It has become increasingly apparent to workers in the behavioral sciences that adoption of a lifestyle that includes a daily program of vigorous physical activity is associated with many health benefits of both a physical and a mental nature.* There has been very little attention paid, however, to the psychological effects, or covariates, oíacute physical activity.
This becomes an important consideration for the psychiatrist, since acute or transitory psychological effects could occur in the absence of observable chronic effects.
For example, the primary psychological effects of daily exercise may be the reduction of tension. Tension may be reduced during the acute physical activity, but the subject's state of anxiety2 might gradually increase during the next 24 hours before he exercises again until it reached its original level - only to decrease once again following acute exercise.
If, in fact, physical activity and the state of anxiety were to covary in such a manner, chronic psychological effects of exercise might not be demonstrable.3 The chief psychological benefit of physical activity then would be seen not as its ability to reduce tension but rather as its ability to maintain a desired tension state or prevent an elevated state of anxiety.
Anxiety neurosis is a major mental-health problem in the United States today, and the psychiatrist understandably will be interested in any therapy that can be demonstrated to be useful in treating such patients. It has been reported that 10 million Americans suffer from anxiety neurosis at the present and that as many as 30 per cent of all patients seen by general practitioners are anxiety neurotics.4 It also has been estimated that between 30 and 70 per cent of all patients examined by general practitioners and internists are suffering from conditions that have their origins in unrelieved stress.5 The potential role of physical activity in the management of anxiety will be the subject of this presentation.
LACTATE METABOLISM IN ANXIETY NEUROSIS: PRO AND CON
It has always been felt by workers in the exercise and sport sciences that physical activity reduces anxiety and produces a feelingbetter sensation.6 This belief system, however, has been based largely on intuition - not research evidence. This intuitive view, which has existed in the exercise sciences, has been shared by psychiatrists. Byrd,7 for example, surveyed 54 psychiatrists and reported that 91 per cent believed that moderate exercise provides relief from tension. In a subsequent survey of 439 physicians, Byrd8 reported that 98 per cent of the respondents indicated that moderate exercise helped relieve tension. Byrd9 also studied 263 bowlers, and 87 per cent of these reported that they felt less tense after bowling.
Positive responses in such a setting, however, may reflect nothing more than compliance with the demand characteristics inherent in such a testing milieu. In view of the fact that bowling is associated with a low metabolic cost, it would be difficult to attribute reductions in anxiety to exercise. A more likely explanation would be the diversional nature of such an activity. At any rate, there seem to be many workers in the exercise and behavioral sciences who believe that physical activity reduces anxiety.
An exception to the view that exercise reduces anxiety is the position of Pitts and McClure,10 who have proposed that lactate, an exercise metabolite, can provoke anxiety symptoms and attacks in anxiety neurotics. It was reported in a subsequent paper by Pitts that "anxiety symptoms could occur in normal individuals under stress as the result of excess lactate accumulation." It has also been noted by Pitts that "the symptoms of anxiety are similar to those produced by physical activity, and exercise may intensify such reactions." The Pitts-McClure hypothesis of lactate-induced anxiety has been supported by Kelly et al.11 and Fìnk et al.,12 and these investigators have proposed the use of a "lactatetolerance test" as a means of diagnosing anxiety neurosis.
The Pitts-McClure hypothesis has been refuted in several theoretic and empiric papers that have appeared since publication of their original paper.10 It was subsequently reported by deVries13 that both acute and chronic physical activity of a vigorous nature (i.e., lactate-p reducing) reduced tension as measured electromyographically. Also, deVries and Adams14 later reported that not only does exercise reduce tension but it was more effective than meprobamate, a frequently used tranquilizer at that time, in the reduction of muscular tension.
