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The influence of exercise on dental pain thresholds and the release of stress hormones
Physiology & Behavior, Vol. 33, pp. 923-926. Copyright©PergamonPress Ltd., 1984. Printedin the U.S.A.
0031-9384/84$3.00 + .00
The Influence of Exercise on Dental Pain Thresholds and the Release of Stress Hormones ANTTI PERTOVAARA, TIMO HUOPANIEMI, ANTTI VIRTANEN AND GUNNAR JOHANSSON
D e p a r t m e n t o f Physiology, University o f Helsinki, Siltavuorenpenger 20 J 00170 Helsinki 17, Finland R e c e i v e d 30 J a n u a r y 1984 PERTOVAARA, A., T. HUOPANIEMI, A. VIRTANEN AND G. JOHANSSON. The influence of exercise on dental pain thresholds and the release of stress hormones. PHYSIOL BEHAV 33(6) 923-926, 1984.--Different levels of exercise (50-200 W) were produced by a bicycle ergometer. In all six subjects the heart rate and blood pressure were increased with increasing work load. Dental pain thresholds tended to increase with increasing work load, too. Plasma ACTH levels were above the normal range during the whole experiment in all subjects, whereas plasma cortisol and prolactin levels were elevated only in one subject. Growth hormone levels had a tendency to elevation at 200 W. There was no correlation between the release of cortisol, prolactin or ACTH and the dental pain threshold elevation. However, there was significant correlation between the release of growth hormone and the dental pain threshold elevation. The results indicate that physical exercise at submaximal work loads is enough to produce a pain threshold elevation in some subjects, with a minor coactivation of stress mechanisms. Dental pain
Exercise
ACTH
Prolactin
Cortisol
SHYU et al. [17] have recently reported that physical exercise produces a pain threshold elevation in rats. The purpose of the present study was to find out if physical exercise at submaximal work loads is enough to produce a dental pain threshold elevation in man. Since activation of stress mechanisms can produce analgesia [14,20] and physical exercise can activate stress mechanisms [8, 11, 15], we also tried to reveal the possible contribution of stress to dental pain threshold elevations. This was done by determining whether ACTH, prolactin, growth hormone or cortisol were released during the exercise and by correlating the hormone concentrations with the possible changes in dental pain thresholds.
Growth hormone
blood pressure, blood sample, pain threshold measurement 3 times. Work load was increased stepwise without rest between different levels. Each work period lasted less than 8 minutes (except one subject who had work periods exceeding 10 minutes). The maximal aerobic power of each subject was determined from linearized load-pulse response curves [3]. Age-correction was made according to Walthuis et al. [ 19]. Dental pain thresholds were determined with a Bofors Pulp tester [1,16]. The cathode was applied to an intact upper tooth through a metal cylinder which was glued to the tooth. The metal cylinder was surrounded by material with a high resistance to prevent the connection between the cathode and extrapulpal tissues. Electrode paste was applied into the metal cylinder to make the contact between the cathode and the tooth better. The test current consisted of constant current pulses of 10 msec duration at a frequency of 5 Hz, which should exclusively activate pulpal A-delta fibers at liminal intensities [18]. The current was slowly increased until the subject felt pain. An intravenous catheter was installed 10 min before the first blood sampling and the first pain determination. The catheter was kept open by periodic injections of 0.9% saline. Blood samples were drawn into hepadnized tubes. Plasma was separated and stored at -20°C for 2 weeks before the determinations were made. The concentrations of ACTH, growth hormone, prolactin and cortisol were measured by radioimmunoassay. Farmos-kit (Finland) was used for cortisol determination (normal range: 120-650 nmol/l), CIS-kit (France) for ACTH (normal range: 10-80 ng/1) and prolactin (normal range: 90-250 mUd) determination. Growth hor-
METHOD Six healthy males volunteered (age range 23-44 years). One of the subjects was an active athlete. An informed consent was obtained before the experiments. Four different levels of exercise (50 W, 100 W, 150 W, and 200 W) were produced by a bicycle ergometer (Tunturi, Finland) operated with a mechanical brake [3]. The subjects pedalled in a sitting position. The pedal frequency was 60 revolutions/min. Heart rate, blood pressure and dental pain thresholds were measured and blood samples were taken before the exercise, at each work load, and 30 minutes after the exercise. Heart rate was monitored with a cardioscope. At each work load the steady state was attained in 3-4 minutes and data collection was performed within additional 4 minutes in the following order: pain threshold measurement 3 times,
923
924
PERTOV AARA l:'7 A L.
mone was determined according to Ylikahri et al. [21]. Blood samples were taken simultaneously with pain threshold determinations. One subject was tested between 9.30-10.00 hr and the other subjects were tested between 14.30-16.30 hr. In each condition pain thresholds (every single measurement included), blood pressure levels, heart rates, and hormone concentrations were calculated over all subjects. Student's paired t-test (two-tailed) was used in statistical calculations, unless otherwise specified. Correlations between the hormone concentrations and the pain threshold elevations were obtained using the Pearson's coefficient of correlation test.
