1.61 1.06 1.39 0.96 -14.3
1.64 1.02 1.31 1.06 - 9.2
1.81 1.43 1.26 1.07 -30.3
1.74 1.35 1.16 1.07 -32.1
1.70 1.44 1.17 1.18 -30.9
1.63 1.42 1.07 0.96 -34.0
1.63 1.37 1.03 0.97 -36.7
1.57 1.31 0.94 0.89 -40.2
1.36 1.17 0.96 0.87 -29.4
1.36 1.22 0.92 0.87 -31.9
1.30 1.20 0.92 0.83 -29.5
1.28 1.23 0.89 0.86 -30.6
1.32 1.26 0.95 0.88 -28.1
1.47 1.73 0.81 0.74 -44.9
1.42 1.74 0.75 0.75 -47.4
1.33 1.67 0.76 0.76 -42.8
1.34 1.61 0.78 0.79 -41.9
1.47 1.47 0.78 0.83 -46.8
1.52 1.62 0.86 0.94 -43.3
1.43 1.73 0.82 0.93 -42.3
61
is illustrated in Figure 5, which shows mean EMG for each 30-second collection
interval for experimental and control groups, with pretest and posttest values indicated
for each group.
For the analysis of EMG scores, the 20 collection scores were divided into 2
groups (MAP 1-10 and MAP 11-20). The reason for this division was that EMG scores
tended to decrease with time in an approximate negative exponential fashion, with the
latter portion becoming asymptotic. Therefore it was postulated that MAP 1-10 might
be more characteristic of the state of the individual, whereas MAP 11-20 might be
more characteristic of the trait of the individual. Significant pretest to posttest
decreases for MAP 1-10 and 11 -20 occurred in the control group but did not reach
significance in the experimental group (Tables 7 and 8). MAP 1-10 for the control
group decreased from 1.60 to 1.12 uV (t = 2.59, p < .02), and MAP 11-20 for the
control group decreased from 1.39 to .83 uV (t =2.55, p < .02). Analysis for the
significance of differences between "within group" changes was conducted, but the
differences were not significant (Table 9), indicating no significant treatment effect.
Experimental and control groups were analyzed for significant pretest to posttest
changes for the remaining physiological parameters, and the results are presented in
Tables 7 and 9, and discussed below. The experimental group showed the following
significant pretest to posttest changes: 1) heart rate before testing (74.2 to 80.0 bpm,
,
t = 2.27, p < .05); 2) diastolic blood pressure 5th phase, before testing (68.1 to 72 mm
Hg, t = 2.21 p < .05); 3) R(.83 to .72, t = 3.85, p < .001); 4) forearm blood flow (2.48
to 3.31 ml/1 00ml/minute, t = 4.14, p < .001 ). The control group exhibited the
following significant pretest to posttest changes: 1) diastolic blood pressure 4th phase,
before testing (75. 7 to 72.5 mm Hg, t = 2.28, p < .05); 2) forearm blood flow (2.65 to
3.57 ml/1 00ml/minute, t = 4.27, p < .001); 3) oxygen consumption (.202 to .214
L/minute, t = 2.61, p < .05; 3.38 to 3.55 ml/kg, t = 2.45, p < .05; .122 to .128 L/M
2
t = 2.75, p < .05).
In order to test ·for treatment effects due to relaxation training, t test analyses
were conducted to determine significance of differences between "within group"
changes (Table 9). Significant decreases existed in diastolic blood pressure 4th phase,
62
0)
w
µV
2.8
C:r-{l- -0
''l::,
'
'
2.5f- ~
2.2
. 1.9
,o ...
/ 'O
... -0
i .6
1.3
1.0
0.70
5
'
"O ...
....
