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runner's high" has even inspired a legal controversy - in 1992, a jogger who was hit by a car brought a lawsuit against the driver. The driver's attorney claimed that the jogger had acted recklessly when crossing the intersection where the accident happened - euphoria brought upon by an extended period of exercise was responsible for giving the jogger a false sense of invincibility. (Shephard 1992)If nothing else before has motivated the slothful to take up an active lifestyle, perhaps the promise of a natural high will finally lure couch potatoes away from the tube and into the gym. For years, long distance joggers and runners have reported feelings of euphoria replacing the pain of physical exertion caused by long bouts of exercise. This euphoria gives them a feeling of effortless movement and has become a mythical goal known as "the zone." (Goldberg 1988) This speculation of the existence of "
Whether or not this "runner's high" physically exists is a topic of heated debate in the scientific community. Scientists have seen many instances in which exercise has benefited the mental health of people. For one thing, physical activity can greatly improve one's self-esteem. Studies conducted on both children and clinically depressed patients show marked improvement in self-esteem, following aerobic and anaerobic exercise training. (Biddle and Mutrie 1991) Exercise does this because it creates a situation in which the participant learns to master a task, thus achieving a feeling of control over their life. Thus, exercise helps to do undo depression, which according to the "learned helplessness" theory of depression, is caused by recurring instances in which patients have no sense of control over the outcome.
The problem is, is there a biochemical explanation for this "runner's high," or is it a purely psychological event (although one can also say psychology is biochemical)? Exercise addiction, similar to substance addiction, seems to suggest that jogger's euphoria could be biochemical. There have been accounts of runners who experience withdrawal symptoms when not exercising - such as edginess, anxiety, and other unpleasant feelings. Research shows that the body produces its own opiate-like peptides, called endorphins, and like morphine, they can cause dependence (Farrell et al. 1982). Thus, this is just one hint suggesting that these "endogenous morphine" compounds may be the chemicals causing all these psychological effects of exercise. In general, endorphins are known to be responsible for pain and pleasure responses in the central nervous system.
Morphine and other opiates bind to the same receptor that the body intended for endorphins, and since we know of morphine's analgesic and euphoric effects, we can appreciate similar effects of endorphins. (Sforzo 1988)
Of all the endorphins, *-endorphin is the most potent, and thus the target of this research. Its precursor, pro-opiomelanocortin, is one of three precursor molecules which gives rise to peptides with opioid activity. Cleaved in various ways, pro-opiomelanocortin can become activated adrenocorticotropic hormone (ACTH), melanotropin (MSH) and *-lipotropin. Further processing of *-lipotropin down to a 31 amino-acid peptide results in activated *-endorphin. What's unusual about this pro-opiomelanocortin is that of all the resulting activated peptides arising from this precursor molecule, only *-endorphin has opioid activity - even its predecessor, *-lipotropin, lacks opioid function. (Sforzo 1988) *-endorphin binds best to *-opioid receptors, although it has an affinity to the other two types, *- and *-. Naloxone, a potent opioid receptor antagonist, also has a strong binding affinity to *-receptors, as does morphine. Opioid binding to receptors inhibits excitatory neural activity, by causing hyperpolarization of synaptic terminals by way of potassium channels. Given their inhibitory nature in the central nervous system, Sforzo (1988) proposes that "If a system is to be activated through opioid function at least one other neural pathway must be involved."
