Thermoregulation during exercise was studied in seven women who were taking oral contraceptive pills for 3 weeks of each month. The subjects were studied once in the 3rd week of taking the pill (P) and once during the following week when they took no pil (N). Rectal temperature (Tre), heart rate (fc) and evaporative water loss (EWL, ventilated capsule technique) were measured while they walked on a treadmill for 60 min at 4.8 km.h-1 at a 10% gradient. Ambient temperature was 22 degrees C. A venous blood sample was drawn 30 min before each experiment for measurement of hematocrit (packed cell volume, PCV), plasma osmolality (Osmpl), and plasma levels of the endogenous pyrogens interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6). Resting Tre was 0.31 degree C higher in P than in N (P < 0.01) and Tre remained higher in P throughout the entire exercise period (P < 0.01). Threshold Tre for the onset of EWL was 0.32 degree C higher in P than in N (P < 0.01). Exercise fc was 6.5 beats.min-1 higher in P than in N (P < 0.01). There was no significant difference in PCV, Osmpl, IL-1 beta or IL-6 between P and N. It was concluded that the administration of synthetic progestins in oral contraceptives causes an upward shift in the threshold for heat loss responses, resulting in higher body core temperatures both at rest and during exercise. There was no evidence that these alterations in thermoregulation were mediated by changes in body fluid balance or in plasma levels of IL-1 beta or IL-6.

The time when blood lactate reaches peak concentration following maximum exercise is unclear. The post exercise venous blood lactate concentration was determined serially for 30 minutes in 13 trained men following maximum exercise on a motor driven treadmill. Lactates were determined enzymatically in duplicate. The VO2 max and percent body fat was 65.1 +/- 4.8 ml.kg-1.min-1 and 11.4 +/- 1.4, respectively. The venous lactate reached a peak concentration at the 6th minute (14.2 mmol.L-1) of an inactive recovery, and declined linearly thereafter to reach a concentration of 7.43 +/- 0.60 mmol.L-1 at the 30th minute. The net rate of lactate removal was .30 mmol.L-1.min-1. Statistical analysis found no significant difference in lactate concentration during the 4th, 5th and 6th minute post exercise, indicating that these post exercise times may be appropriate to sample venous blood for peak lactate concentration.

Introduction: Post-menopausal women have lower resting cardiac function than premenopausal women, but whether the menopause influences maximal cardiac output and hence exercise capacity is unclear. It is possible that pre-and post-menopausal women achieve similar improvements in peak aerobic capacity (V O 2peak ) and cardiac output with exercise training via different regional left ventricular muscle function ("LV mechanics"), as suggested by in vitro and animal studies. The aim of this study was to investigate the effects of the menopause on LV mechanics and adaptations to exercise training. Methods: Twenty-five healthy untrained middle-aged women (age 45-58 years; 11 pre-menopausal, 14 post-menopausal) completed 12 weeks of exercise training. Before and after exercise training, (i)V O 2peak and blood volume were determined, and (ii) LV mechanics were assessed using echocardiography at rest and during two submaximal physiological tests -lower body negative pressure (LBNP) and supine cycling. Results: The increase in relativeV O 2peak after exercise training was 9% smaller in post-menopausal than premenopausal women, concomitant with a smaller increase in blood volume (P < 0.05).However, cardiac output and LV volumes were not different between pre-and postmenopausal women (P > 0.05) despite altered regional LV muscle function, as indicated by higher basal mechanics in pre-menopausal women during the physiological tests after exercise training (P < 0.05). Conclusion: These findings are the first to confirm altered LV mechanics in post-menopausal women. In addition, the reduced aerobic adaptability to exercise training in post-menopausal women does not appear to be a central cardiac limitation, and may be due to altered blood volume distribution and lower peripheral adaptations.1 removed: Twenty-five healthy untrained 2 removed: completed

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