MECHANISMS OF CARDIOVASCULAR ADJUSTMENTS ASSOCIATED WITH PRESYNCOPAL-LIMITED LOWER BODY NEGATIVE PRESSURE TOLERANCE (ORTHOSTASIS).

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