'O ... ~
'~
\
\
4-
'
'
~
\
\
\
\
------o CONTROL PRETEST
---• CONTROL POSTTEST
-- - - - -o EXPERIMENTAL PRETEST
----.a• EXPERIMENTAL POSTTEST
'
~--0
... \
'Q ~
'
\ '
' n
\ \
0--o, 'vP--o.. p-'-0..,
"O--o-..0\ '-o--O,' '()
10
COLLECTION
\
\
~
15
PERIOD
--0 ... -Cl
20
Fig. 5. EMG Time Course Showing Mean MAP Values for Each of the 20 30-Second Colledtion Periods
m
~
TABLE 7
Pretest Posttest Analysis for Experimental Group
Pretest Posttest
X SD X
HR before testing (bpm) 74.2 13.0 80.0
HR after testing (bpm) 68.5 11. 7 69.8
Systolic BP before testing (mm Hg) 118.1 11.1 116.1
Diastolic BP (4th) before testing (mm Hg) 74.5 8.9 76.2
Diastolic BP (5th) before testing (mm Hg) 68.1 10.2 72.0
Systolic BP after testing (mm Hg) 116.1 10.1 111.6
Diastolic BP (4th) after testing (mm Hg) 74.2 8.2 73.9
Diastolic BP (5th) after testing (mm Hg) 69.5 10.9 69.6
MAP X 1-10 (uV) 2.69 4.19 1.24
MAP X 11-20 (uV) 1.23 0.74 1.03
VO2 ( Uminute) 0.200 0.050 0.209
R 0.83 0.13 0.72
VO
2
(ml/Kg) 3.01 0.53 3.15
VO2 (UM
2
) 0.113 0.018 0.110
Blood Flow (ml/100 ml/minute) 2.48 0.99 3.31
t
p
-
SD
14.2 -2.27 0.035
12.0 -0.84 0.410
9.9 1.20 0.243
7.4 -1.36 0.190
9.8 -2.21 0.039
9.0 3.20 0.005
8.9 0.28 0.786
11.1 -0.06 0.950
0.88 1.34 0.195
0.65 0.97 0.344
0.04 -0.95 0.354
0.06 3.85 0.001
0.50 -1.08 0.292
0.020 -1.06 0.303
0.92 -4.14 0.001
0,
01
TABLE 8
Pretest Posttest Analysis for Control Group
Pretest Posttest
Variable X SD X
HR before testing (bpm) 74.3 12.0 77.6
HR after testing (bpm) 71.0 11.2 72.1
Systolic BP before testing (mm Hg) 118.9 15.8 117.5
Diastolic BP (4th) before testing (mm Hg) 75.7 9.6 72.5
Diastolic BP (5th) before testing (mm Hg) 70.7 9.3 67.6
Systolic BP after testing (mm Hg) 115.C 14.2 113.2
Diastolic BP (4th) after testing (mm Hg) 75.4 9.1 73.5
Diastolic BP (5th) after tes'dng (mm Hg) 70.2 9.4 67.6
MAP X 1-10 (uV) 1.60 1.17 1.12
MAP X 11-20 (uV) 1.39 1.49 0.83
VO2 ( Uminute) 0.202 0.034 0.214
R 0.78 0.07 0.70
VO
2
(ml/Kg) 3.38 0.41 3.55
VO2 (UM
2
) 0.122 01015 0.128
Blood Flow (ml/100 ml/minute) 2.65 0.84 3.57
t
p
- -
SD
13.0 -1.46 0.161
9.8 0.58 0.5666
11.6 0.49 0.630
8.6 2.28 0.034
10.6 1.68 0.110
11. 7 0.92 0.368
8.9 1.17 0.257
9.8 1.40 0.177
0.95 2.59 0.018
0.78 2.55 0.020
0.042 -2.61 0.017
0.07 4.45 0.001
0.45 -2.45 0.024
0.017 -2.75 0.013
1.13 -4.27 0.001
a,
a,
TABLE 9
t Test Analysis of Mean Difference Scores for Experimental and Control Groups
Experimental Group Control Group
Variable X SD X SD
HR before testing (bpm) -5.8 11.3 -3.3 10.1
HR after testing (bpm) -1.3 6.9 -1.1 8.4
Systolic BP before testing (mm Hg) 2.0 7.4 1.4 12.8
Diastolic BP (4th} before testing (mm Hg) -1.7 5.6 3.2 6.3
Diastolic BP (5th} before testing (mm Hg) -3.9 7.9 3.1 8.3
Systolic BP after testing (mm Hg) 4.5 6.3 1.8 8.7
Diastolic BP (4th} after testing (mm Hg} 0.3 4.9 1.8 7.1
Diastolic BP (5th} after testing (mm Hg} -0.1 7.1 2.6 8.3
