To test how leukocyte responses to endurance exercise were modified by clamping body temperature, nine men (27.3 +/- 6.0 yr) completed four 80-min immersions to midchest at water temperatures of 23 or 39 degrees C; two tests included 40-min of cycle ergometer exercise at 65% of aerobic power. When the subjects were exercising, rectal temperature peaked at 39.1 +/- 0.4 degrees C in the warm water and 37.8 +/- 0.3 degrees C in the cool water. When the subjects were sitting in warm water, rectal temperature closely matched the core temperature during exercise in cool water, whereas when they were sitting in cool water, rectal temperatures decreased to 36.4 +/- 0.6 degrees C. Total and differential white cell counts were determined by using a Coulter counter, and cortisol and growth hormone concentrations were determined by radioimmunoassay; all data were adjusted for changes of blood and plasma volumes. Heat clamping during exercise substantially reduced the rise in white cell, lymphocyte, and granulocyte counts but not the increase in monocyte count. Clamping also abolished previously observed associations between cell counts and cortisol and weakened associations with growth hormone concentrations (D. A. McCarthy and M. M. Dale. Sports Med. 6: 333-363, 1988). We conclude that both exercise and a rise of core temperature contribute to the changes in white cell and subset counts during and immediately after moderate exercise. Both cortisol and growth hormone concentrations appear to be mediators of these responses.

Five normal men, aged 20-30 years, participated in three types of exercise (I, II, III) of equal duration (20 min) and total external work output (120-180 kJ) separated by ten days of rest. Exercises consisted of seven sets of squats with barbells on the shoulders (I; Maximal Power Output Wmax = 600-900 W), continuous cycling at 50 rev X min-1 (II; Wmax = 100-150 W) and seven bouts of intermittent cycling at 70 rev X min-1 (III; Wmax = 300-450 W). Plasma cortisol, glucagon and lactate increased significantly (P less than 0.05) during the exercise and recovery periods of the anaerobic, intermittent exercise (I and III) but not in the continuous, aerobic exercise (II). No consistent significant changes were found in plasma glucose. Plasma insulin levels decreased only during exercise II. The highest increase in cortisol and glucagon was not associated with the highest VE, VO2, Wmax or HR; however it was associated with the anaerobic component of exercise (lactic acid). It is suggested that in exercises of equal duration and total external work output, the continuous, aerobic exercise (II) led to lowest levels of glucogenic hormones.

Five normal male volunteers performed two intermittent weight lifting exercises of equal total external work output and duration (20 min) with identical work-rest intervals but different load and frequency of movements. Exercise I consisted of seven sets of seven vertical leg lifts at 85% of the subject's Seven Repetition Maximum (SRM) and, 5 days later, seven sets of 21 vertical leg lifts with one-third of the previously used load (Exercise II). Blood was sampled throughout the exercise and recovery periods for growth hormone, lactate, and glucose analysis. Growth hormone increased after 20 min of Exercise I to a peak during the recovery period. Significantly elevated growth hormone (GH) levels were found 5, 10, and 15 min (P less than 0.025, P less than 0.05, P less than 0.025 respectively) of recovery after Exercise I. No significant elevations of GH occurred in Exercise II. Significant linear correlations (r = 0.99, P less than 0.01) with a time lag of 16 min were found between lactate and GH levels in Exercise I (lactate increases preceded those of GH). No significant differences in plasma glucose concentrations were detected. The results suggests that in intermittent weight lifting exercises of equal total external work output and duration as well as identical work-rest intervals, the load and/or frequency of an exercise are determinant factors in the regulation of plasma GH levels.

Growth hormone (GH) and lactic acid levels were measured in five normal males before, during and after two different types of exercise of nearly equal total duration and work expenditure. Exercise I (aerobic) consisted of continuous cycling at 100 W for 20 min. Exercise II (anaerobic) was intermittent cycling for one minute at 285 W followed by two minutes of rest, this cycle being repeated seven times. Significant differences (P less than 0.01) were observed in lactic acid levels at the end of exercise protocols (20 min) between the aerobic (I) and anaerobic (II) exercises (1.96 +/- 0.33 mM X 1(-1) vs 9.22 +/- 0.41 mM X 1(-1), respectively). GH levels were higher in anaerobic exercise (II) than in aerobic (I) at the end of the exercise (20 min) (2.65 +/- 0.95 micrograms X 1(-1) vs 0.8 +/- 0.4 micrograms X 1(-1); P less than 0.10) and into the recovery period (30 min) (7.25 +/- 6.20 micrograms X 1(-1) vs 2.5 +/- 2.9 micrograms X 1(-1); P less than 0.05, respectively).

The purpose of the present study was to investigate the intramuscular temperature fluctuations in the human forearm immersed in water at 15 degrees C. Tissue temperature (Tt) was continuously monitored by a calibrated multicouple probe during 3 h immersion of the forearm. The probe was implanted approximately 90 mm distal from the olecranon process along the ulnar ridge. Tt was measured every 5 mm, from the longitudinal axis of the forearm (determined from computed tomography scanning) to the skin surface. Along with Tt, rectal temperature, skin temperature and heat loss of the forearm were measured during the immersions. Five of the six subjects tested showed evidence of cyclic temperature fluctuations in the forearm limited to the muscle tissue. The first increase of the muscle temperature was observed 75 (SE 6) min after the onset of the immersion, and the duration of the cycle averaged 36 (SE 3) min. The maximum increase of the muscle temperature, which ranged between 0.4 degrees C and 1.0 degrees C, was measured at the axis of the forearm, and was inversely correlated to the circumference of the subject's forearm (P less than 0.05). No corresponding increases of the skin temperature and heat loss of the forearm were observed for the complete duration of the immersion. These data support the hypothesis of a significant contribution of the muscle vessels during cold-induced vasodilatation in the forearm.