Competition/Exercise and Pain 1 Running Head: EFFECTS OF COMPETITION AND EXERCISE ON PAIN The Effects of Competition and Exercise on Pain Perception

One of the most ubiquitous examples of stress-induced analgesia that is easily observed is the pain reduction athletes experience during competition. There is anecdotal evidence for this phenomenon but there is an omission in the literature of conclusive systematic investigations of athletes' responses to noxious stimuli under competitive stress. The purpose of the present study was to examine the nature of stress involved in interpersonal competition, and to determine which component of athletic competition, psychological stress or physical exertion, is a trigger for endogenous pain inhibitory systems. The results demonstrate stress-induced analgesia as a result of strenuous exercise in athletes and non-athletes—an increase in pain threshold and a reduction in pain ratings that increases under competitive stress. The present study will add to the research on the contribution of stress to athletic competition induced analgesia and identifies how the circumstances necessary to elicit a stress-induced analgesic response during competition interact with gender and athletic status. Competition/Exercise and Pain 3 The Effects of Competition and Exercise on Pain Perception In competition athletes will often continue to compete even after sustaining painful injuries. The ability of athletes to perform when injured is anecdotal evidence of pain modulation systems in humans responsible for a reduction in sensitivity to noxious stimuli. The effective inhibition of nociceptive afferent fibers is a form of endogenous analgesia. Environmental stressors such as threatening or aversive events can activate the mechanisms of this system. The existence of “stress-induced analgesia” has been well established in laboratory animals but few studies have reliable evidence of analgesic states in human subjects confronted with stressors in experimental or naturalistic situations. The objective of the present experiment is to systematically study the effects of competitive exercise on the perception of noxious stimuli. Previous studies have shown that competing in athletic events can produce analgesic states in college athletes (Sternberg, Bailin, Grant, & Gracely, 1998; Sternberg, Bokat, Kass, Alboyadjian, & Gracely, 2001). Efforts were made to discriminate between the different components of competition, the physical exertion involved in competition and the cognitively stressful components of competition that are independent of exercise. Researchers demonstrated that there are differences in the analgesic effects produced by the different components of the experience of competition, and that these differences may be sex dependent. In females, a low intensity treadmill run produced analgesia, whereas in males only, sedentary video game competition had this effect (Sternberg et al., 2001). However, the exercise component of that previous study may not have been significantly stressful enough to elicit a stress-induced analgesic response in males. In response to these findings researchers suggest that exercise produces analgesia if, perhaps only if, it is construed as stressful (Sternberg et al., 2001). Competition/Exercise and Pain 4 Thus, based on previous research the hypothesis of the present study is that physical exertion must include some element of “stress” in order to activate pain suppressing mechanisms. The goal of the present study is to examine this phenomenon by manipulating the psychological state associated with interpersonal competition while holding physical exertion constant. In the current experiment, subjects will exercise and also participate in contrived competition while physical exertion remains the same under both conditions. This design will allow the experimenters to address the question of whether or not the exercise component of competition is solely responsible for the observed analgesic effects, or if there is something unique about the notion of interpersonal competition—if competition is an environmental stressor capable of activating the pain suppressing mechanism of stress-induced analgesia. Nociception, Pain and Analgesia The physiological system being studied in the current experiment is the neural mechanism of pain perception. Noxious stimuli applied to the skin activate specialized sensory receptors called nociceptors (Basbaum & Jessell, 2000). There are different classes of nociceptors that differ in mode of activation, speed of transmission and size. For example, some Aδ fibers are thermal nociceptors, myelinated, small in diameter (2-5 μM), and are activated by extreme temperatures (greater than 45°C and less than 5°C). Polymodal nociceptors, C fibers are unmyelinated and have the smallest diameter (0.3-3.0 μM). Polymodal axons like C fibers are activated by chemical, mechanical, and thermal stimuli. These primary afferent nociceptors are characterized by different rates of conduction; C axons conduct signals at velocities less than 1-2 m/s whereas Aδ fibers conduct signals at 5-30 m/s (Basbaum & Jessell, 2000; Fields, 1987). Not only do nociceptive C primary afferents constitute the majority of axons in peripheral nerves, but experimental evidence has also demonstrated that