This investigation examined the distinct and interactive effects of initial hydration state, exercise-induced dehydration, and water rehydration in a hot environment. On four occasions, 10 men performed a 90-min heat stress test (treadmill walking at 5.6 km/h, 5% grade, 33 degrees C, 56% relative humidity). These heat stress tests differed in pretest hydration [2 euhydrated (EU) and 2 hypohydrated (HY) trials] and water intake during exercise [2 water ad libitum (W) and 2 no water (NW) trials]. HY+NW indicated greater physiological strain than all other trials (P < 0.05-0.001) in heart rate, plasma osmolality (Posm), sweat sensitivity (g/degrees C.min), and rectal temperature. Unexpectedly, final HY+W and EU+W responses for rectal temperature, heart rate, and Posm were similar, despite the initial 3.9 +/- 0.2% hypohydration in HY+W. We concluded that differences in pretest Posm (295 +/- 7 and 287 +/- 5 mosmol/kg for HY+W and EU+W, respectively) resulted in greater water consumption (1.65 and 0.31 liter for HY+W and EU+W, respectively), no voluntary dehydration (0.9% body mass increase), and attenuated thermal and circulatory strain during HY+W.

This study examined the immunological responses to cold exposure together with the effects of pretreatment with either passive heating or exercise (with and without a thermal clamp). On four separate occasions, seven healthy men [mean age 24.0 +/- 1.9 (SE) yr, peak oxygen consumption = 45.7 +/- 2.0 ml. kg(-1). min(-1)] sat for 2 h in a climatic chamber maintained at 5 degrees C. Before exposure, subjects participated in one of four pretreatment conditions. For the thermoneutral control condition, subjects remained seated for 1 h in a water bath at 35 degrees C. In another pretreatment, subjects were passively heated in a warm (38 degrees C) water bath for 1 h. In two other pretreatments, subjects exercised for 1 h at 55% peak oxygen consumption (once immersed in 18 degrees C water and once in 35 degrees C water). Core temperature rose by 1 degrees C during passive heating and during exercise in 35 degrees C water and remained stable during exercise in 18 degrees C water (thermal clamping). Subsequent cold exposure induced a leukocytosis and granulocytosis, an increase in natural killer cell count and activity, and a rise in circulating levels of interleukin-6. Pretreatment with exercise in 18 degrees C water augmented the leukocyte, granulocyte, and monocyte response. These results indicate that acute cold exposure has immunostimulating effects and that, with thermal clamping, pretreatment with physical exercise can enhance this response. Increases in levels of circulating norepinephrine may account for the changes observed during cold exposure and their modification by changes in initial status.

Heart rate (HR), hematocrit, hemoglobin, blood glucose, and plasma concentrations of lactate, cortisol, and testosterone were monitored in 10 male subjects (Division I, 20.3 +/- 2.5 yrs, VO2max: 58.5 +/- 9.4 ml.kg-1.min-1) during singles tennis and a treadmill test. During the on-court session, HR was 144.6 +/- 13.2 beats.min-1 for the 85 min of play. Plasma lactate rose 50% from a post-warmup value of 1.6 +/- 0.6 mmol.l-1 to 2.3 +/- 1.2 mmol.l-1 during play (p greater than 0.05). Blood glucose slightly decreased (8%, p greater than 0.05) from a pre-exercise value of 4.6 +/- 0.8 mmol.l-1 as a result of the 10-min warmup. This was followed by a 23% rise (p less than 0.05) from 4.2 +/- 1.0 mmol.l-1 to 5.2 +/- 0.6 mmol.l-1, measured after the first 30 min of play. Blood glucose subsequently remained steady at slightly above the pre-exercise value. Plasma cortisol rose (9%, p greater than 0.05) during the warmup and subsequently decreased (p less than 0.05) from a post-warmup value of 558.2 +/- 285.2 nmol.l-1 to 337.1 +/- 173.3 nmol.l-1 (a 40% decrease), and remained decreased during recovery. Plasma testosterone rose 22% (p less than 0.05) from pre-exercise to recovery (13.5 +/- 3.8 nmol.l-1 and 16.5 +/- 2.6 nmol.l-1, respectively). Although tennis is characterized by periods of high-intensity exercise, the overall metabolic response resembles prolonged moderate-intensity exercise.

This investigation examined the influence of pre-exercise hydration status, and water intake during low intensity exercise (5.6 km.h-1 at 5% gradient) in the heat (33 degrees C), on plasma testosterone (TEST), cortisol (CORT), adrenaline (A), and noradrenaline (NA) concentrations at baseline (BL), pre-exercise (PRE), and immediately (IP), 24 h (24 P), and 48 h postexercise (48 P). Ten active men participated in four experimental treatments. These treatments differed in pre-exercise hydration status [euhydrated or hypohydrated (HY, -3.8 (SD 0.7)% body mass)] and water intake during exercise (water ad libitum or no water intake during exercise, NW). There were no significant changes in TEST, CORT, or A concentrations with time (BL, PRE, IP, 24 P, and 48 P), or among treatments. However, significant increases from BL and PRE plasma NA concentrations were observed at IP during all four treatment conditions. In addition, HY+NW resulted in significantly higher plasma NA concentrations at IP compared to all other treatments. These results suggest that moderate levels of hypohydration during prolonged, low intensity exercise in the heat do not influence plasma TEST, CORT, or A concentrations. However, plasma NA appears to respond in a sensitive manner to these hydration and exercise stresses.

To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age = 27.6 (SD 3.8) years, VO2max = 46.1 (SD 8.5) ml min-1 kg-1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO2max, 40 min at 60% VO2max, 20 min at 70% VO2max, and 40 min at 70% VO2max). O2 uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO2 rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P < 0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO2 returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO2max) or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.