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RESULTS
In all subjects the heart rate and blood pressure were increased as a function of increasing work load (Fig. 1, two upper graphs). The maximal aerobic power of the subjects varied from 230 to 310 W. The mean was 275 W. The subjects had to use on the average 70.7% of their maximal aerobic work capacity at the highest work load (200 W). Heart rate measured 30 min after the exercise was at the pre-exercise level, whereas all subjects had lower blood pressure levels after the exercise. The decrease of systolic blood pressure 30 min after the exercise was significant (,o<0.05) if compared to the pre-exercise level. Five subjects had an elevation of dental pain thresholds during the exercise, and this elevation varied from 5 to 53%. One subject had no pain threshold elevation during the exercise. The average pain threshold elevation over all subjects at 200 W was significant 6o<0.001) if compared to the pre-exercise level (Fig. 1, the lowest graph). In four subjects the dental pain threshold measured 30 min after the exercise remained higher than before the exercise. ACTH level was above the normal range in all subjects before, during, and after the exercise. However, there was no marked change in the ACTH level with increasing exercise (Fig. 2). The cortisol level was above the normal range only in one subject, and there was no change of cortisol level during the experiment (Fig. 2). The subject with high cortisol levels was also the only subject with prolactin levels above the normal range, and no average change of prolactin level was found with increasing work load (Fig. 2). Repeated measures A N O V A (one-way) with load as a within subject factor revealed that the load had no significant effect on ACTH, prolactin, or cortisol release. However, the load had a significant effect on growth hormone release (.o<0.03). All six subjects had an elevation of growth hormone level with the highest work load (significant finding according to the sign-test too: p<0.03). The subjects with the highest cortisol levels before the exercise had the lowest dental pain thresholds, although this correlation was not significant (r= -0.618, N=6). There was no correlation between the pre-exercise ACTH, growth hormone, or prolactin level and the pre-excercise dental pain threshold level. During the exercise the correlation of growth hormone level to the elevation of dental pain thresholds was significant (r= 0.444, N=24, p<0.05). The correlation between the ACTH, prolactin, or cortisol level and the dental pain threshold elevation was not significant. DISCUSSION
The results of this study indicate that physical exercise at a submaximal work load is enough to produce a dental pain threshold elevation at least in some subjects. The correlation of growth hormone level with the dental pain threshold ele-
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FIG. 1. Average heart rates, systolic blood pressures, and dental pain thresholds over all subjects at different work loads. Vertical bars represent _+S.E.M. (N=6, except in the lowest graph N=36).
vation suggests that stress-induced mechanisms may contribute to the reduction of pain sensibility during physical exercise. The level of A C T H was above the normal range during the whole experiment which probably reflects the anticipation of an aversive experiment. However, the highest work load used in the present study (200 W), which required on the average 70% of the maximal aerobic work capacity of our subjects, was not enough to produce a marked change in ACTH, prolactin or cortisol release. In some previous studies, too, a work load exceeding 80-85% of the maximal aerobic work capacity has been needed to produce a significant increase in stress hormone release [8,15]. Since
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FIG. 2. Average plasma levels of stress hormones over all subjects at different work loads. Vertical bars represent _+S.E.M. (N=6)