C and Aδ nociceptors are the primary Competition/Exercise and Pain 5 contributors to pain sensation. They are also responsible for the quality and intensity of the sensation (Fields, 1987). Nociceptors have peripheral terminals innervated throughout the skin. Transduction begins in the primary afferent with the activation of receptors in peripheral tissues in the form of chemical, mechanical, or thermal energy, which is then converted into electrochemical nerve impulses. The coded information is then transmitted to structures in the central nervous system. Specifically, primary afferent nociceptors terminate in the dorsal horn of the spinal cord and activate ascending tracts that relay the pain message to the brain. There are nociceptive-specific neurons that respond exclusively to noxious stimulation, and these signals ascend to the brainstem, through the thalamus, and finally to the cortex to be processed (Fields, 1987; Basbaum & Jessell, 2000). It is important to recognize the distinction between nociception and pain perception. As Basbaum and Jessell (2000) explain, while nociceptors are activated by noxious stimuli, pain is a mental perception, “An unpleasant sensory and emotional experience...[is] a product of the brain’s elaboration of sensory input,” which is separate from the actual neural mechanics of the pathway (pp.473-474). This is an important distinction to make because pain is the basis of the dependent variable measured in the present study, which is different than nociception. Pain is an individual and subjective experience; different painful stimuli will be experienced differently between individuals. “There are no ‘painful stimuli’—stimuli that invariably elicit the perception of pain in all individuals...[For example] athletes often do not detect their injuries until their game is over,” (Basbaum & Jessell, 2000, pp.474). This issue and the distinction between pain and nociception are important for experimenters to be cognizant of when studying the experience of pain. Competition/Exercise and Pain 6 In order to study pain it is also crucial to understand that there are two components of the sensation of pain. First, pain intensity is considered the sensory aspect of painful sensations (Gracely, McGrath, Dubner, 1978). Secondly, there is also evidence for an affective dimension of pain which may be defined as the cognitive component or the emotional arousal of a painful experience, referred to in this study as "unpleasantness" (Gracely et al., 1978; Jensen & Karoly, 1992). Positron emission tomography studies have confirmed that there are different brain areas responsible for coding different components of pain: intensity and unpleasantness (Tolle et al., 1999). Pain responses in the current study will be quantified using ratio scales that separately assess the sensory intensity and affective dimensions of pain. The Gracely Box Scales will be used for measures of intensity and unpleasantness (Gracely et al., 1978). This measure is a 20point scale composed of a combination of numerical rating scales and verbal analogue scales, in other words, each numerical value is associated with a verbal descriptor (see Appendix A) (Jensen & Karoly, 1992; Gracely et al., 1978). The perception of noxious stimuli before and after the experimental manipulation is essentially what is measured in the current study—how competition induces changes in pain sensitivity. The present study involves pain testing on three different measures. Pain responses will be obtained for the following measures: cold pressor test (ischemic pain), thermal heat threshold test, and suprathreshold thermal scaling test (pain ratings obtained for different temperatures). These are standard pain tests widely used in the field of pain research and in clinical settings (Nielsen, 1997). Some pain researchers believe that stimulus response tasks, such as the thermal scaling procedure, are better and more informative than threshold Competition/Exercise and Pain 7 determination because not only is the data from suprathreshold procedures more descriptive in terms of response characteristics (intensity and unpleasantness) than pain thresholds, but also thresholds are relatively consistent and thus not a good measure of changes in pain perception (Nielsen, 1997; Price & Harkins, 1992). Multiple pain measures have been included in the present study in order to measure pain and assess analgesia as thoroughly, fully, and accurately as possible. Experimenters in the field of pain research have observed that the sensation of pain does not always coincide with nociception. This occurs because pain is not a direct result of nociception alone, but can be regulated by non-nociceptive activity. Discrepancies arise as a result of endogenous pain modulation systems that affect pain perception. Melzack and Wall proposed the Gate Control Theory of Pain in 1965 to address why the experience of pain and nociception do not always correspond. Their primary theory involves a “gate” at the level of the spinal cord that determines the upward flow of information based on communication between afferents. Excitatory and inhibitory afferents incoming from the periphery interact in the spinal cord. This local circuitry in the spinal cord is the gate-keeper that influences and modulates the transmission