The endorphin hypothesis behind jogger's euphoria draws its strength from findings that show changing levels of *-endorphin in blood plasma during and after periods of exercise. Experiments have demonstrated that aerobic exercise in various forms cause *-endorphin levels to rise. Research has been conducted on both men and women who were examined while cycling, running on a treadmill, participating in aerobic dance and running marathons. In one instance, aerobic exercise caused *-endorphin levels to multiply five times greater than the normal level in the body. (Biddle and Mutrie 1991) The level of athletic training of the subjects seems to be irrelevant as both trained and untrained individuals experience an increase in *-endorphin levels, although metabolism of *-endorphin is more efficient in trained athletes (Goldfarb and Jamurtas 1997). Recently, Goldfarb et al. (1998) explored gender effects on *-endorphin production during exercise. The results showed that *-endorphin response is independent of gender, also. All of these studies have demonstrated over and over that both intensity and duration are factors in increasing *-endorphin concentrations, which means exercising at above 60% maximum oxygen uptake (VO2 max) (Goldfarb and Jamurtas 1997) and performing for a minimum of 3 minutes. (Kjaer and Dela 1996)
Scientists have taken these findings further by looking for a direct correlation between increased b-endorphin levels and mood changes (as well as analgesic effects). The current method for measuring mood involves administering the Profile of Mood States (POMS) to each subject, before and after their exercise session. Subjects assign numerical ratings to five negative categories of mood (tension, depression, anger, fatigue and confusion) and one positive category (vigor). A composite mood score is then computed by adding the five negative affects and subtracting the vigor score. To produce the most accurate psychological data, Farrell et al. (1982) took care not to inform subjects of the purpose of the study when they took the POMS questionnaire. POMS scores improved by 15 and 16 raw score units from the baseline, after subjects exercised at 60% and 8002 max. Quantitatively, mood improved about 50%, which corresponds to clinical observations that people's moods are elevated after vigorous workouts. Farrell et al. (1982) obtained seemingly parallel results in the radioimmunoassay used to measure b-endorphin concentrations in blood samples before and after exercise sessions. b-endorphin levels increased after exercise sessions at 6002 Max, 8002 Max and at a self-selected pace of exercise.
However, these results cannot prove conclusively that b-endorphin causes mood elevations, since there are some flaws in the experiment. First of all, the task of collecting accurate psychological data is difficult, since the experimental results depend solely on subjective responses from human subjects and trying to quantify them to produce objective, numerical values. Therefore, any evidence gathered from these types of studies is less convincing than rote numerical data. Moreover, statistical analyses of the mood scores failed to yield statistical significance (P> 0.05) because the subjects had high variability of moods. (Farrell et al. 1982)
Another problem recognized by Farrell et al. is that the b-endorphin measure in the experiment comes from plasma - which means that this type of b-endorphin is located in the periphery. Because of its makeup, b-endorphin can not cross the blood brain barrier back into the brain once it is released into the bloodstream. Consequently, plasma b-endorphin fluctuations do not concretely reflect b-endorphin involvement in CNS-controlled sensations of euphoria and analgesia. Some researchers claim that plasma levels do act centrally and therefore can be used to trace CNS activity (Biddle and Mutrie 1991). At this time, such a theory concerning b-endorphin can only rely on circumstantial evidence - so far, met-enkephalin and dynorphin are the only two opioids which show a modification mechanism that can transport them back across the BBB. (Sforzo 1988) Unfortunately, the only other way to measure changes in brain b-endorphin is to cut open the brain and do a radioimmunoassay on brain slices. Rat studies of this type have been done and they have shown an increase in opioid receptor binding. (Pert and Bowie 1979)
To work around this problem, researchers proposed that naloxone could be a useful tool in observing whether b-endorphin played a role in CNS-mediated responses like euphoria and analgesia. Since it is a potent m-opioid receptor antagonist, it competes with b-endorphin to bind the same receptor. Thus, injection of naloxone into human subjects should negate the euphoric and analgesic effects produced by exercise - if b-endorphin perpetrates these effects. Haier et al. (1981) found that naloxone decreased the analgesic effect reportedly caused by runner's high, but other researchers who conducted similar experiments remain divided about these results. As for naloxone's effects on mood elevation, Markoff et al. (1982) observed that naloxone did not reverse "runner's high."
