The influence of alterations in plasma volume on physiological responses to dynamic exercise

Abstract

This thesis investigated the hypothesis that the level of resting plasma volume (PV) is an important determinant of the responses that occur in the cardiovascular, metabolic and substrate, thermoregulatory and endocrine systems during prolonged exercise. Two strategies were employed to alter resting PV, namely diuretics, which produced a reduction in resting PV, and Pentispan or Dextran, which produced increase in PV.

In the plasma volume expansion study (PVX), eight healthy untrained males performed 90 min of cycle ergometry at 62% of peak aerobic power (VO2peak) twice, prior to (CON) and following acute plasma volume expansion (PVX). Oxygen uptake (VO2) was similar between the two conditions. The PVX condition resulted in a calculated 15.8% increase in resting PV (P<0.05). During PVX, heart rate was lower and stroke volume and cardiac output were higher during the exercise. Mean arterial pressure and total peripheral resistance were not different between the two conditions. The core temperature response to exercise was not affected by PVX. It was also observed that acute PV expansion altered both the fluid regulatory hormones and catecholamine responses to exercise. Exercise induced increases in plasma norepinephrine, renin, aldosterone, and vasopressin were attenuated with PVX. No differences in the glucose rate of appearance/disappearance, glycerol rate of appearance, and rates of substrate oxidation were observed between conditions. Muscle glycogen depletion and muscle metabolite concentrations were also unaltered by PVX during exercise.

In the PV reduction study, ten untrained males performed 60 min of cycle exercise at 61% of VO2 peak while on a diuretic (DIU) and under control (CON) conditions. Participants consumed either a diuretic (Novotriamazide) or a placebo, in random order, for 4 days prior to the exercise. The diuretic resulted in a 14.3% reduction in resting PV. Hypovolemia resulted in a reduction in SV and an increase in HR, both at rest and during exercise. The reduced PV led to greater circulating concentrations of norepinephrine during exercise. The hormonal response to the exercise was also altered, such that greater circulating concentrations of plasma renin, aldosterone, and angiotensin I, and a reduction in atrial natriuretic peptide were observed, during exercise. Furthermore, plasma glucagon concentrations were also increased during DIU. The diuretic induced reduction in PV also led to alterations in the response of glucose kinetics, but not whole body lipolysis, during exercise. Rates of total carbohydrate and fat oxidation during exercise were not affected by the two conditions. Muscle metabolism was also unaltered by DIU, as indicated by the concentrations of muscle glycogen, ATP, PCr, Cr, Pi and lactate, both at rest and during exercise.