an activation of stress-induced mechanisms can produce analgesia [14,20] it is possible that higher work loads producing a marked increase of stress hormone release produced a higher elevation of dental pain thresholds. Since four of the six subjects had higher pain thresholds 30 rain after the exercise than before the exercise, it is possible that exercise had a tonic effect; this assumption is supported by the significant decrease of systolic blood pressure 30 min after the exercise. Increased activity in proprioceptive afferents and muscle afferents during exercise may activate inhibitory mechanisms at spinal or supraspinal levels in a way suggested by the gate control theory of pain [13]. With increasing work load the number of impulses increases especially in muscle afferents, which could explain the elevation of dental pain thresholds with increasing work load too. Movement has been shown to modulate activity in the somatosensory cortex [5], and somatosensory evoked responses in lemniscal [7] and extralemniscal [6] pathways. In addition to the gate control type mechanisms, other intracortical and descending cortical mechanisms too could contribute to the movementinduced modulation (cf. [2]). Some of the structures (bulbar nucleus gigantocellularis, thalamic centrum medianum) in which movement modulates somatosensory responses [6] include nociceptor-activated neurons which probably are mediating the sense of pain [4]. However, in these studies very low work loads have been used (e.g., moving of one
finger or front paw), and moreover, the movement-induced modulation of somatosensory responses has been limited to the area which has been moving [12]. Thus, previous studies on movement-induced modulation of somatosensation may deal with mechanisms different from the nonsegmental mechanisms activated by exercise at considerable work loads ([17], this study). Increased blood pressure has been shown to produce dental pain threshold elevation [22]. In the present study the blood pressure increased with increased work load similarly to pain thresholds. However, after the exercise there was a significant blood pressure decrease in contrast to pain threshold increase in some subjects. Thus, it does not seem probable that the dental pain threshold elevation in the present study was due to the activation of analgesic mechanisms by a blood pressure elevation. Attention modulates the activity in tactile neurons of the somatosensory cortex [10] and in nociceptive neurons of the spinal trigeminal nucleus [9]. However, in the present study the task of the subjects was to focus their attention to the dental stimulation; thus, a change in attention is not a plausible explanation for the reduction of pain sensibility in this study. A change in attention may contribute significantly to the reduction of pain sensibility during physical exercise in other kinds of conditions, e.g., during an ice hockey match. The results of this study indicate that physical exercise at submaximal work loads is enough to produce a pain
926
PERTOVAARA El' AL.
t h r e s h o l d e l e v a t i o n in s o m e s u b j e c t s , with a m i n o r c o a c t i v a tion o f s t r e s s m e c h a n i s m s . F u r t h e r studies with h i g h e r work loads a n d e.g., with d e x a m e t h a s o n e s u p p l e m e n t a t i o n are n e e d e d to clarify the role o f s t r e s s m e c h a n i s m s in e x e r c i s e i n d u c e d analgesia.
ACKNOWLEDGEMENTS This study was supported by grants from the Finnish Cultural Foundation and from the Finnish Dental Society.
REFERENCES
1. Anderson, S. A., T. Ericsson, E. Holmgren and G. Lindqvist. Electro-acupuncture. Effect on pain threshold measured with electrical stimulation of teeth. Brain Res 63: 393-396, 1973. 2. Angel, R. W. and R. C. Malenka. Velocity-dependent suppression of cutaneous sensitivity during movement. Exp Neurol 77: 266-274, 1982. 3. Astrand, P.-O. and K. Rodahl. Textbook o f Work Physiology. New York: McGraw-Hill, 1970. 4. Casey, K. L., J. J. Keene and T. Morrow. Bulboreticular and medial thalamic unit activity in relation to aversive behavior and pain. In: Advances in Neurology, vol 4, edited by J. J. Bonica. New York: Raven Press, 1974, pp. 197-205. 5. Chapin, J. K. and D. J. Woodward. Modulation of sensory responsiveness of single somatosensory cortical cells during movement and arousal behaviors. Exp Neurol 72: 164-178. 1981. 6. Ciancia, F., M. Maitte and J.-M. Coquery. Reduction during movement of the evoked potentials recorded along the extralemniscal pathways of the cat. Electroencephalogr Clin Neurophysiol 48: 197-202, 1980. 7. Coulter, J. D. Sensory transmission through lemniscal pathway during voluntary movement in the cat. J Neurophysiol 37: 831845, 1973. 8. Gaibo, H. Endocrinology and metabolism in exercise, lnt .I Sports Med 2: 203-211, 1981. 9. Hayes, R. L., R. Dubner and D. S. Hoffman. Neuronal activity in medullary dorsal horn of awake monkeys trained in a thermal discrimination task. II. Behavioral modulation of responses to thermal and mechanical stimuli. J Neurophysiol 46: 428-443. 1981. 10. Hyviirinen, J., A. Poranen and Y. Jokinen. Influence of attentive behavior on neuronal responses to vibration in primary somatosensory cortex of the monkey. J Neurophysiol 43: 870882, 1980.