MAP X 1-10 (uV) 1.20 4.01 0.48 0.83
MAP X 11-20 (uV} 0.28 1.28 0.56 0.98
VO2 ( I/minute} -0.009 0.044 -0.012 0.020
R 0.110 0.13 0.07 0.07
VO
2
(ml/kg} 0.14 0.58 0.17 0.31
VO2 (UM
2
) -0.005 0.023 -0.006 0.010
Blood flow (ml/100 ml/minute} -0.83 0.90 -0.92 0.96
t
p
-
-0.72 0.475
-0.08 0.935
0.18 0.857
-2.61 0.013
-2.74 0.009
1.12 0.269
-0.81 0.425
-1.11 0.275
0.79 0.438
0.78 0.442
0.21 0.838
1.09 0.285
0.20 0.845
0.13 0.894
0.30 0.763
before testing (t = 2.61, p < .05) and diastolic blood pressure 5th phase, before testing
(t =2. 74, p < .01) with no other significant differences found. The experimental
group's diastolic blood pressures increased from pretest to posttest ( 118/74.5/68.1 to
116/76.2/72.0), while control group's diastolic blood pressures decreased from pretest
to posttest ( 118.9/75. 7 /70.7 to 117.5/72.5/67.6). These changes did not support the
experimental hypothesis.
67
CHAPTER V
DISCUSSION
Jacobson (1943) and Steinhaus and Norris (1964) demonstrated a significant
reduction in resting EMG occurred as a result of Progressive Relaxation. Mathews and
Gelder ( 1969) used abbreviated relaxation training for six weeks and found no
significant changes in EMG due to relaxation training. The data from the current
investigation support the work of Mathews and Gelder, and suggest that abbreviated
relaxation training may not be effective in producing a reduction in resting EMG.
Tables 5 and 6, and Figure 5 show the changes in mean EMG with time, with
EMG for both groups decreasing over the 10 minute collection period in a relatively
similar fashion. The experimental group had high pretest values due to one subject
having very high EMG values. The EMG values for this subject decreased markedly
during the pretest session, dropping from 19 uV at the first 30-second interval, to
11.3 uV at the 13th interval, to 3.4 uV at the 14th interval, to 1.8 uV at the 15th
interval. These changes are readily apparent upon inspection of Figure 5. When the
subject reached lower, more normal values, the experimental group had lower mean
EMG values than the control group. At the 20th interval, mean experimental EMG was
1.23 uV, and the control value was 1.43 uV. On the posttest this subject had much
lower EMG values, measuring 4.4 uV at the first interval, and . 77 uV at the 14th
interval. Inspection of Figure 5 shows that the experimental group's mean posttest
values were far less influenced by the one subject with high EMG values than the
pretest mean values. Inspection of the last 5 intervals on Figure 5 shows that the
control group posttest values were lower than the experimental groups posttest values.
The control group also had higher pretest values than the experimental group. The data
suggest strongly that there were no chronic effects on muscle EMG due to abbreviated
relaxation training and practice.