of nociceptive input from peripheral fibers to higher order processing structures in the brain. Melzack and Wall's theory also included the possibility that “downward” modulation could play a role in the experience of pain and introduced the idea that exogenous factors are important to the process of pain perception (Melzack & Wall, 1965; Gatchel, 1999). Support for the existence of descending internal pain modulation systems were based on evidence that stimulation of the brain, in the periaqueductal gray region (PAG), induces selective analgesia in animals and humans, a phenomenon referred to as stimulation produced analgesia. There is converging evidence that these effects are reversed by naloxone and are mediated by changes in Competition/Exercise and Pain 8 the descending pathways. (Reynolds, 1969; Hosobuchi, Adams, & Linchitz,1977; Akil, Mayer & Liebeskind, 1976). The evidence shows that stimulation of the PAG blocks spinally mediated responses to noxious stimuli because the blockade involves the descending pathways that inhibit nociceptive neurons. The descending pathway is composed of neurons in the PAG, which make excitatory connections with neurons of the raphe nucleus that in turn have inhibitory connections in the dorsal horn of the spinal cord (Basbaum & Jessell, 2000). As Melzack and Wall suspected, there are descending analgesic pathways involved in pain modulation. This system relies on endogenous opioids, which are largely responsible for and involved in the body’s intrinsic analgesia systems. Opioid peptides are analgesic agents that lead to a reduction in pain sensitivity. Opiate receptors are located at key points in the pain pathway including the central terminals of the primary afferent fibers, the spinal cord, areas of the brain, and in peripheral areas in skin, joints, and muscles (Basbaum & Jessell, 2000). Since opiate receptors are located throughout the body, the release of endogenous opioids can produce analgesia in response to many different factors. In fact, opioid mediation was found to play a crucial role in stimulation produced analgesia; the release of opioids occurs in response to electrical stimulation and results in analgesia (Hosobuchi, Adams, & Linchitz, 1977; Akil, Mayer & Liebeskind, 1976). Stress Induced Analgesia Since endogenous opioids are capable of reducing the sensation of pain, it is logical to conclude that stimuli that activate the release of these analgesic agents will lead to decreases in pain perception. Stress is an example of a naturalistic psychological factor, the experience of which is correlated with endorphin release that induces analgesia. Experiments have shown that in response to stressful stimuli, opioid peptides (such as β-endorphin) are released (Yamada & Competition/Exercise and Pain 9 Nabeshima, 1995). However, the release of β-endorphin is not conclusive evidence of opioid mediated stress-induced analgesia; experimental proof of naloxone antagonism is more conclusive evidence of opioid mediation. Opiate antagonists, like naloxone, effectively block opioid activity. Subsequently, this mechanism of action is used as a helpful diagnostic tool to investigate the occurrence of opioid mediation. Stress-induced analgesia is difficult to study in humans. In order to investigate these effects, stress must be induced in the lab in an ethical way. Some investigators rely on observations of real-life psychological stress. For example, researchers have investigated opiate mediation systems and stress-induced analgesia in novice parachute jumpers (Janssen & Arntz, 2001). Subjects were given naloxone or a placebo immediately after a jump and the results showed a decrease in pain sensitivity in the placebo condition only, accompanied by an increase in plasma β-endorphin levels in both groups (Janssen & Arntz, 2001). This evidence demonstrates that stressors can result in elevated levels of endogenous opioids and analgesia but these effects are inhibited by naloxone. The experimenters concluded that their data represent opioid mediated stress-induced analgesia in humans, and they suggest that real life stress triggers an endogenous opioid system to attenuate the potential pain of actual or imminent physical harm (Janssen & Arntz, 2001). In addition to opioid mediated stress-induced analgesia, there is also non-opioid mediated analgesia (Yamada & Nabeshima, 1995). The stress-induced analgesia response, in some cases, can be sensitive to naloxone or not (Lewis, Cannon, & Liebeskind, 1980). Evidence indicates that the nature of the stress-induced analgesia may be dependent on the intensity, duration, and temporal pattern of the stressor (Yamada & Nabeshima, 1995). One such theory suggests that the decision to recruit the activation of opioid or non-opioid analgesia systems is determined by the Competition/Exercise and Pain 10 intensity and duration of the stimulus. Opioid mediated pain inhibition occurs when a stressor is brief or weak, and when stressors are more intense and prolonged non-opioid mediation occurs (Terman, Shavit, Lewis, Cannon, & Liebeskind, 1984). The relationship between opioid and non-opioid systems of mediation has been classified as a mutually inhibitory interaction, in what is referred to as the collateral inhibition model (Kirshgessner, Bodnar, & Pasternak, 