Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects, during a 80-min exercise period on ergocycle with ingestion of 140 g of (13)C-labelled glucose, in normoxia and acute hypobaric hypoxia (445 mmHg or 4,300 m), at the same relative [77% V(.-)((O)(2)(max))] and absolute workload (161+/-8 W, corresponding to 77 and 54% V(.-)((O)(2)(max)) in hypoxia and normoxia). The oxidation rate of exogenous glucose was not significantly different in the three experimental situations: 21.4+/-2.9, 20.2+/-1.2 and 17.2+/-0.6 g over the last 40 min of exercise at approximately 77 and approximately 54% V(.-)((O)(2)(max)) in normoxia and in hypoxia, respectively, providing 12.5+/-1.5, 16.8+/-1.1 and 14.9+/-1.1% of the energy yield, although ingestion of glucose during exercise resulted in a higher plasma glucose concentration in hypoxia than normoxia. The contribution of carbohydrate (CHO) oxidation to the energy yield was significantly higher in hypoxia (92.0+/-2.1%) than in normoxia for both a given absolute (75.3+/-5.2%) and relative workload (78.1+/-1.8%). This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield: 75.9+/-1.7% versus 66.6+/-3.3 and 55.2+/-3.7% in normoxia at the same relative and absolute workload.

The effects of hydromineral hormones and catecholamines on renal concentrating ability at different hydration states were examined in five male volunteers while they performed three trials. Each of these trials comprised a 60-min exercise bout on a treadmill (at 50% of maximal oxygen uptake) in a warm environment (dry bulb temperature, 35 degrees C; relative humidity, 20-30%). In one session, subjects were euhydrated before exercise (C). In the two other sessions, after thermal dehydration (loss of 3% body mass) which markedly reduced plasma volume (PV) and increased plasma osmolality (osm[pl]), the subjects exercised either not rehydrated (Dh) or rehydrated (Rh) by drinking 600 ml of mineral water before and 40 min after the onset of exercise. During exercise in the Dh compared to C state, plasma renin, aldosterone, arginine vasopressin (AVP), noradrenaline and adrenaline concentrations were increased (P < 0.05). A reduction in creatinine clearance and urine flow was also observed (P < 0.05) together with a decrease in urine osmolality, osmolar clearance and sodium excretion, while free water clearance increased (P < 0.05). However, compared to Dh, Rh partially restored PV and osm(pl) and induced a marked reduction in the time courses of both the plasma AVP and catecholamine responses (P < 0.05). Values for renal water and electrolyte excretion were intermediate between those of Dh and C. Plasma atrial natriuretic peptide presented similar changes whatever the hydration state. These results demonstrate that during moderate exercise in the heat, renal concentrating ability is paradoxically reduced by prior dehydration in spite of high plasma AVP levels, and might be the result of marked activation of the sympatho-adrenal system. Rehydration, by reducing this activation, could partially restore the renal concentrating ability despite the lowered plasma AVP.

Eight healthy men, unacclimated to heat, were submitted to variations in body hydration. The subjects were kept euhydrated, dehydrated by controlled passive hyperthermia or exercise on a treadmill up to a weight loss of 2.8%, or hyperhydrated using a solution containing glycerol, with a total ingested volume equal to 21.4 ml/kg of body weight. On completion of a 90-min recovery period, the subjects were assigned a pedaling exercise on an arm-crank ergometer. Psychological tests were administered 30 min after the phase of hydration variation and 15 min after the arm crank exercise. Both dehydration conditions impaired cognitive abilities (i.e., perceptive discrimination, psycho-motor skills, and short-term memory) as well as subjective estimates of fatigue, without any relevant differences between them. Short-term memory was significantly greater following hyperhydration when compared to euhydration (P < .05). Following arm crank exercise, further effects of dehydration were found for tracking performance only (P < .05). Moreover, long-term memory was impaired in both control and dehydration situations, whereas there was no decrement in performance in the hyperhydration condition.

This study examined plasma volume changes (deltaPV) in humans during periods with or without changes in body hydration: exercise-induced dehydration, heat-induced dehydration and glycerol hyperhydration. Repeated measurements of plasma volume were made after two injections of Evans blue. Results were compared to deltaPV calculated from haematocrit (Hct) and blood haemoglobin concentration ([Hb]). Eight well-trained men completed four trials in randomized order: euhydration (control test C), 2.8% dehydration of body mass by passive controlled hyperthermia (D) and by treadmill exercise (60% of their maximal oxygen uptake, VO2max) (E), and hyperhydration (H) by glycerol ingestion. The Hct, [Hb], plasma protein concentrations and plasma osmolality were measured before, during and after the changes in body hydration. Different Hct and [Hb] reference values were obtained to allow for posture-induced variations between and during trials. The deltaPV values calculated after two Evans blue injections were in good agreement with deltaPV calculated from Hct and [Hb]. Compared to the control test, mean plasma volume declined markedly during heat-induced dehydration [-11.4 (SEM 1.7)%] and slightly during exercise-induced dehydration [-4.2 (SEM 0.9)%] (P < 0.001 compared to D), although hyperosmolality was similar in these two trials. Conversely, glycerol hyperhydration induced an increase in plasma volume [+7.5 (SEM 1.0)%]. These results would indicate that, for a given level of dehydration, plasma volume is dramatically decreased during and after heat exposure, while it is better maintained during and after exercise.