11. Kuoppasalmi, K. Effects of exercise stress on human plasma hormone levels. (D.M.S. Thesis) University of Helsinki, 1981. 12. Lee, R. G. and D. G. White. Modification of the human somatosensory evoked response during voluntary movement. Electroencephalogr Clin Neurophysiol 36: 53-62, 1974. 13. Melzack, R. and P. D. Wall. Pain mechanisms: a new theory. Science 150: 971-979, 1965. 14. Millan, M. J., R. Przewlocki and A. Herz. A non-/3endorphinergic adenohypophyseal mechanism is essential for an analgetic response to stress. Pain 33: 343-353, 1980. 15. Moretti, C., M. Cappa, D. Paolucci et al. Pituitary response to physical exercise: sex differences. In: Medicine and Sport. vol 14, edited by E. Jokl. Basel: S. Karger, 1981, pp. 180-186. 16. Pertovaara, A., P. Kemppainen, G. Johansson and S.-L. Karonen. Ischemic pain nonsegmentally produces a predominant reduction of pain and thermal sensitivity in man: a selective role for endogenous opioids. Brain Res 251: 83-92, 1982. 17. Shyu, B.-C., S. A. Andersson and P. Thorrn. Endorphin mediated increase in pain threshold induced by long-lasting exercise in rats. Life Sci 30: 833-840, 1982. 18. Virtanen, A., M. Niirhi, T. Huopaniemi and T. Hirvonen. Thresholds of intradental A- and C-nerve fibres in the cat to electrical current pulses of different duration. Acta Physiol S t a n d 119: 393-398, 1983. 19. Walthuis, R. A., V. F. Froehlicher, J. Fischer and J. H. Triclermasser. The response of healthy men to treadmill exercise. Circulation 55: 153-163, 1971. 20. Wilier, J. C. and D. Albe-Fessard. Electrophysiological evidence for a release of endogenous opiates in stress-induced "analgesia" in man. Brain Res 198: 419-426, 1980. 21. Ylikahri, R. H., M. O. Huttunen, M. H~irk6nen, T. Leino, T. Helenius, K. Liewendahl and S.-L. Karonen. Acute effects of alcohol on anterior pituitary secretion of the tropic hormones. J Clin Endorcrinol 46: 715-720, 1978. 22. Zamir, N. and E. Shuber. Altered pain perception in hypertensive humans. Brain Res 201: 471-474, 1980.
0031-9384/84$3.00 + .00
The Influence of Exercise on Dental Pain Thresholds and the Release of Stress Hormones ANTTI PERTOVAARA, TIMO HUOPANIEMI, ANTTI VIRTANEN AND GUNNAR JOHANSSON
D e p a r t m e n t o f Physiology, University o f Helsinki, Siltavuorenpenger 20 J 00170 Helsinki 17, Finland R e c e i v e d 30 J a n u a r y 1984 PERTOVAARA, A., T. HUOPANIEMI, A. VIRTANEN AND G. JOHANSSON. The influence of exercise on dental pain thresholds and the release of stress hormones. PHYSIOL BEHAV 33(6) 923-926, 1984.--Different levels of exercise (50-200 W) were produced by a bicycle ergometer. In all six subjects the heart rate and blood pressure were increased with increasing work load. Dental pain thresholds tended to increase with increasing work load, too. Plasma ACTH levels were above the normal range during the whole experiment in all subjects, whereas plasma cortisol and prolactin levels were elevated only in one subject. Growth hormone levels had a tendency to elevation at 200 W. There was no correlation between the release of cortisol, prolactin or ACTH and the dental pain threshold elevation. However, there was significant correlation between the release of growth hormone and the dental pain threshold elevation. The results indicate that physical exercise at submaximal work loads is enough to produce a pain threshold elevation in some subjects, with a minor coactivation of stress mechanisms. Dental pain
Exercise
ACTH
Prolactin
Cortisol
SHYU et al. [17] have recently reported that physical exercise produces a pain threshold elevation in rats. The purpose of the present study was to find out if physical exercise at submaximal work loads is enough to produce a dental pain threshold elevation in man. Since activation of stress mechanisms can produce analgesia [14,20] and physical exercise can activate stress mechanisms [8, 11, 15], we also tried to reveal the possible contribution of stress to dental pain threshold elevations. This was done by determining whether ACTH, prolactin, growth hormone or cortisol were released during the exercise and by correlating the hormone concentrations with the possible changes in dental pain thresholds.