1982). Stress-induced analgesia is a phenomenon that has been well documented, at least in animal studies, using a number of different stimuli such as inescapable shock, cold water swim, restraint, and centrufrugal rotation (e.g., Drugan, Ader, & Maier, 1984; LaBuda, Sora, Uhl, & Fuchs, 2000; Rizzi et al., 2001). Stress stimulates an endocrine response involving stimulation of the hypothalamic pituitary adrenocortical axis and results in the secretion of various hormones and activation of sympathetic nervous system activity (Yamada & Nabeshima, 1995; Terman et al., 1984). Cortisol is a physiological marker of stress-induced adrenal cortical activity (Janssen & Arntz, 2001). Psychological stimuli have particularly potent effects on the pituitary adrenal system, therefore, cortisol levels should reflect the amount of stress the subject is experiencing (Mason, 1971). In an experimental situation hormone assays can quantify the level of cortisol present in the sample and can be used in research as a measure to observe stress. Previous research has demonstrated that competitive situations result in such hormonal changes. A large portion of these studies show an increase in cortisol after contests, however, in addition to competition, these situations also usually involve physical effort which may be sufficient to produce hormonal changes (Serrano, Salvador, González-Bono, Sanchís, & Suay, 2000). In the present study, hormonal responses will be assessed through the analysis of cortisol levels, which will permit us to measure the levels of stress experienced and hopefully allow Competition/Exercise and Pain 11 insight into differences in the physical and psychological stress of exercise with and without the impression of competition. Exercise Induced Analgesia As described above, stress is one example of a mechanism that activates endogenous pain modulatory systems. In addition, the experience of exercise is shown to result in analgesia. Research has demonstrated that exercise stimulates endogenous opioid activity in human subjects (Thorén, Floras, Hoffman, & Seals, 1990; Goldfarb & Jamurtas, 1997). Thus, it seems logical to conclude that exercise may serve as a trigger for endogenous analgesia pathways (Sternberg et al., 1998; Fuller & Robinson, 1993). This phenomenon is referred to as “Exerciseinduced analgesia.” Researchers have reported evidence to support the existence of exerciseinduced analgesia. For example, one study demonstrated that a 6.3-mile run resulted in analgesia in runners (Janal, Colt, Clark, & Glusman, 1984). Experimenters also determined that βendorphin levels increased and that the exercise-induced analgesic effects could be blocked by naloxone, which indicates the involvement of opioid mediation (Janal et al., 1984). However, research results on the effects of exercise-induced analgesia have been unpredictable. One study found hypoalgesia, decreased pain sensitivity, after intense exercise and increased β-endorphin levels, but failed to find a correlation between increased β-endorphin levels and decreases in pain perception (Oktedalen, Solberg, Haugen, & Opstad, 2001). Also in a review of the literature, Kotlyn (2000) found that results of studies vary in consistency depending on the mode of pain assessment. Studies that use painful electrical and pressure stimuli show more consistent results than studies that rely on temperature stimuli to produce pain (Koltyn, 2000). This summary of human studies also revealed that naloxone administration does Competition/Exercise and Pain 12 not always influence the exercise-induced analgesic response, and this finding indicates that there is a parallel non-opiate mediation system at work (Kotlyn, 2000). Padawer and Levine (1992) proposed that the experimental evidence of the relationship between exercise-induced opioid activity and exercise-induced analgesia is an artifact of testing procedure. These researchers showed no analgesic effects for exercise and instead identified pain testing as a confounding variable. The inclusion of a control group that did not exercise eliminated differences in pain perception after exercise and showed that reduced pain sensitivity may occur on the second pain assessment of most studies regardless of exercise due to the effects of repeated testing (Padawer & Levine, 1992). However, there is debate in the literature regarding the criticisms presented by Padawer and Levine. Researchers claim that their results are in fact evidence of an exercise-induced analgesia system but it is unclear whether exercise produces analgesia in all testing situations and on all pain tests. (Fuller & Robinson, 1993; Pertovaara & Kemppainen, 1992; Droste & Greenlee, 1992). The confounds of analgesia associated with pain assessment represent an inadequacy present in most previous studies that had reported evidence of exercise-induced analgesia (Sternberg et al., 1998; Padawer & Levine, 1992). Perhaps the evidence of exercise-induced analgesia, if it is not an artifact of repeated testing, has been misinterpreted. The reduction in pain perception after exercise observed in the literature, may actually be due to acute stress as a result of the pain testing procedure. As mentioned earlier, stress-induced analgesia is produced in the presence of an environmental stressor that is