With decreased resting EMG values one could hypothesize decreased resting
68
oxygen consumption. de Vries et al ( 1976) found a positive correlation between resting
oxygen consumption and electrical activity in the right elbow flexors. Decreases in
oxygen consumption during the practice of Transcendental Meditation have been
demonstrated (Wallace, 1970; Wallace, Benson, & Wil:;on, 1971), but no studies prior
to the present investigation were found that measured the long term, chronic changes
in resting oxygen consumption as a result of relaxation training. The hypothesized
chronic effect of decreased oxygen consumption due to relaxation training was not
found in this investigation. This might be expected because no reductions in EMG were
found for the relaxation group. There may be some question regarding the validity of
the oxygen consumption measurements, due to the very low R values (some approach ing R= .6), in the posttest measurements (Tables 7 and 8). Mean pretest values for
experimental and control groups were .83 and .78 respectively, while mean posttest
values were . 78 and . 70. During the course of the experiments there were some
concerns with the CO
2
analyzer. Although it was calibrated daily, difficulties with the
analyzer may possibly have accounted for the low R Values, and subsequent possible
errors in oxygen consumption values.
Increased resting forearm blood flows have been reported during the practice of
Transcendental Meditation ( Levander et al, 1972; Riechert, 1967). Mathews and Gelder
( 1969) studied abbreviated relaxation training effects on blood flow and found no
significant changes in experimental or control groups. Significant pretest to posttest
increases in blood flow were found in the present investigation in both control and
experimental groups, while no significant differences between the groups were found as
a result of the treatment. The pretest to posttest changes could not be accounted for.
Steinhaus and Norris ( 1964) found no significant long term changes in heart rate
and blood pressure due to relaxation training in normal subjects; with hypertensive
subjects, systolic and diastolic blood pressures showed significant reductions. The
present population of subjects in the experimental and control groups was normo
tensive (mean experimental group blood pressure was 118.1 /74.5/68.1; mean control
group blood pressure was 118.9/75. 7 /70. 7). No significant long term changes were
found with either blood pressure or heart rate.
69
In this present investigation 6 weeks of abbreviated relaxation training and
practice failed to demonstrate the hypothesized long term changes characteristic of the
Relaxation Response. This leads to the conclusion that under the conditions of this
experiment no significant measurable training effects were brought about due to
abbreviated relaxation training and practice. This conclusion casts some doubt upon
the validity of the abbreviated relaxation training methods. This investigation provided
a fair test for abbreviated relaxation methods. Six weeks of instruction (total of 6
hours) and practice were used for this test, where normally 1-6 sessions (total of 3
hours) is used in practical application. Highly sensitive EMG equipment was used to
detect any changes in resting muscle tension. The right elbow flexors were used for the
EMG measurements. This muscle group is considered to be most representative of
general muscule tension (Nidever, 1959; Balshan, 1962; deVries et al, 1976). The
integrated effect of relaxation training on the body was measured using 5 physiological
dependent variables. Mathews and Gelder ( 1969) examined several physiological and
psychological parameters, but only had a group size of 5, while this investigation had a
group size of 20, providing a much greater opportunity for small changes to attain
significance. The data from this investigation do not support the position that
abbreviated relaxation training is effective in bringing about chronic physiological
changes characteristic of the Relaxation Response. Reasons for this lack of significant
results warrant further discussion.
The first factor to be considered was the nature of the subjects. The subject
groups for this investigation were relatively normal by physiological standards. Mean
blood pressure values for the experimental group were 118.1 /74.5/68.1, while control
group had mean blood pressure values of 118.9/75. 7 /70.7 (Table 4). The mean age of
the subjects was 37. Shoemaker and Tasto (1975) found that abbreviated relaxation
training brought about changes in hypertensive subjects, but not in normal subjects,
and suggested that relaxation training brings elevated blood pressure down toward
normal levels, but not lower than normal. The screening values for EMG were also
reasonably low (Tables 2 and 3). Although the subjects in the investigation felt subjec
tively that they were tense, and seemed to show the symptoms listed in the procedure
70
section, perception may differ from actual physiological measures. Mean screening
EMG values for controls was 1.24 uV compared to 1.90 uV for the experimental
group. The experimental group had one subject with a very high screening EMG value
of 15.49 uV, which accounted for an elevated experimental group mean value. With
the exception of this one subject, the groups were relatively similar, due to matching
procedures used to divide the subjects into the control and experimental groups.