A direct and far more convincing refutation of the Pitts-McClure hypothesis has been presented by Grosz and Farmer.15 These investigators correctly pointed out that infusion of sodium lactate, as used in the study by Pitts and McClure,10 does not produce the same physiologic changes as those that follow anaerobic exercise. Specifically, the infusion of sodium lactate results in a metabolic alkalosis, while exercise- induced elevation in lactic acid produces a metabolic acidosis. It was also found by Grosz and Farmer15 that infusion of sodium lactate also "... produces a rise in sodium bicarbonate and adaptive hypoventilation (compensatory respiratory acidosis) and concomitant feelings of discomfort" (p. 618). These investigators noted that experimentally provoked anxiety produces a lactate level of approximately 30-40 mg./100 ml., which they did not believe was sufficient to produce an anxiety attack. This seems reasonable, since maximal exercise results in lactate levels of 90-120 mg./100 ml.
Pitts and McClure10 also theorized that the anxiety symptoms and attacks observed in their study were due to hypocalcemia brought about by the lactate ions complexing with calcium. However, both Grosz and Farmer15 and Lassers and Nimmo16 reported that the fall in the amount of interstitial calcium produced with the lactate concentrations used in the Pitts and McClure10 study was not enough to account for the anxiety symptoms produced in their study.
The Pitts-McClure hypothesis of lactateinduced anxiety has become institutionalized in certain sectors of psychiatry and psychology. It is for this reason that an attempt is being made here to deinstitutionalize their hypothesis. The crucial test of the lactate hypothesis, however, entails comparison of anxiety responses to anaerobic exercise in normal and high-anxious subjects. A series of such investigations have been performed since the appearance of the initial paper by Pitts and McClure,10 and these are reviewed in the following section.
ANXIETY LEVELS FOLLOWING EXERCISE
Walking is one of the most frequently prescribed exercises,7·8 and for this reason Morgan et al.17 tested the effects of walking one mile at 3.6 mph on the state anxiety of young men and women. The subjects were randomly assigned to exercise groups that walked on level grade or 5 per cent grade, and their responses were compared with those of a control group consisting of subjects who simply rested quietly in the supine position. The control, 0-grade, and 5 per cent grade walks resulted in heart rates of 73, 126, and 144 beats per minute, respectively, for the women, and 69, 111, and 125 bpm for the men. This particular experiment did not demonstrate an exercise effect on anxiety.
One possible explanation is that exercise needs to be more vigorous in order to demonstrate an effect. A second possibility is that the anxiety scale employed in this investigation, the IPAT 8-Parallel- Anxiety Battery, was not sensitive to changes, since it appears to be more of a trait than a state measure. On the other hand, shifts in anxiety have consistently been demonstrated with this instrument under a variety of circumstances.
Sime's18 recent research indicating that light exercise does not modify state anxiety corroborates the earlier work17 reported above. It is also noteworthy that Sime employed the State-Trait Anxiety Inventory (STAI),2 which is regarded as a more appropriate measure by today's standards. These reports seem to suggest that exercise of a light nature does not alter state anxiety.
The aerobic, or non- 1 acta te-prò du ein g, work of Morgan et al.17 has been extended at the University of Wisconsin19 to include vigorous exercise. The exercise stimulus in these later investigations produced postexercise lactate values ranging from 30 mg./100 ml. to 120 mg./100 ml. The state anxiety scale was administered before and following exercise in order to quantify shifts in anxiety. In the first investigation 40 men completed the STAI before, immediately following, and 20 to 30 minutes after a vigorous physical workout lasting approximately 45 minutes. Anxiety was found to increase slightly in the immediate postexercise setting, but a substantial and significant (P <0.001) decrease below the baseline level was observed at 20 to 30 minutes postexercise. It is also noteworthy that high-anxious individuals experienced a significant reduction (P <0.05) in state anxiety.
The above findings were replicated in a second study of 15 adult males who completed the STAI (1) before a vigorous run of 15 minutes' duration, (2) five minutes following the exercise, and (3) 20 to 30 minutes following exercise. Significant decreases in state anxiety occurred in both postexercise settings.19
Subjects scoring high on tests of aerobic power are known to produce significantly less lactic acid than less fit ones. Therefore, even if anxiety neurotics produced abnormal quantities of lactic acid with exercise, this might very well reflect the level of fitness, not psychopathology.
