Behr et al.: Cortisol responses to exercise
www.brjb.com.br ORIGINAL PAPER (ARTIGO ORIGINAL)
CORTISOL RESPONSES TO SUPRA-MAXIMAL EXERCISE Melissa B. Behr, Laura E. Gerraughty, Kristin S. Ondrak, Claudio L. Battaglini, and Anthony C. Hackney Endocrine Section - Applied Physiology Laboratory, Department of Exercise & Sport Science - University of North Carolina, Chapel Hill, NC, USA
Submitted for publication: July 2009 Accepted for publication: August 2009 ABSTRACT BEHR, M. B.; GERRAUGHTY, L. E.; ONDRAK, K. S.; BATTAGLINI, C. L.; HACKNEY, A. C. Cortisol responses to supra-maximal exercise. Brazilian Journal of Biomotricity, v. 3, n. 3, p. 281-286, 2009. Exercise is a stressor that elicits responses within the hypothalamic-pituitary-adrenal (HPA) axis. Cortisol is a key hormonal component and major resultant of HPA activation. While the cortisol responses to sub-maximal and near-maximal exercise are well-known, the response of this hormone to supra-maximal exercise (i.e., exercise beyond 100% of the work output elicited by the maximal oxygen uptake [VO2max]) is not wellcharacterized. Therefore, this study was conducted to examine and characterize the cortisol responses to supra-maximal exercise. Ten male participants completed a 30-sec cycle-ergometry test at 175% VO2max (peak lactate [LA] = 11.6 ± 1.0 mM/L [Mean ± SD]) and two 90-sec cycle-ergometry tests at 135% VO2max (peak LA = 11.9 ± 1.3 mM/L) and 110% VO2max (peak LA =13.6 ± 0.8 mM/L), respectively. Blood cortisol was measured pre-exercise (resting), 3 minutes post-exercise, and 30 minutes post-exercise. Each participant also completed a control trial, during which no exercise was performed. Peak cortisol responses after exercise occurred at 30 min of recovery and were significantly (p < 0.001) different from respective preexercise and control values. However, the peak cortisol responses did not differ significantly from one another (175% = 19.7 ± 3.0, 135% = 24.0 ± 3.6, 110% = 22.1 ± 2.5 ug/dL; p > 0.05, respectively). These results are limited by a small sample size, but suggest a physiological ceiling with respect to the magnitude of the circulating cortisol response to supra-maximal exercise, beyond which no further increase is seen despite increasing exercise intensity. Key Words: Endocrine, hormones, glucocorticoids, stress reactivity
INTRODUCTION Cortisol is a hormone released by the adrenal cortex in humans. It has many physiological roles and is critical in the maintenance of health. In response to an exercise session, circulating concentrations of cortisol change substantively. At exercise intensities of 40% of maximal oxygen uptake (VO2max) or less, the concentrations typically decrease, while at intensities greater than 50-60% of VO2max concentrations typically increase (in a relatively linear fashion proportional to the increasing intensity) (MCMURRAY & HACKNEY, 2000).
Brazilian Journal of Biomotricity, v. 3, n. 3, p. 281-286, 2009 (ISSN 1981-6324)
Corresponding Author: Anthony C. Hackney, PhD, DSc University of North Carolina CB# 8700 - Fetzer Building Chapel Hill, NC 27599 USA Email:
[email protected] Fax: 919-962-0489
281
Behr et al.: Cortisol responses to exercise
www.brjb.com.br
The mechanism of cortisol release is typically linked to the pituitary hormone adrenocorticotropic hormone (ACTH) which stimulates cortisol production at the zona fasciculata region of the adrenal cortex (TORTORA & DERRICKSON, 2006). However, several well-controlled studies by Radomski et al. (1998) using thermal clamping procedures suggest that core temperature changes with exercise also serve as a stimulant to induce cortisol release. Work from our research group has provided evidence that there may be a limit to the increase in cortisol response observed at maximal or near maximal efforts of exercise (VIRU et al., 2001). That is, in statistical terms, there is a ceiling effect in the magnitude of the hormonal response (WINER, 1971). The ceiling effect is defined as a situation in which values of a variable have an upper limit to what can be observed, and this limit is encountered during the course of an observation or experiment (conversely, a variable having a lower limit of response is referred to as the basement effect) (WINER, 1971). The present study was conducted in an attempt to address aspects of the regulation of cortisol and its potential limit to increase in the blood in response to an exercise stimulus. Specifically trained male subjects performed differing intensities of supra-maximal exercise to see if cortisol responses varied significantly; therefore the purpose of this study was to examine and characterize the cortisol responses to supra-maximal exercise.