Sixty-five percent of the total subjects had screening EMG values less than 1 uV. On
the basis of EMG and blood pressure, the groups did not deviate greatly from normal,
and effects due to relaxation training and practice, had they occurred, would have
been very smal I.
A second factor to be considered was that abbreviated relaxation training methods
may be ineffective in bringing about physiological changes. It is necessary to consider 3
possibilities: 1) treatment did not occur over long enough period of time, 2) learning
sessions were not long enough in duration, or 3) the method itself is ineffective. The
first possibility, that the treatment did not occur over a long enough period of time, is
probably not valid. Common usage of abbreviated relaxation training is up to 180
minutes of instruction (1-6 sessions at 30 minutes/session), and 360 minutes of
instruction over 6 weeks was used in this investigation. However, abbreviated relaxation
training involves far less time than Progressive Relaxation. Table 10 summarizes data
regarding instruction time for each of the investigations which dealt with long term
chronic physiological changes.
The second possibility, that learning sessions were not long enough, can probably
be rejected because common usage does not exceed 30 minutes/session, the amount of
time used in the investigation (Table 10). Mathews and Gelder (1969) used one hour
sessions, and no significant results were found.
The third possibility, that the method itself is ineffective merits some further
consideration. There exist definable differences in methodology between abbreviated
relaxation training and Progressive Relaxation training. Abbreviated relaxation training
consists of one protocol, with this protocol repeated at each session. A limited amount
of time is spent on each muscle group (i.e. 4-5 minutes for the arms). Progressive
71
"
"->
INVESTIGATOR TRAINING
Weeks Session
per Week
Progressive Relaxation
1) Steinhaus &
Norris ( 1964) 8 2
2) Jacobson ( 1943) 10 1
Abbreviated Relaxation Training
3) Mathews and
Gelder (1969) 6 1
4) Present
Investigation 6 2
* I = Student Group
II = General Population
TABLE 10
Analysis of Relaxation Training Duration
NUMBER OF SUBJECTS RESULTS
Minutes Total Experimental Control
per Session Minutes
80 1280 *I 56 76 +
II 61 21
60 600 7 10 +
60 360 5 5
30 360 20 20
relaxation, on the other hand, allows much greater time for instruction. Each lesson
(normally one hour in duration) is devoted to 1 or 2 muscle groups. One may
hypothesize that during Progressive Relaxation instruction, a sufficient amount of time
is allowed for individual practice, allowing time for a genuine learning effect to occur.
However, in abbreviated relaxation, the subject merely follows directions, with little
time to practice and experiment with tensing and relaxing the muscles on his own.
This lack of practice time may limit the genuine learning effect. The abbreviated
relaxation training instructions are presented in the appendix.
Grossberg (1965), Paul (1969), and Mathews and Gelder (1969) demonstrated
decreased EMG "during" the practice of abbreviated relaxation training, indicating an
acute effect. This present investigation, as wel I as Mathews and Gelder ( 1969)
examined EMG before and after (but not during) abbreviated relaxation training. The
tensing and relaxation methods may enable a subject to achieve the acute effect of
decreased EMG levels. However, data from this study suggest that when asked to relax,
omitting the relaxation exercises, abbreviated relaxation trained subjects are not able to
relax significantly better than control subjects. This may indicate a lack of learning
effect, which may account for the lack of chronic changes due to abbreviated relaxa
tion training. However, the fact that abbreviated relaxation training brought about
reductions in blood pressure for hypertensive subjects (Shoemaker & Tasto, 1975), but
not in normotensive subjects, plus the fact that the subject population for this study
did not deviate widely from normal, suggest that abbreviated relaxation training may
have some effectiveness for subjects who have measurably elevated levels of physio
logical parameters, which are characteristic of tension.
