In man, tolerance to an orthostatic stress varies widely. Compensatory cardiovascular responses to orthostatic stressors such as head-up tilt, +Gz acceleration, and lower body negative pressure (LBNP) have been identified. However, physiologic reactions associated with the capacity to withstand a presyncopal- limited orthostatic exposure requires additional clarification. The relationship between maximal oxygen uptake (‘VO₂ max) and presyncopal-limited LBNP tolerance was examined in adult male subjects categorized into high (HAC) and low (LAC) aerobic capacity groups. In addition to similar (N.S.) cardiovascular responses, the (mean) and cumulative LBNP stress indices (CS)) observed in the HAC (722 torr•min) and LAC (784 torr•min) groups were also similar (N.S.). These data fail to support a relationship between LBNP tolerance and ‘VO₂ max. Cardiovascular responses associated with LBNP tolerance were measured during the control period (pre-LBNP) and final minute (peak LBNP) of decompression. The CSI criterion distinguished high (HT, n = 10) and low (LT, n = 8) LBNP tolerant groups was 640 torr•min. A greater (p < 0.05) end-diastolic volume and cardiac output was observed in the HT subjects during pre-LBNP may have provided a larger reserve to utilize throughout exposure to LBNP. At peak LBNP, both groups demonstrated similar (N.S.) cardiac outputs despite a higher (p < 0.05) HT heart rate. These data suggest that a major mechanism in prolonging LBNP tolerance may have been a greater LBNP-induced tachycardia. Blood samples were drawn to determine group differences in vasoactive neuroendocrine response. During peak LBNP, concentrations of norepinephrine increased (p < 0.05) in both groups. The HT group displayed greater (p < 0.05) LBNP-induced increases in vasopressin and plasma renin activity. These data suggest that HT subjects may have supplemented the catecholamine pressor response by involving the vasopressin and renin-angiotensin systems. The affect of cholenergic and beta-adrenergic blockades on cardiovascular responses to LBNP were examined in six HT and five LT subjects. CSI in both groups were unchanged (N.S.) by administration of atropine as compared to a placebo LBNP exposure. Propranolol however, reduced (p < 0.05) LBNP tolerance in both groups. This CSI reduction was greater (p < 0.05) in the HT subjects. The reduction in LBNP tolerance appeared closely associated with the negative chronotropic effect.

The effects of moderate workload exercise at different pedal rates on circulatory and respiratory parameters were studied. Five subjects performed seven discontinuous constant-load cycle ergometer tests of 30 minutes duration at pedal rates of 40, 50, 60, 70, 80, 90 and 100 rpm. Oxygen uptake and carbon dioxide production were determined by standard open circuit spirometry, while heart rate was recorded by electrocardiograph. The CO₂ rebreathing procedure was administered during the exercise bout in order to determine cardiac output. Blood pressure was determined for each test, and total peripheral resistance was calculated. The findings indicate that progressive increases in pedal frequency during discontinuous constant-load cycle ergometry produce progressive increases in cardiovascular, respiratory and metabolic responses and a decrease in gross exercise mechanical efficiency. The results indicate that oxygen uptake, cardiac output, heart rate, ventilation and arterial-venous oxygen difference increases curvilinearly as pedal rate increases, possibly as a result of increases in recruitment of muscle fibers and/or muscle groups. These findings suggest that circulatory and respiratory responses are due to "central command" which sets the basic efferent response pattern. However, this effector pattern is modulated by afferent input originating from the legs during progressive increases in pedal rate.