Healthy, physically active male subjects (n = 10) were recruited to participate in this study. All subjects signed a written informed consent statement prior to participation in the study in accordance with the Helsinki Declaration. The physical characteristics (mean ± SD) of the subjects were; age = 25.7 ± 4.5 yr, body mass = 74.4 ± 11.3 kg, height = 176.5 ± 8.6 cm. All subjects were physically active and involved in exercise training on a regular basis (i.e., 5+ days/week for ≥ 60 minutes/day). The subjects completed three supra-maximal exercise trials; each of which occurred on a separate day in a random order. The exercise trials consisted of cycle ergometry using a Wingate test style-protocol, as outlined by Pearman and Hackney (1996). The subjects exercised at relative workloads corresponding to calculated percentages of their maximal oxygen uptake (VO2max), which had been determined for each individual subject prior to this study. These exercise intensities were: (a) 175% of VO2max for 30 seconds, (b) 135% of VO2max for 90 seconds, and (c) 110% of VO2max for 90 seconds. The duration for each exercise trial was based upon the work of Pearman and Hackney (1996) and Sale (1991). The total work performed (kg·m) within each of the three exercise trials varied for every individual subject by no more than ~ 5%. As noted, each exercise trial was conducted on a different day, with at least two days rest between each of the trials. Also on another separate day the subjects completed a resting, control trial in which no exercise was performed and subjects rested quietly. Each of the exercise and control trials were controlled for times of day, diet (subjects were four hours post-prandial), and prior physical activity (subjects did not exercise for 24 hours prior). In each of the four experimental trials, blood specimens were collected from an indwelling forearm catheter at rest (pre-trial), at 3 minutes of recovery, and at 30 minutes of recovery (i.e., following each of the exercise trials or the rest period in the control trial). All blood specimens were analyzed in duplicate for lactate and cortisol levels. Lactate analysis was performed via a DT-60 Johnson & Johnson automated blood analyzer (Rochester, NY, USA) and cortisol was assessed by radioimmunoassay procedures (Siemens-DPC Inc., Los Angles, CA, USA). Standard clinical quality controls procedures were utilized to insure
Brazilian Journal of Biomotricity, v. 3, n. 3, p. 281-286, 2009 (ISSN 1981-6324)
METHODS
282
Behr et al.: Cortisol responses to exercise
www.brjb.com.br
viable assay analyses for all biochemical outcomes. Descriptive statistics on all measures are reported as mean ± SD. A repeated measures ANOVA and Tukey post-hoc analysis procedures were used to compare the separate lactate and cortisol responses within the trials to determine statistical significance. The alpha level for statistical significance was set at p ≤ 0.05. RESULTS
In Figure 1 the blood lactate responses to the exercise and control trials are depicted. Exercise resulted in a significant increase in lactate from pre-exercise levels (p < 0.001); however, the magnitude of the peak increase (3 minutes post-exercise) was not significantly different between the individual exercise trials (p > 0.05). Although, the peak lactate levels for the 110% and 175% trials did approach statistical significance in the magnitude of the difference observed (p = 0.06). Lactate levels declined throughout the recovery following exercise, but remained substantially elevated above their respective pre-exercise resting levels (p < 0.01) at 30 minutes of recovery. Again, no significant differences between the exercise trial responses were noted (p > 0.05) at 30 minutes of recovery. Furthermore, all of the corresponding 3 minute and 30 minute post-exercise lactate responses were substantially different from their corresponding control trial levels (p < 0.01), which remained stable and unchanged throughout that trial (p > 0.05).
18 16 Lactate (mM/L)
14 12
Control 110% Test 135% Test 175% Test
10 8 6 4 2 0 Pre
3 min Post
30 min Post
Time Figure 1 - Blood lactate responses in male subjects (n=10) due to the three supra-maximal exercise sessions of this study as well as the control, resting session. All 3 minute and 30 minute post-exercise lactate levels are significantly (p 0.05). Cortisol continued to increase up to the 30 minutes of recovery measurement and the magnitude of the responses at that point were significantly greater (p < 0.05) than the 3 minute levels for the 110% and 135% trials, but not for the 175% trial (p > 0.05). Furthermore, all 3 minute and 30 minute post-exercise cortisol responses were significantly different from corresponding control trial (p < 0.001) time points. The control cortisol levels did not change significantly from one another during that trial (p > 0.05).