In order to circumvent this problem, a study was carried out in which six men diagnosed as anxiety neurotics and six normals possessing comparable levels of aerobic power ran on a treadmill to complete exhaustion. The two groups possessed comparable resting lactate levels (12 mg./100 ml.), and their lactate response following maximal exercise was essentially identical (95-100 mg./100 ml.). None of the participants in this experiment experienced an anxiety attack. The findings were replicated in a subsequent study of 17 adult women and, in addition, state anxiety decreased significantly following maximal exercise in both the normal and high-anxious subjects.18
These investigations were next amplified to include additional measures of mood. The Profile of Mood States20 was administered to 16 men before and following an exercise stress test performed at 80 per cent of the individual's predicted maximum. The only factor to change was tension-anxiety, and this decrease was statistically significant.
Morgan and Horstman21 replicated these earlier findings19 measuring the anxiety state by means of the modified STAI22 during exercise, as well as before and afterwards. In this study, the subjects walked to complete exhaustion on a motor-driven treadmill operated at a speed requiring them to utilize 80 per cent of their maximal aerobic power. The experiment was carried out with two separate samples of 30 men, and the results were identical: anxiety increased during early exercise, reached an asymptote about halfway through the exercise session, and then decreased rapidly following exercise. In both experiments, lactate levels, plasma epinephrine, and plasma norepinephrine were elevated significantly. These biochemical changes in the subjects were associated with significant decreases in anxiety for both normal subjects and for those who were clinically anxious.
These two studies19'21 challenge the PittsMcClure hypothesis, for they demonstrated that vigorous physical activity was consistently observed to be associated with a significant decrease in anxiety, not only in anxious subjects, but in normal controls as well. The exercise employed in these experiments was sufficiently intense to produce significant increments in lactic acid and plasma catecholamines.
The research described above was carried out for the most part in a laboratory setting. A more recent investigation was performed by Mitchum23 in a more natural setting. Twenty males and 20 females completed the STAI before and following 15 minutes of racketball, and a significant decrement in state anxiety was observed.
The state anxiety of 62 males and 44 females was recently studied by Wood24 before and following exercise that also took place in a relatively natural setting. The STAI was completed before and following a 12-minute run. A significant decrease in state anxiety was observed for the males, but the females did not change. This finding is in disagreement with the earlier report19 that state anxiety decreases for both males and females following vigorous exercise. At any rate, there is no logical explanation as to why a sex difference should exist, and inspection of Wood's data suggests that statistical regression may have been responsible for the reported sex differences.
Additional evidence supporting the view that exercise may be useful in the management of anxiety comes from the work of Orwin.25 Orwin has employed exercise to treat agoraphobia, as well as other specific phobias. This work seems to suggest that anxiety responses can be inhibited as a result of exercise- induced arousal "competing" with the anxiety response. In other words, the perceived autonomie arousal is attributed to the exercise rather than phobic stimuli. It has also been reported by DriscolP that systematic desensitization and exercise along with "pleasant fantasies" are comparable in their ability to reduce anxiety. While exercise or fantasy alone also produced decrements in anxiety, the decreases were not as great as that produced with exercise and fantasy combined. This represents an important therapeutic point when taken in concert with the observation that many distance runners routinely fantasize during training runs as well as during competition.27,28
Persons who exercise regularly know that exercise makes them feel good. There seems to be universal agreement on this particular benefit of vigorous physical activity. Furthermore, a convincing theoretical rationale can easily be presented to explain why exercise is thought to produce positive affect. The empiric evidence reviewed in this article provides additional support for such a view in a traditional psychometric sense. In other words, significant decrements in anxiety have consistently been observed following vigorous physical activity.
A theoretic and applied issue that has not been addressed, however, relates to the important question of whether or not exercise causes tension reduction. The tacit assumption seems to have been that decreases in anxiety were preceded by exercise, and, therefore, exercise caused the tension reduction. In fact, however, there has been little if any evidence presented to support the notion of causality. If one were to assume that anxiety was reduced by exercise, another important question would be the extent to which such a treatment was more efficacious than other treatments. It would be of major theoretic and applied importance if exercise were no more effective in reducing anxiety than "passive" therapies, such as progressive relaxation, meditation, hypnosis, biofeedback, and so on.