73
CHAPTER VI
SUMMARY AND CONCLUSIONS
Summary
It was the purpose of this investigation to test the hypothesis that abbreviated
relaxation training and practice leads to chronic physiological changes. Evidence
(Benson, Beary, & Carol, 1974; Gellhorn 1958a, b), was presented which supports
existence of an integrated hypothalamic relaxation response, with muscle tension and
proprioceptive input playing an important role in the mechanism of this response. The
hypothesis was developed that with training and practice in decreasing resting muscular
activity (through relaxation training and practice), chronic physiological changes,
characteristic of the "Relaxation Response," would occur. These changes include 1)
decreased resting muscle potentials ( l\~APs), 2) decreased resting oxygen consumption,
3) increased forearm blood flow, 4) decreased resting heart rate, and 5} decreased
resting arterial blood pressure.
In this investigation 103 volunteer subjects were screened for EMG activity, and
40 subjects, with the highest EMG scores, were chosen and divided into 2 groups,
experimental and control. A pretest measuring heart rate, blood pressure, EMG, oxygen
consumption, and forearm blood flow was administered to both groups. The
experimental group underwent 6 weeks of abbreviated relaxation training and practice
(2 times/week, 30 minutes per session) using the method of Jacobson as modified by
Wolpe and Lazarus (1966), while the controls continued with their normal schedules.
An identical posttest was administered to both groups after the relaxation training
period was completed. The two groups vvere considered to be reasonably well equatec
on the basis of t test analyses of pretest data, which showed only one variable was
significantly different between control and experimental groups, which may have been
due to chance.
In order to test ·for treatment effects due to relaxation training, t test analyses
74
were conducted for all physiological parameters to test ·for significance of differences
between within group change scores (pretest minus posttest). It was found that
significant differences existed only in diastolic blood pressures 4th and 5th phases,
before testing, with no other significant differences found.
In the discussion of resu Its, reasons for the lack of significant changes due to
abbreviated relaxation training were suggested. The two major considerations were the
insufficient deviation from normalcy of subjects and questionable effectiveness of the
method itself to bring about a learning effect. It was suggested that the method does
provide some acute effects, due to tensing and relaxing the muscles, but does not yield
chronic changes for normal subjects. There is data, however, which supports the
contention that abbreviated relaxation training may be effective in subjects who have
measurable elevated levels of physiological parameters, characteristic of tension.
Conclusions
The findings suggest that under the experimental conditions of this investigation,
abbreviated relaxation training and practice over a period of 6 weeks is not effective in
bringing about chronic physiological changes characteristic of the Relaxation Response.
Recommendations
There is still a need for further investigation of the chronic physiological changes
due to abbreviated relaxation training and practice. Further investigation is needed to:
1. Test the hypothesis that chronic physiological changes can be brought about
by abbreviated relaxation training in subjects with elevated levels of physio
logical parameters, which are characteristic of tension.
2. Examine the time course changes in physiological parameters due to relaxation
training and practice over an extended period of time.
3. Examine the integrated acute physiological changes that occur during the
practice of methods other than Transcendental Meditation, 1.e. Progressive
Relaxation, Yoga (Shavasana), or Autogenic Training.
4. Examine the long term physiological changes due to relaxation training using
75
other methods of relaxation.
5. Examine the relationship between MAPs and arterial blood pressure before
and after 8 or more weeks of relaxation training, using a group of hyper
tensive subjects as the experimental group.
76
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APPENDIX I
RELAXATION TECHNIQUES*
RELAXATION OF ARMS (time: 4-5 min.)
Settle back as comfortably as you can. Let yourself relax to the best of your
ability ... Now, as you relax like that, clench your right fist, just clench your fist
tighter and tighter, and study the tension as you do so. Keep it clenched and feel
the tension in your right fist, hand, forearm ... and now relax. Let the fingers of
your right hand become loose, and observe the contrast in your feelings ... Now,
let yourself go and try to become more relaxed all over ... Once more, clench
your right fist really tight ... hold it, and notice the tension again ... Now let go,
relax; your fingers straighten out, and you notice the difference once more ...
Now repeat that with your left fist. Clench your left fist while the rest of your
body relaxes; clench that fist tighter and feel the tension ... and rKJW relax. Again
enjoy the contrast. . . Repeat that once more, clench the left fist, tight and
tense. . . Now do the opposite of tension - relax and feel the difference.
