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American Pain Society
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Richard H. Gracely, PhD, Department Editor
Wendy F. Sternberg, PhD
Research carried out over the past three decades has demonstrated the complex nature of the pain experience. The perception of pain is not always a reflection of nociceptive activity in the periphery resulting from tissue injury. Pain can be experienced in the absence of nociception (as in many chronic pain sufferers), and it is well known that tissue damage does not always result in pain. Psychological factors also can modify the relationship between nociception and pain in a given situation. It is now well accepted that descending influences from the brain serve to modulate activity in the pain pathways that arise in the periphery such that pain perception, depending on situational factors, can be diminished or enhanced. At any time, the experience of pain is a reflection of activity in pathways ascending from the periphery to the brain and descending from the brain to the periphery. In the pain modality, as is in most sensory realms, the brain is not a passive recipient of incoming information; high-level processing modifies attributes of the peripheral stimulus (analogous to the top-down processing that prevents us from being aware of the blind spot in the visual field).
Laboratory studies of endogenous pain-modulating pathways rely on the activation of such pathways by electrical stimulation of centrifugal pain controls, pharmacological activation of receptors in the pain inhibition pathway, and environmental stressors. These methods are believed to represent different means of activating the same multifaceted analgesic substrate. Environmental stressors, such as exposure to predators and extremes in temperature or physical exertion, are believed to represent the ecologically relevant stimuli that conferred a survival advantage on these evolutionary ancestors that possessed such pain-modulating circuitry. Although pain is generally believed to be an adaptive response to tissue injury, animals that were able to ignore pain arising from injury sustained during fight-or-flight were certainly more apt to survive. Neurophysiological, pharmacological, and behavioral studies of pain-modulating circuitry have led to much useful information regarding the neuroanatomical locus and neurochemical nature of endogenous pain inhibition.
The study of stress-induced analgesia (SIA) in the laboratory is not limited to laboratory rodents. Several investigators have demonstrated nonpharmacological analgesia in humans. Vaginal stimulation (Whipple & Komisaruk, 1985), acupuncture (Clark & Yang, 1976), and anticipatory stress (Willer & Ernst, 1986) are effective in producing analgesia in the laboratory setting. The fact that psychological manipulations can produce analgesia suggests that endogenous pain inhibition in humans is under descending control. In addition, numerous anecdotal reports document reduced pain sensitivity during conditions of extreme stress, such as that experienced by soldiers in the heat of battle. Beecher (1959) noted that the pain reported by injured World War II soldiers was markedly lower than the pain reported by their similarly injured civilian counterparts. Thus, situational factors may play a modulatory role in the experience of pain in humans.
Controlled or passive studies of SIA occurring in human subjects often leads to speculation regarding the real-life experiences that trigger pain-related inhibitory mechanisms in humans. Well-publicized anecdotal reports of athletes continuing to compete despite sustaining painful injury, as well as the general belief that certain athletes (such as marathon runners, for example) have altered pain capacities when compared with nonathletes, have led us to become interested in athletes as research subjects. Specifically, we were interested in whether athletic competition represents one of the real-life experiences that serve to modulate pain perception.
The most relevant background literature for this field of study was that of exercise-related stress. In laboratory animals, forced exercise is a commonly used environmental manipulation resulting in activation of the hypothalamo-pituitary-adrenal axis and pain inhibition. In man, exercise is known to cause the release of endogenous opioids. Although some studies examining the pain-altering effects of exercise find evidence on some pain tests for exercise-induced analgesia (e.g., Janal, Colt, Clark, & Glusman, 1984; Gurevich, Kohn, & Davis, 1994), others do not (Padawer & Levine, 1992). It also been suggested that most studies in which exercise-induced analgesia has been reported are hampered by methodological problems that may confound exercise-related analgesia with repeated-testing analgesia (Padawer & Levine, 1992). A particularly well-controlled study using highly trained runners in a naturalistic setting showed that exercise reduced pain sensitivity only to low-intensity noxious stimuli but did not inhibit pain resulting from high-intensity stimuli (Fuller & Robinson, 1993). The inconsistencies in the literature led us to suspect that contrived laboratory exercise situations may fail to activate pain-inhibitory circuitry, especially in physically fit subjects or athletes. It seemed likely to us that only stressful exercise, such as that experienced during a personally meaningful competition situation (or forced exercise in physically unfit individuals), would result in pain inhibition. We set out to test this hypothesis in Haverford College varsity athletes.