significant enough to warrant pain suppression. The pain testing may be a confounding variable in previous studies due to the stressful nature of the testing itself. Pain testing certainly qualifies as a stressor according to Yamada and Nabeshima (1995), who define Competition/Exercise and Pain 13 a stressor as, “ An event, internal or external to an animal, that poses a real or perceived threat to the maintenance of the animal’s homeostasis,” (pp.133). Padawer and Levine (1992) indicate that the pain testing that occurs before exercise may be the source of analgesia as opposed to the act of exercising. “The measurement of pain is not a passive procedure, however; it can be highly reactive. Given the range of environmental stimuli known to produce stress-induced analgesia (SIA) via stress mechanisms...one would expect that pain, as a stressor, would of itself produce SIA, and results cited as evidence for an EIA [exercise-induced analgesia] effect may just as well be due to the analgesic effect of the pain pretest (or repeated testing) as to the exercise per se.” (Padawer & Levine, 1992, pp.132) However, there is an alternative explanation for the lack of conclusive evidence of exercise-induced analgesia. Inconsistent findings may be a result of inconsistent appraisal of particular exercise paradigms as stressful; exercise manipulations used in previous contrived experimental circumstances may not be uniformly stressful to all subjects. Perhaps, activation of the stress-induced analgesia pathways requires cognitive appraisal of a situation as stressful, which is a primary unanswered question that led to a need for the present study (Sternberg et al., 1998). Stress Induced Analgesia in Athletic Competition One of the most ubiquitous examples of stress-induced analgesia observed in everyday life is the pain reduction athletes experience during competition. Sternberg et al. (1998) interpreted this observation as evidence for the activation of endogenous analgesia mechanisms and began systematically studying the influence of athletic competition on analgesia in an experiment that tested athletes on various pain measures before and immediately following a competition. The results demonstrated that participating in athletic competition significantly reduced pain sensitivity to noxious stimuli (Sternberg et al., 1998). However, there were several Competition/Exercise and Pain 14 methodological concerns that need to be addressed in future studies. For example, there was a need to use improved testing equipment and to address previous difficulties testing athletes immediately after competition. The duration of pain modulation induced by competition is not known and earlier studies varied in the duration between the conclusion of the competition and when the pain testing was conducted. Also, the athletic competition involved exercise, and the design of previous experiments did not allow experimenters to discern between competition specific effects and exercise only effects. Thus, in order to separately assess the pain inhibitory effects of the stressful components of athletic competition, (stress of interpersonal competition vs. physical activity) a later study also included the study of sedentary competition and non-competitive exercise. Experimenters tested male and female athletes after a track meet, but also included lab sessions where subjects were asked to compete head-to-head against another subject in a video game competition or to engage in exercise on a treadmill for a fixed period of time. Sternberg et al. (2001) reported analgesia in male and female athletes after the track meet, but the results of the lab sessions were sex-specific. Male subjects (but not females) exhibited analgesia after the video game competition, where as females (but not males) showed an analgesic response to the treadmill exercise (Sternberg et al., 2001). In response to these findings, researchers suggest that exercise produces analgesia only if it is construed as stressful (Sternberg et al., 2001). Also, it is possible that men and women may experience competition differently in that men find competition stressful and women find the exercise involved in competition stressful. The Sternberg et al. (2001) study was possibly limited by the intensity of the exercise and sex biases in the video game task, which may have been arousing or salient only to males. The researchers suggested that the threshold for exercise-induced activation of endogenous opioid systems in humans may Competition/Exercise and Pain 15 differ between the sexes, and if the treadmill intensity is too low, then their ability to test men's response to exercise is compromised (Sternberg et al., 2001). Regardless, the results of this study demonstrate a need for further investigation of this phenomenon and lead directly to the questions addressed by the current study. Is it the case that competition needs to be accompanied by physical exertion to trigger analgesic responses in women? Could exercise alone trigger stress-induced analgesia in men if it is strenuous enough? The purpose of the present study is to investigate the role of competitive stress in activating endogenous pain suppressing mechanisms in response to exercise, in order to determine if the psychological state of competition or strenuous