Continue relaxing like that for a while ... Clench both fists tighter and tigher,
both fists tense, forearms tense, study the sensations ... and relax; straighten out
your fingers and feel that relaxation. Continue relaxing your hands and forearms
more and more ... Now bend your elbows and tense your biceps, tense them
harder and study the tension feelings ... all right, straighten out your arms, let
them relax and feel that difference again. Let the relaxation develop ... Once
more, tense your biceps; hold the tension and observe it carefully ... Straighten
the arms and relax; relax to the best of your ability ... Each time, pay close
attention to your feelings when you tense up and when you relax. Now straighten
your arms, straighten them so that you feel most tension in the triceps muscles
along the back of your arms; stretch your arms and feel that tension ... And now
relax. Get your arms back into a comfortable position. Let the relaxation proceed
on its own. The arms should feel comfortably heavy as you allow them to
relax ... Straighten the arms once more so that you feel ~he tension in the triceps
muscles; straighten them. Feel that tension ... and relax. Now let's concentrate on
pure relaxation in the arms without any tension. Get your arms comfortable and
let them relax further and further. Continue relaxing your arms ever further. Even
when your arms seem fully relaxed, try to go that extra bit further; try to achieve
deeper and deeper levels of relaxation.
* Relaxation Script taken directly from Wolpe and Lazarus (1966, p. 259)
87
RELAXATION OF FACIAL AREA WITH NECK, SHOULDERS, AND UPPER
BACK (time: 4-5 min.)
Let all your muscles go loose and heavy. Just settle back quietly and
comfortably. Wrinkle up your forehead novv; wrinkle it tighter ... And now stop
wrinkling your forehead, relax and smooth it out. Picture the entire forehead and
scalp becoming smoother as the relaxation increases ... Now frown and crease
your brows and study the tension ... Let go of the tension again. Smooth out the
forehead once more. . . Now, close your eyes tighter and tighter . . . feel the
tension ... and relax your eyes. Keep your eyes closed; gently, comfortably, and
notice the relaxation. . . Now clench your jaws, bite your teeth together; study
the tension throughout the jaws. . . Relax your jaws now. Let your lips part
slightly ... Appreciate the relaxation ... Now press your tongue hard against the
roof of your mouth. Look for the tension ... All right, let your tongue return to
a comfortable and relaxed position. . . Now purse your lips, press your lips
together tighter and tighter ... Relax the lips. Note the contrast between tension
and relaxation. Feel the relaxation all over your face, all over your forehead and
scalp, eyes, jaws, lips, tongue and throat. The relaxation progresses further and
further ... Now attend to your neck muscles. Press your head back as far as it can
go and feel the tension in the neck; roll it to the right and feel the tension shift;
now roll it to the !eft. Straighten your head and bring it forward, press your chin
against your chest. Let your head return to a comfortable pos:tion, and study the
relaxation. Let the relaxing develop ... Shrug your shoulders, right up. Hold the
tension. . . Drop your shoulders and feel the relaxation. Neck and shoulders
relaxed. . . Shrug your shoulders again and move them around. Bring your
shoulders up and forward and back. Feel the tension in your shoulders and in
your upper back ... Drop your shoulders once more and relax. Let the relaxation
spread deep into the shoulders, right into your back muscles; relax your neck and
throat, and your jaws and other facial areas as the pure relaxation takes over and
grows deeper. . . deeper. . . ever deeper.
RELAXATION OF CHEST, STOMACH AND LOWER BACK (time: 4-5 min.)
Relax your entire body to the best of your ability. Feel that comfortable
heaviness that accompanies relaxation. Breathe easily and freely in and out.
Notice how the relaxation increases as you exhale ... as you breathe out just feel
that relaxation. . . Now breathe right in and fill your lungs; inhale deeply and
hold your breath. Study the tension ... Now exhale, let the walls of your chest
grow loose and push the air out automatically. Continue relaxing and breathe
freely and gently. Feel the relaxation and enjoy it ... With the rest of your body
as relaxed as possible, fill your lungs again. Breathe in deeply and hold it again ...
