Jiri Zamecnik

The Impact of heat exposure and repeated exercise on circulating stress hormones

Abstract To determine if heat exposure alters the hormonal responses to moderate, repeated exercise, 11 healthy male subjects [age = 27.1 (3.0) years; maximal oxygen consumption, V˙O2max = 47.6 (6.2) ml · kg · min−1; mean (SD)] were assigned to four different experimental conditions according to a randomized-block design. While in a thermoneutral (23°C) or heated (40°C, 30% relative humidity) climatic chamber, subjects performed either cycle ergometer exercise (two 30-min bouts at ≈50% V˙O2max, separated by a 45-min recovery interval, CEx and HEx conditions), or remained seated for 3 h (CS and HS conditions). Blood samples were analyzed for various exercise stress hormones [epinephrine (E), norepinephrine (NE), dopamine, cortisol and human growth hormone (hGH)]. Passive heating did not alter the concentrations of any of these hormones significantly. During both environmental conditions, exercise induced significant (P < 0.001) elevations in plasma E, NE and hGH levels. At 23°C during bout 1: E = 393 (199) pmol · l−1 (CEx) vs 174 (85) pmol · l−1 (CS), NE = 4593 (2640) pmol · l−1 (CEx) vs 1548 (505) pmol · l−1 (CS), and hGH = 274 (340) pmol · l−1 (CEx)vs 64 (112) pmol · l−1 (CS). At 40°C, bout 1: E = 596 (346) pmol · l−1 (HEx) vs 323 (181) pmol · l−1 (HS), NE = 7789 (5129) pmol · l−1 (HEx) vs 1527 (605) pmol · l−1 (HS), and hGH = 453 (494) pmol · l−1 (HEx) vs 172 (355) pmol · l−1 (HS). However, concentrations of plasma cortisol were increased only in response to exercise in the heat [HEx = 364 (168) nmol · l−1 vs HS = 295 (114) nmol · l−1). Compared to exercise at room temperature, plasma levels of E, NE and cortisol were all higher during exercise in the heat (P < 0.001 in all cases). The repetition of exercise did not significantly alter the pattern of change in cortisol or hGH levels in either environmental condition. However, repetition of exercise in the heat increased circulatory and psychological stress, with significantly (P < 0.001) higher plasma concentrations of E and NE. These results indicate a differential response of the various stress hormones to heat exposure and repeated moderate exercise.

Melatonin has no effect on tolerance to uncompensable heat stress in man

Abstract This study examined whether a 5 mg dose of melatonin induced a lower rectal temperature (Tre) response at rest in both a cool and hot environment while wearing normal military combat clothing, and then examined the influence of this response on tolerance to exercise in the heat while wearing protective clothing. Nine men performed four randomly ordered trials involving 2 h of rest at ambient temperatures of either 23 °C or 40 °C followed by exercise at an ambient temperature of 40 °C. The double-blind ingestion of placebo or melatonin occurred after 30 min of rest. The mean Tre during rest at 23 °C had decreased significantly from 36.8 (SD 0.1) °C to 36.7 (SD 0.2) °C at 90 min following the ingestion of the drug, whereas values during the placebo trial did not change. The lower Tre response during the melatonin trial remained during the first 50 min of exercise in the heat while wearing the protective clothing. Since the final mean Tre at the end of exercise also was significantly reduced for the melatonin [39.0 (SD 0.4) °C] compared with the placebo [mean 39.1 (SD 0.3) °C] trial, tolerance times approximated 95 min in both conditions. During rest at 40 °C, melatonin did not affect the mean Tre response which increased significantly during the last 90 min from 36.9 (SD 0.1) °C to 37.3 (SD 0.1) °C. This increase in Tre during the rest period prior to donning the protective clothing decreased tolerance time approximately 30 min compared with the trials that had involved rest at 23 °C. Total heat storage summated over the rest and exercise periods was not different among the trials at 15 kJ · kg−1. It was concluded that the small decrease in Tre following the ingestion of 5 mg of melatonin at rest in a cool environment had no influence on subsequent tolerance during uncompensable heat stress.

β-Endorphin and natural killer cell cytolytic activity during prolonged exercise. Is there a connection?

This study was designed to test whether a single 50-mg dose of the opioid antagonist naltrexone hydrochloride, ingested 60 min before 2 h of moderate-intensity exercise (i.e., 65% peak O2 consumption), influenced the exercise-induced augmentation of peripheral blood natural killer cell cytolytic activity (NKCA). Ten healthy male subjects were tested on four occasions separated by intervals of at least 14 days. A rested-state control trial was followed by three double-blind exercise trials [placebo (P), naltrexone (N), and indomethacin] arranged according to a random block design. The indomethacin exercise trial is discussed elsewhere (S. G. Rhind, G. A. Gannon, P. N. Shek, and R. J. Shepherd. Med. Sci. Sports Exerc. 30: S20, 1998). For both the P and N trials, plasma levels of beta-endorphin were increased (P < 0.05) at 90 and 120 min of exercise but returned to resting (preexercise) levels 2 h postexercise. CD3(-)CD16(+)CD56(+) NK cell counts and NKCA were significantly (P < 0.05) elevated at each 30-min interval of exercise compared with correspondingly timed resting control values. However, there were no differences in NK cell counts or NKCA between P and N trials at any time point during the two trials. Changes in NKCA reflected mainly changes in NK cell count (r = 0.72; P < 0.001). The results do not support the hypothesis that the enhancement of NKCA during prolonged submaximal aerobic exercise is mediated by beta-endorphin.This study was designed to test whether a single 50-mg dose of the opioid antagonist naltrexone hydrochloride, ingested 60 min before 2 h of moderate-intensity exercise (i.e., 65% peak O2 consumption), influenced the exercise-induced augmentation of peripheral blood natural killer cell cytolytic activity (NKCA). Ten healthy male subjects were tested on four occasions separated by intervals of at least 14 days. A rested-state control trial was followed by three double-blind exercise trials [placebo (P), naltrexone (N), and indomethacin] arranged according to a random block design. The indomethacin exercise trial is discussed elsewhere (S. G. Rhind, G. A. Gannon, P. N. Shek, and R. J. Shepherd. Med. Sci. Sports Exerc. 30: S20, 1998). For both the P and N trials, plasma levels of β-endorphin were increased ( P < 0.05) at 90 and 120 min of exercise but returned to resting (preexercise) levels 2 h postexercise. CD3-CD16+CD56+NK cell counts and NKCA were significantly ( P < 0.05) elevated at each 30-min interval of exercise compared with correspondingly timed resting control values. However, there were no differences in NK cell counts or NKCA between P and N trials at any time point during the two trials. Changes in NKCA reflected mainly changes in NK cell count ( r = 0.72; P < 0.001). The results do not support the hypothesis that the enhancement of NKCA during prolonged submaximal aerobic exercise is mediated by β-endorphin.