35
25 20 15 10 Pre
3 min Post
30 min Post
Time Figure 2 - Blood cortisol responses in male subjects (n=10) due to the three supra-maximal exercise sessions of this study as well as the control, resting session. All 3 minute and 30 minute post-exercise cortisol levels are significantly (p 175%, p = 0.05). While this sample size is not unheard of, it suggests that the lack of significance we observed for cortisol (i.e., the similarity in the peak cortisol responses) was not simply a factor of too few subjects within the research study (WINER, 1971). A critical physiological question is why would there be a limit to the maximal cortisol responses to a stressor such as exercise? Cortisol is an important hormonal component to the responses and adaptation to exercise (VIRU & VIRU, 2004). Nevertheless, when produced in an over abundance it can induce negative physiological consequences. Perhaps the most profound medical illustration of this are the negative health outcomes associated with Cushing's Syndrome (TORTORA & DERRICKSON, 2006). If there is a limit to cortisol release by the adrenal cortex in normal healthy people, it might be a self regulating means to prevent some of the results of excessive circulating cortisol from manifesting themselves. It is unclear if such auto-regulation would be at the level of production from the zona fasciculata cells of the cortex (i.e., product inhibition) or at a more central neuro-endocrine system level with reduced corticotropin releasing-hormone or ACTH release from within the hypothalamic-pituitary-adrenal axis. This speculation on our part is in need for further evaluation and presents interesting prospects for future research. To conclude, this study attempted to characterize the cortisol responses to short-term supra-maximal exercise of various intensities. Such exercise resulted in substantial and significant cortisol elevations; however, the magnitude of the cortisol increases in response to the exercise did not differ between the various supra-maximal intensities studied. This
Brazilian Journal of Biomotricity, v. 3, n. 3, p. 281-286, 2009 (ISSN 1981-6324)
As noted in the methods, the total work performed in each of the exercise trials did not vary considerably (~ 5%). This was intentional and an attempt on our part to manipulate primarily intensity within this study and not the work performed. It is known that the total work performed can be an influential factor on the cortisol response to exercise, although this seems to be primarily driven by the input of core temperature changes during extended durations of exercise (RADOMSKI et al., 1998). Nevertheless, we did not wish to have varying amounts of work performed during the exercise trials be a major confounder in our data and thus attempted to control it. Extending the duration of each of the supramaximal exercise trials could have produced differing results from those herein, but at the high level of intensities we studied, extending the duration may have resulted in an inability of the subjects to maintain the desired intensity level (SALE, 1991).
285
Behr et al.: Cortisol responses to exercise
www.brjb.com.br
finding suggests that perhaps there may be a ceiling to the magnitude of cortisol response that can be observed with intensive exercise. Such a limitation to the cortisol response might represent a safety mechanism to prevent aspects of the negative physiological consequences from excessive cortisol release in otherwise healthy individuals. REFERENCES BOUCHARD. C.; TAYLOR, A. W.; SIMONEAU, J.; DULAC, S. Testing anaerobic power and capacity. Physiological Testing of the High-Performance Athlete. JD MacDougall et al. Ed. Human Kinetics Publisher, Champaign, IL.1991. DALY, W.; SEEGERS, C. A.; RUBIN, D. A.; DOBRIDGE, J. D.; HACKNEY, A. C. Relationship between stress hormones and testosterone with prolonged endurance exercise. European Journal Applied Physiology, v. 93, p. 375-380, 2005. DAVIES, C. T. M.; FEW, J. D. Effect of exercise on adrenal cortical function. Journal of Applied Physiology, v. 35, p. 887-891, 1973. MCMURRAY, R. G,; HACKNEY, A. C. The endocrine system and exercise. In: Exercise and Sport Science. Editor, W. Garrett. Williams & Wilkins Publisher. New York, NY. p. 135162, 2000.
PEARMAN, S. N.; HACKNEY, A. C. Development of a 90 second cycle ergometer test to assess anaerobic ability. Sports Medicine, Training & Rehabilitation, v. 6, p. 279-286, 1996. RADOMSKI, M. W.; CROSS, M.; BUDGET, A. Exercise-induced hyperthermia and hormonal responses to exercise. Canadian Journal of Physiology and Pharmacology, v. 76, p. 547-552, 1998. SALE, D. G. Testing of strength and power. Physiological testing of the High-Performance Athlete. JD MacDougall et al. Ed. Human Kinetics Publisher, Champaign, IL.1991. STEGEMANN, J. Exercise Physiology: Physiological Bases of Work and Sport. G. Thieme Verlag, Stuttgart - New York, NY.1981. TORTORA, G. J.; DERRICKSON, B. Principles of Anatomy and Physiology 11th Edition. Wiley & Son, Hoboken, NJ. 2006. VIRU, A.; HACKNEY, A. C.; VALJA, E.; KARELSON, K.; JANSON, T.; VIRU, M. Influence of prolonged continuous exercise on hormonal responses to subsequent intensive exercise. European Journal of Applied Physiology, v. 85, p. 578-585, 2001. VIRU, A.; VIRU, M. Cortisol – essential adaptation hormone in exercise. International Journal Sports Medicine, v. 25, p. 461-464, 2004. VIRU, M.; HACKNEY, A. C.; JANSON, T.; KARELSON, K.; VIRU, A. Characterization of the cortisol response to incremental exercise in physically active young men. Acta Physiological Hungarica, v. 95, p. 219-227, 2008. WINER, B. J. Statistical Principles in Experimental Design. McGraw-Hill, New York, NY. 1971.
Brazilian Journal of Biomotricity, v. 3, n. 3, p. 281-286, 2009 (ISSN 1981-6324)
OLBRECHT, J.; MADER, O.; ISEN, H.; HOLLMANN, W. Relationship between swimming velocity and lactic acid concentration during continuous and intermittent training exercises. International Journal Sports Medicine, v. 6, p. 74-77, 1985.
286