The importance of the causality vs. association issue has been reinforced in several recent papers on anxiety management. It has been demonstrated by Michaels et al.,29 for example, that transcendental meditation (TM) is associated with a decrease in plasma epinephrine, a biochemical measure of anxiety. Hence, it would be easy to jump to the conclusion that TM causes anxiety or plasma epinephrine to decrease. However, the control group in their investigation29 experienced comparable reductions in plasma epinephrine and norepinephrine. This, of course, raises the classic question of causality, and it forces one to conclude that while TM may reduce plasma catecholamines, it is no more effective in doing so than a simple rest in a quiet room!
In a somewhat related investigation, deVries et al.30 compared the effectiveness of relaxation training and biofeedback in reducing tension as measured electromyographically. A rest break was also employed in this study as a control, and it was found that EMG activity was reduced just as much with this simple rest period.
Recent psychometric evidence31 has been presented that corroborates the above biochemical20 and ne uro physio logic30 data. In this more recent investigation Bahrke and Morgan31 randomly assigned 75 men to conditions consisting of 20 minutes of (1) exercise at 70 per cent of maximal aerobic power, (2) noncultic meditation, or (3) a control condition of quiet rest in a sound-filtered room. The exercise and meditation groups both experienced significant decreases in state anxiety, as expected. An unexpected result, however, was the observation that the control group also experienced a decrease in state anxiety. A control or placebo group was employed in an attempt to quantify the Hawthorne effect, or any treatment versus no treatment. These biochemical,29 ne uro physio logic,30 and psychometric32 findings have led Bahrke and Morgan31 to speculate that diversion, not exercise, biofeedback, or meditation, is the crucial ingrethent.
In other words, it appears that "time our," or simple rest breaks, may be effective in the management of anxiety. A common clinical observation is that many distance runners spontaneously report that running permits them to "drift away from the concerns of the day" and become deeply relaxed as a consequence.27 Needless to say, exercise causes many physiologic changes that are not observed with biofeedback, relaxation training, meditation, or "time-out" therapy. For example, substantial increases in core temperature, cardiac frequency, systolic blood pressure, ventilatory minute volume, and catecholamine production accompany vigorous physical activity, whereas the converse occurs with aforementioned "passive" therapies. Furthermore, it is possible that vigorous exercise may also alter brain biochemistry in such a way as to cause improved affect. The important point is that causal evidence has not been presented.
This represents a significant méthodologie issue in view of the observation that quiet rest breaks, or "time out," are associated with decrements in anxiety as measured biochemically,29 neurophysiologically,30 or by selfreport,31 which quantitatively equals reductions in anxiety following meditation, biofeedback, or exercise. Whether or not reduced anxiety following "time-out" therapy is qualitatively equal to more traditional approaches, such as exercise, has not yet been addressed. Also, generalizability of this experimental research to the clinical setting has not been examined.
The present clinical and experimental evidence overwhelmingly supports the view that vigorous physical activity of an acute nature is consistently associated with a decrease in state anxiety. This generalization holds for both normal and clinically anxious subjects. The view that lactate, an exercise metabolite, produces anxiety has been convincingly refuted at both a theoretical and an experimental level. It is unfortunate that exercise scientists have not addressed, at least in a serious and systematic fashion, the question of why, relative to tension reduction following vigorous physical activity. While the tacit assumption seems to be that exercise per se causes anxiety to be reduced, there has simply not been evidence presented to support causality. This is particularly important, since placebo and control conditions have been observed to be associated with comparable quantitative reductions in anxiety. It is conceivable that reduced anxiety following exercise, biofeedback, meditation, and "time-out" treatments differs qualitatively.
Future research on the efficacy of vigorous exercise in the management of anxiety should (1) focus on the mechanisms responsible for reduced anxiety, (2) determine the time course or persistence of the "exercise high," and (3) compare the qualitative effects of various therapies. At this particular point it is reasonable to conclude that acute physical activity of a vigorous nature has consistently been associated with reduced anxiety. Whether exercise causes such tension reduction, is equal or superior to traditional therapies, or persists across time remains to be demonstrated.
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