Growth hormone
blood pressure, blood sample, pain threshold measurement 3 times. Work load was increased stepwise without rest between different levels. Each work period lasted less than 8 minutes (except one subject who had work periods exceeding 10 minutes). The maximal aerobic power of each subject was determined from linearized load-pulse response curves [3]. Age-correction was made according to Walthuis et al. [ 19]. Dental pain thresholds were determined with a Bofors Pulp tester [1,16]. The cathode was applied to an intact upper tooth through a metal cylinder which was glued to the tooth. The metal cylinder was surrounded by material with a high resistance to prevent the connection between the cathode and extrapulpal tissues. Electrode paste was applied into the metal cylinder to make the contact between the cathode and the tooth better. The test current consisted of constant current pulses of 10 msec duration at a frequency of 5 Hz, which should exclusively activate pulpal A-delta fibers at liminal intensities [18]. The current was slowly increased until the subject felt pain. An intravenous catheter was installed 10 min before the first blood sampling and the first pain determination. The catheter was kept open by periodic injections of 0.9% saline. Blood samples were drawn into hepadnized tubes. Plasma was separated and stored at -20°C for 2 weeks before the determinations were made. The concentrations of ACTH, growth hormone, prolactin and cortisol were measured by radioimmunoassay. Farmos-kit (Finland) was used for cortisol determination (normal range: 120-650 nmol/l), CIS-kit (France) for ACTH (normal range: 10-80 ng/1) and prolactin (normal range: 90-250 mUd) determination. Growth hor-
METHOD Six healthy males volunteered (age range 23-44 years). One of the subjects was an active athlete. An informed consent was obtained before the experiments. Four different levels of exercise (50 W, 100 W, 150 W, and 200 W) were produced by a bicycle ergometer (Tunturi, Finland) operated with a mechanical brake [3]. The subjects pedalled in a sitting position. The pedal frequency was 60 revolutions/min. Heart rate, blood pressure and dental pain thresholds were measured and blood samples were taken before the exercise, at each work load, and 30 minutes after the exercise. Heart rate was monitored with a cardioscope. At each work load the steady state was attained in 3-4 minutes and data collection was performed within additional 4 minutes in the following order: pain threshold measurement 3 times,
923
924
PERTOV AARA l:'7 A L.
mone was determined according to Ylikahri et al. [21]. Blood samples were taken simultaneously with pain threshold determinations. One subject was tested between 9.30-10.00 hr and the other subjects were tested between 14.30-16.30 hr. In each condition pain thresholds (every single measurement included), blood pressure levels, heart rates, and hormone concentrations were calculated over all subjects. Student's paired t-test (two-tailed) was used in statistical calculations, unless otherwise specified. Correlations between the hormone concentrations and the pain threshold elevations were obtained using the Pearson's coefficient of correlation test.
r-~ 140 t 100-1 60
i
|
o
5;
i
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,s'o
i
2;o
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RESULTS
In all subjects the heart rate and blood pressure were increased as a function of increasing work load (Fig. 1, two upper graphs). The maximal aerobic power of the subjects varied from 230 to 310 W. The mean was 275 W. The subjects had to use on the average 70.7% of their maximal aerobic work capacity at the highest work load (200 W). Heart rate measured 30 min after the exercise was at the pre-exercise level, whereas all subjects had lower blood pressure levels after the exercise. The decrease of systolic blood pressure 30 min after the exercise was significant (,o<0.05) if compared to the pre-exercise level. Five subjects had an elevation of dental pain thresholds during the exercise, and this elevation varied from 5 to 53%. One subject had no pain threshold elevation during the exercise. The average pain threshold elevation over all subjects at 200 W was significant 6o<0.001) if compared to the pre-exercise level (Fig. 1, the lowest graph). In four subjects the dental pain threshold measured 30 min after the exercise remained higher than before the exercise. ACTH level was above the normal range in all subjects before, during, and after the exercise. However, there was no marked change in the ACTH level with increasing exercise (Fig. 2). The cortisol level was above the normal range only in one subject, and there was no change of cortisol level during the experiment (Fig. 2). The subject with high cortisol levels was also the only subject with prolactin levels above the normal range, and no average change of prolactin level was found with increasing work load (Fig. 2). Repeated measures A N O V A (one-way) with load as a within subject factor revealed that the load had no significant effect on ACTH, prolactin, or cortisol release. However, the load had a significant effect on growth hormone release (.o<0.03). All six subjects had an elevation of growth hormone level with the highest work load (significant finding according to the sign-test too: p<0.03). The subjects with the highest cortisol levels before the exercise had the lowest dental pain thresholds, although this correlation was not significant (r= -0.618, N=6). There was no correlation between the pre-exercise ACTH, growth hormone, or prolactin level and the pre-excercise dental pain threshold level. During the exercise the correlation of growth hormone level to the elevation of dental pain thresholds was significant (r= 0.444, N=24, p<0.05). The correlation between the ACTH, prolactin, or cortisol level and the dental pain threshold elevation was not significant. DISCUSSION
The results of this study indicate that physical exercise at a submaximal work load is enough to produce a dental pain threshold elevation at least in some subjects. The correlation of growth hormone level with the dental pain threshold ele-
E,
200
t. 09 U) tCL "0 0
o 100
~'
I
i
0
50
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18
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',
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FIG. 1. Average heart rates, systolic blood pressures, and dental pain thresholds over all subjects at different work loads. Vertical bars represent _+S.E.M. (N=6, except in the lowest graph N=36).