That's fine, breathe out and appreciate the relief. Just breathe normally. Continue
relaxing your chest and let the relaxation spread to your back, shoulders, neck
88
and arms. Merely let go ... and enjoy the relaxation. Now let's pay attention to
your abdominal muscles, your stomach area. Tighten your stomach muscles, make
your abdomen hard. Notice the tension ... And relax.
RELAXATION TECHNIQUES
Let the muscles loosen and notice the contrast ... Once more, press and tighten
your stomach muscles. Hold the tension and study it ... And relax. Notice the
general well-being that comes with relaxing your stomach ... Now draw your
stomach in, pull the muscl~s right in and feel the tension this way ... Now relax
again. Let your stomach out. Continue breathing normally and easily and feel the
gentle massaging action all over your chest and stomach. . . Now pull your
stomach in again and hold the tension ... Now push out and tense like that; hold
the tension ... once more pull in and feel the tension ... now relax your
stomach fully. Let the tension dissolve as the relaxation grows deeper. Each time
you breathe out, notice the rhythmic relaxation both in your lungs and in your
stomach. Notice thereby how your chest and your stomach relax more and
more ... Try and let go of all contractions anywhere in your body ... Now direct
your attention to your lower back. Arch up your back, make your lower back
quite hollow, and feel the tension along your spine . . . and settle down
comfortably again relaxing the lower back ... Just arch your back up and feel the
tensions as you do so. Try to keep the rest of your body as relaxed as possible.
Try to localize the tension throughout your lower back area ... Relax once more,
relaxing further and further. Relax your lower back, relax your upper back,
spread the relaxation to your stomach, chest, shoulders, arms and facial area.
These parts relaxing further and further and further and ever deeper.
RELAXATION OF HIPS, THIGHS AND CALVES FOLLOWED BY COMPLETE
BODY RELAXATION
Let go of all tensions and relax ... Now flex your buttocks and thighs. Flex
your thighs by pressing down your heels as hard as you can .. . Relax and note
the difference ... Straighten your knees and flex your thigh muscles again. Hold
the tension ... Relax your hips and thighs. Allow the relaxation to proceed on its
own ... Press your feet and toes downwards, away from your face, so that your
calf muscles become tense. Study that tension ... Relax your feet and calves ...
This time, bend your feet towards your face so that you feel tension along your
shins. Bring your toes right up ... Relax again. Keep relaxing for a while ... Now
let yourself relax further all over. Relax your feet, ankles, calves and shins, knees,
thighs, buttocks and hips. Feel the heaviness of your lower body as you relax still
further ... Now spread the relaxation to your stomach, waist, lower back. Let go
more and more. Feel that relaxation all over. Let it proceed to your upper back,
chest, shoulders, and arms and right to the tips of your fingers. Keep relaxing
89
more and more deeply. Make sure that no tension has crept into your throat;
relax your neck and your jaws and all your facial muscles. Keep relaxing your
whole body like that for a while. Let yourself relax.
Now you can become twice as relaxed as you are merely by taking in a
really deep breath and slowly exhaling. With your eyes closed so that you become
less · aware of objects and movements around you and thus prevent any surface
tensions from developing, breathe in deeply and feel yourself becoming heavier.
Take in a long, deep breath and let it out very slowly. Feel how heavy and
relaxed you have become.
In a state of perfect relaxation you should feel unwilling to move a single
muscle in your body. Think about the effort that would be required to lift your
right arm. As you think about raising your right arm, see if you notice any
tensions that might have crept into your shoulder and your arm ... Now you
decide not to lift the arm but to continue relaxing. Observe the relief and the
disappearance of the tension . ..
Just carry on relaxing like that. When you wish to get up, count backwards
from four to one. You should then feel fine and refreshed, wide awake and calm.
90
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Hopper, Robert Thorenz
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An investigation of the chronic physiological changes due to relaxation training and practice
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Physical Education
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1976-04
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04/01/1976
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