physical exertion are necessary to trigger a stress induced analgesic response. To accomplish our goal of separating stress from the exercise involved in competition, “competition” will be manipulated (absent or present) while exercise intensity is held constant. Subjects will first exercise in the lab and later will exercise in a contrived competition followed on each occasion by assessment of pain perception. Subjects will be under the impression that they are competing, however, the actual power that they exert will be controlled by the experimenter; exercise intensity will be the same when they completed the non-competitive exercise task. This manipulation will allow us to observe individual differences in pain sensitivity resulting from exercise versus competitive exercise. Thus, the effect of the competitive stress on pain sensitivity will be identified. Stress-Induced Analgesia: Influence of Sex and Athletic Status There are additional questions the present experiment intends to investigate in regards to stress-induced analgesia in competition. Through a review of the literature it is clear that sex and athletic status may influence this process. Competition/Exercise and Pain 16 This study will explore sex differences in the ability of competition to produce stressinduced analgesia. The evidence from previous studies in this area suggest that physical exertion must include an element of “stress” to activate pain suppressing mechanisms in males, whereas exercise alone may be considered a stressor for women capable of eliciting stress-induced analgesia (Sternberg et al., 2001). Female and male track athletes have exhibited analgesia after competition, which certainly involves both physical exertion and stress (Sternberg et al., 1998). Taken in consort, these findings suggest that the contributions of stress to athletic competition induced analgesia are different in men and women. For example, in males the stress of competition induces analgesia, but for females the exercise component of competition is stressful and is responsible for inducing analgesia, not necessarily the psychological state of competition. There is also evidence to suggest that males and females perceive pain differently overall. Often, females demonstrate decreased thresholds, greater ability to discriminate between stimuli, higher pain ratings, and less tolerance for noxious stimuli compare to males (Berkley, 1997). The data on sex differences is considered by some to be inconclusive because they are inconsistently observed and small, however when they do appear, the differences are usually in the same direction and replicable in animals (Miaskowski, 1999; Berkley, 1997). Regardless, some studies do report that male and female subjects show differential responses to painful stimuli (Ellermeier & Westphal, 1995; Paulson, Minoshima, Morrow, & Casey, 1998; Sheffield, Biles, Orom, Maxiner, & Sheps, 2000). Women rate thermal stimuli more unpleasant and intense than men (Sheffiled et al., 2000; Sternberg et al, 2001). One study confirms that there are sex differences in the brain areas involved in pain perception via positron emission tomography (Paulson et al., 1998). This study demonstrated that there may be a unique pattern of cerebral and cerebellar activity in response to pain, and that in males and females, Competition/Exercise and Pain 17 patterns of activity overlap in general (Paulson et al., 1998). However, females do rate perceived intensity of noxious heat stimuli higher and this difference is correlated with greater activation in certain structures of the forebrain, the contralateral thalamus and the anterior insula (Paulson et al., 1998). There is also evidence that experimenter gender is a psychosocial factor that influences pain responses and is dependent on gender in that men report less pain to female experimenters (Ellermeier & Westphal, 1995; Miaskowski, 1999). All of the experimenters in the present study are female. Therefore, if female experimenters have an effect on only male subjects, then sex differences found in the current study may be exaggerated by or an artifact of experimenter gender. However, experimenter gender will not be a confound in assessing the analgesic manipulations because subjects will be tested by a female experimenter on all testing days. An additional variable the present study will investigate is how athletic status (athlete vs. non-athlete) influences individual differences in pain and analgesic responses. Previous research has demonstrated that there are differences in pain sensitivity between athletes and non-athletes. Athletes consistently report significantly lower pain ratings than non-athletes on experimentally delivered somatic noxious stimuli (Sternberg et al., 2001; Hall & Davies, 1991; Janal, Glusman, Kuhl, & Clark, 1994). For example, the noxious cold threshold for male runners is significantly higher than control males who do not perform regular exercise (Janal et al., 1994). In this study male runners also discriminated among noxious thermal stimuli better than controls (Janal et al., 1994). Researchers concluded that athletes' capacity to tolerate pain better, at least decreased sensitivity to noxious cold, is attributed to adaptation to athletic training (Janal et al., 1994; Freischlag, 1981). However, the