As we reported in a recent issue of Pain, we found that both male and female track athletes, basketball players, and fencers exhibited altered pain sensations immediately after vigorous athletic competition compared with baseline pain measures taken 2 days prior to and 2 days after competition (Sternberg, Bailin, Grant, & Gracely, 1998). Ratings of sensory intensity and unpleasantness related to a cold pressor stimulus decreased significantly in all athletes on the day of competition. Threshold withdrawal responses to noxious heat also increased (indicating pain inhibition) as a function of competition in track runners and basketball players when heat was applied to the inner surface of their forearms, but it is interesting that sensitivity to noxious heat actually increased in all athletes (evidenced by faster withdrawal latencies on the competition day) when heat was applied to their fingertips. No changes were observed in the pain responses (withdrawal latencies and cold pressor ratings) of nonathlete controls across time, however.
Although the effect of body site on the heat withdrawal test was complex and difficult to interpret, our cold pressor findings are consistent with the hypothesis that engaging in athletic competition results in pain inhibition. The fingertips, and possibly other body sites with extremely dense peripheral sensory innervation, may experience heightened sensitivity, which could also play an adaptive role in stressful situations.
Of course, since our study examined the pain-modulating effects of athletic competition, we are unable to distinguish between the effects of exercise and the cognitive sequelae associated with stressful competition (athletes also reported greater levels of stress, anxiety, and anger on the day of competition). We are currently attempting to separate these aspects of the competitive situation by comparing the pain responses of college track athletes engaged in sedentary competition (a head-to-head video racing game), solitary exercise (running on a treadmill), and athletic competition (track meet). We suspect that these well-conditioned track runners will experience minimal levels of analgesia as a result of running on a treadmill, and more pronounced analgesia from sedentary competition. It is expected that pain responses will be most profoundly altered from baseline levels during the competitive situation. Thus, we suspect that the cognitive state is a sufficient condition to activate pain-modulatory circuitry, although a combination of exercise and competition will result in the greatest changes from baseline responses to pain.
Competitive athletes represent a unique population for studying pain and related phenomena. Several investigators have addressed the hypothesis that athletes are different from other individuals in terms of their pain threshold and tolerance. Some support for this idea exists, although as in the exercise literature, reports have conflicted with each other. One particularly relevant factor appears to be the noxious stimulus that is employed. Athletes have been shown to be less sensitive to noxious cold and more tolerant to ischemic stimulation and noxious pressure than nonathletes but not different in their responses to noxious heat (Hall & Davies, 1991; Janal, Glusman, Kuhl, & Clark, 1994; Jaremko, Silbert, & Mann, 1981; Ryan & Kovacic, 1966; Scott & Gijsbers, 1981).
In our study on athletic competition, we compared the basal pain responsiveness of athletes and nonathletes; male runners and basketball players showed significantly lower cold-pressor-related pain intensity ratings than male nonathletes. The pain ratings of male fencers were intermediate when compared with the ratings of the other athletes and the nonathlete controls but not significantly different from any other group. Upon careful examination of our cold-pressor-related data, it appeared that fencers were more similar to nonathletes than they were to basketball players or track runners. The rate of rise in cold-pressor-related ratings was remarkably similar in fencers and nonathletes. In these groups, initial pain ratings were in fact lower than in basketball players and track runners (who were no different from each other) but became higher than those of the other athletes by the time 60 seconds had elapsed after immersion of an arm in the cold water. Subjects reported the frequency with which they used ice as a therapeutic tool. Fencers and nonathlete controls used ice less frequently than track runners and significantly fewer times per week than basketball players. Perhaps the frequency with which subjects were exposed to extreme cold contributed to the effect of participation in a sport on cold-pressor-related pain ratings and the rate at which they increased. These apparent differences in some measures of pain perception may be due to any number of factors. For example, one criterion for becoming a competitive athlete may be a relatively high pain tolerance that enables a person to effectively cope with pain associated with training and exertion. Conversely, frequent experience with varying degrees of pain may alter future pain reports. Indeed, Janal et al. (1994) attribute the higher threshold of runners to noxious cold to their experience with exposure to very low temperatures.
The unique experiences of competitive athletes with pain make them ideal subjects for future study.
The research described above indicates that situational factors can influence competitive athletes' reports of pain, and that athletes and nonathletes can have different criteria for labeling stimuli as painful. Competitive athletes and the psychological and physical factors associated with competition represent an interesting avenue for future research about pain modulation. Such studies could prove useful for athletic trainers and coaches who assess the condition of injured athletes. Self-reports of pain during competition may not be reflective of the true nature of an injury. Failure to attend to real or potential tissue damage during the course of a competition can impair recovery and healing, diminish athletic performance, and can ultimately lead to chronic pain conditions.
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Wendy F. Sternberg is a professor in the department of psychology at Haverford College in Haverford, PA.