Mounting evidence demonstrates that b-endorphins are not necessary for the euphoria experienced by exercise. Harte et al. (1995) noted that although exercise produces both a positive emotional effect and a rise in the levels of b-endorphin, one is not necessarily cause for the other. In other words, rising b-endorphin levels may be physiologically specific to exercise and the absence of such an event in other mood-elevating activities suggests that other links need to be explored. Meditation is one alternative activity which produces a comparable elevation in mood, although it does not involve stressing the body as in exercise. Another mood scale called visual analogue mood scale (VAMS) demonstrated that both runners and meditators experienced significant positive effects from their activities. (VAMS differs from POMS because it gives greater consideration of positive mood affects to produce a more global index of mood - happiness and relaxation are "measured" along with sadness, irritation and anxiety.) To find a biochemical explanation of these mood changes, simultaneous measurements were made of three neurohormones - corticotropin-released hormone (CRH), cortisol, and of course, b-endorphin. Meditators did not show a rise in b-endorphin levels corresponding with mood elevation, but both groups showed strong statistical correlation (p < 0.05) between positive affects of mood and CRH levels. These results seem to further question the link between b-endorphin increases and exercise-induced mood elevation, but at the same time, they don't completely discount b-endorphin involvement. (Harte et al. 1995)
Results such as these simply reinforce the fact that behavior and biochemistry share a complex relationship. Experiments in which significant amounts of b-endorphin were directly injected into the bloodstream of non-depressed subjects failed to show any changes in mood. (Biddle and Mutrie 1991) On the other hand, b-endorphin injections had an effect on clinically depressed patients. (Biddle and Mutrie 1991) Interestingly enough, electroconvulsive therapy, used to treat patients with depression, increases b-endorphin
This result, and the lack of b-endorphin release during meditation (Harte et al. 1995) calls attention to the physical stress that influences b-endorphin. In an effort to consolidate peripheral b-endorphin data with the central nervous effects, some scientists realize that the peripheral opioid system requires further investigation. Taylor et al. (1994) proposed that acidosis is the physiological trigger of b-endorphin release in the bloodstream during exercise. The results showed that blood pH strongly correlates to the b-endorphin levels (acidic conditions raise the concentration of b-endorphin, buffering the blood attenuates this response). An explanation of these events suggests that acidosis increases respiration and stimulates a feedback inhibition mechanism in the form of b-endorphin. b-endorphins interact with neurons responsible for respiratory control, and b-endorphin thus serves the purpose of preventing hyperventilation. (Taylor et al. 1994) How is this physical aspect of stress (mediated in the periphery) connected to the emotional, CNS-mediated aspect? Sforzo (1988) noted that since opioids have an inhibitory role in the CNS, he proposed that "if a system is to be activated through opioid function at least one other neural pathway must be involved." Thus, instead of trying to establish how peripheral amounts of b-endorphin act on the CNS, researchers could develop an alternate physiological model demonstrating how "anti-stress effects of opioids might be activated by inhibition of peripheral sympathetic activity." (Sforzo 1988)
While "runner's high" may never be empirically established as fact and b-endorphin's importance in this event is questionable, other studies have shown how peripheral b-endorphins affect centrally-mediated behavior. Electroacupuncture, used to treat morphine addiction by diminishing cravings and relieving withdrawal symptoms, causes b-endorphin levels to rise. (McLachlan et al. 1994) Since exercise also increases b-endorphin levels in the bloodstream, McLachlan et al. (1994) set out to observe whether exercise could decrease exogenous opiate intake. Rats were fed morphine and methadone for several days and then randomly divided into two groups of exercisers and non-exercisers. At that time, voluntary exogenous opiate intake was recorded to see if the exercise would affect the consumption of opiate in the group of exercised rats. The results showed that although both groups increased consumption of the opiate, exercised rats did not consume as much as the non-exercised rats and the difference was statistically significant. (McLachlan et al. 1994) This suggests that exercise does decrease craving. b-endorphin levels were higher in the rats that exercised, although statistical analysis failed to produce significant difference. However, this could simply mean that b-endorphin binding to receptor happens at a faster rate than b-endorphin production. (McLachlan 1994) While exercise is not a useful treatment for drug addiction, it does reinforce the positive benefits of exercise for improving mental health. More studies need to be done to ascertain whether this is because of b-endorphin fluctuations or, if other links can be established, as Harte et al. (1995) discovered.
The story of b-endorphin and "runner's high" provides valuable lessons for the scientific community. Over and over again, scientists have met dead ends in their research by trying to explain a centrally-mediated phenomenon with peripheral system data. Perhaps the next approach entails developing new models of looking at the opioid system - such as Sforzo's (1988) proposal mood enhancement can be affected via peripheral pathways. Clearly, science has not uncovered all there is to know about the opioidergic pathways, but luckily, research focusing on its effects have simultaneously allowed discovery of its components. This form of serendipitous discovery has characterized the scientific process, but it can also stall progress when scientists do not explore all the options being uncovered.
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