generalizability of the Janal et al. (1994) study across sex is limited because only male athletes were studied. Competition/Exercise and Pain 18 Hall and Davies (1991) observed differences in pain perception related to athletic status and found interactions between athletic status and gender on responses for different pain dimensions. The results showed that non-athletes reported higher affective pain ratings than athletes (Hall & Davies, 1991). Also, female non-athletes rated pain intensity higher than female athletes, male athletes, and male non-athletes (Hall & Davies, 1991). Athletes in general reported higher pain intensity than affect, but the reverse was true for non-athletes whose affective reports were significantly higher than intensity reports (Hall & Davies, 1991). Therefore, pain tolerance may in part depend upon the type and the frequency of painful experiences the individual is exposed to. Athletes may experience more pain than non-athletic individuals on a regular basis, due to strenuous training and painful injuries sustained in competition, subsequently influencing their pain sensitivity (Hall & Davies, 1991; Janal et al., 1994). An alternative explanation is that an altered sensitivity to pain is required to become an athlete or that such individuals are drawn to sports. These ideas are particularly relevant to the current study because athletic status may mediate differences in pain sensitivity, but also exercise may be more stressful for non-athlete since athletes participate in strenuous exercise during training. Hypotheses The major theoretical hypothesis of the present study is that exercise must be stressful in order to activate analgesic mechanisms. Therefore, if competitive exercise is considered stressful it should produce a greater analgesic response than exercise alone. If there are sex differences in this process, females may find the non-competitive exercise task stressful and demonstrate decreased pain sensitivity and no increase in analgesia in response to competition. Males may find the competition stressful showing more analgesia after competitive exercise than just Competition/Exercise and Pain 19 exercise. Alternatively, the exercise task may be sufficiently stressful to produce analgesia in both sexes. Stress in the current study is observed and measured as individual differences in perception in pain, effort exerted, and sympathetic arousal. As evidence of the effectiveness of the experimental manipulation an increase in cortisol should be observed under stressful conditions, primarily during competitive exercise and to a lesser extent during exercise only. Overall, it is expected that pain ratings reported by females will be higher than those given by males. Also in accord with previous research, athlete’s pain ratings should be lower than ratings reported by non-athletes (e.g. Hall & Davies, 1991; Janal et al., 1994). The purpose of the control group is to determine the effects of repeated testing on pain ratings. There is no change expected in the non-exercising control group across testing sessions. Experimental and control groups should not significantly differ in pain sensitivity during the initial session. Method Participants A total of fifty-two subjects from Haverford College participated in the study. Forty subjects participated in the exercise manipulation and twenty participants, who did not engage in exercise, serve as repeated testing control subjects. The subject population was composed of both athletes and non-athletes, including an equal number of male and females in each category. Athletes were recruited from the Haverford track team and non-athletes were recruited from the general campus population via signs posted around campus and in athletic buildings. There were exclusion criteria for participating in the study because of the high intensity exercise involved; subjects for whom exercise is contraindicated were not able to participate. Eligibility was Competition/Exercise and Pain 20 determined by a series of questions given to potential subjects during initial contact with the experimenter and repeated again on the first day subjects report to the lab. Eligible subjects were monetarily compensated at the conclusion of their participation. Exercising subjects received fifty dollars and repeated testing control subjects were given twenty-five dollars. Forms and Questionnaires In order to verify eligibility for participation, subjects completed the Medical History Questionnaire (see Appendix B). Subjective ratings of physiological arousal were assessed by the Body Awareness Questionnaire that asks subjects to rate, on a 4 point scale, the degree to which they were currently experiencing symptoms of sympathetic arousal (see Appendix C). Also, subjects were asked to rate the perceived effort (RPE) exerted during the exercise tasks on the Borg's RPE scale (see Appendix D), which measures the amount of personal investment in the task. Physiological Measures Subjects had their blood pressure and heart rate measured using the Omron Blood Pressure and Heart Rate Meter, an inflatable pressure cuff that is placed on the wrist. Experimenters also obtained the subject's skin temperature. Hormone Assay Salivary samples were collected from each subject for analysis of the levels of the stress