vation suggests that stress-induced mechanisms may contribute to the reduction of pain sensibility during physical exercise. The level of A C T H was above the normal range during the whole experiment which probably reflects the anticipation of an aversive experiment. However, the highest work load used in the present study (200 W), which required on the average 70% of the maximal aerobic work capacity of our subjects, was not enough to produce a marked change in ACTH, prolactin or cortisol release. In some previous studies, too, a work load exceeding 80-85% of the maximal aerobic work capacity has been needed to produce a significant increase in stress hormone release [8,15]. Since
EXERCISE A N D D E N T A L PAIN
925
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"-4
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FIG. 2. Average plasma levels of stress hormones over all subjects at different work loads. Vertical bars represent _+S.E.M. (N=6)
an activation of stress-induced mechanisms can produce analgesia [14,20] it is possible that higher work loads producing a marked increase of stress hormone release produced a higher elevation of dental pain thresholds. Since four of the six subjects had higher pain thresholds 30 rain after the exercise than before the exercise, it is possible that exercise had a tonic effect; this assumption is supported by the significant decrease of systolic blood pressure 30 min after the exercise. Increased activity in proprioceptive afferents and muscle afferents during exercise may activate inhibitory mechanisms at spinal or supraspinal levels in a way suggested by the gate control theory of pain [13]. With increasing work load the number of impulses increases especially in muscle afferents, which could explain the elevation of dental pain thresholds with increasing work load too. Movement has been shown to modulate activity in the somatosensory cortex [5], and somatosensory evoked responses in lemniscal [7] and extralemniscal [6] pathways. In addition to the gate control type mechanisms, other intracortical and descending cortical mechanisms too could contribute to the movementinduced modulation (cf. [2]). Some of the structures (bulbar nucleus gigantocellularis, thalamic centrum medianum) in which movement modulates somatosensory responses [6] include nociceptor-activated neurons which probably are mediating the sense of pain [4]. However, in these studies very low work loads have been used (e.g., moving of one
finger or front paw), and moreover, the movement-induced modulation of somatosensory responses has been limited to the area which has been moving [12]. Thus, previous studies on movement-induced modulation of somatosensation may deal with mechanisms different from the nonsegmental mechanisms activated by exercise at considerable work loads ([17], this study). Increased blood pressure has been shown to produce dental pain threshold elevation [22]. In the present study the blood pressure increased with increased work load similarly to pain thresholds. However, after the exercise there was a significant blood pressure decrease in contrast to pain threshold increase in some subjects. Thus, it does not seem probable that the dental pain threshold elevation in the present study was due to the activation of analgesic mechanisms by a blood pressure elevation. Attention modulates the activity in tactile neurons of the somatosensory cortex [10] and in nociceptive neurons of the spinal trigeminal nucleus [9]. However, in the present study the task of the subjects was to focus their attention to the dental stimulation; thus, a change in attention is not a plausible explanation for the reduction of pain sensibility in this study. A change in attention may contribute significantly to the reduction of pain sensibility during physical exercise in other kinds of conditions, e.g., during an ice hockey match. The results of this study indicate that physical exercise at submaximal work loads is enough to produce a pain
926
PERTOVAARA El' AL.
t h r e s h o l d e l e v a t i o n in s o m e s u b j e c t s , with a m i n o r c o a c t i v a tion o f s t r e s s m e c h a n i s m s . F u r t h e r studies with h i g h e r work loads a n d e.g., with d e x a m e t h a s o n e s u p p l e m e n t a t i o n are n e e d e d to clarify the role o f s t r e s s m e c h a n i s m s in e x e r c i s e i n d u c e d analgesia.
ACKNOWLEDGEMENTS This study was supported by grants from the Finnish Cultural Foundation and from the Finnish Dental Society.
REFERENCES
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