No abstract

To determine the influence of hydration state upon circulatory controls, we studied four relatively fit subjects during duplicate 30-min cycle ergometer exercise bouts (55% VO2max) in euhydrated, hypohydrated, and hyperhydrated conditions. Ambient temperature was 35 degrees C. Hypohydration was achieved by 4 days of diuretic administration and resulted in a whole-body weight loss of 2.2 kg and a plasma volume decrease of approximately 700 ml. Hyperhydration was achieved by ADH administration plus ingestion of 2 liters water but caused only a minor increase volume. Hypohydration resulted in a significantly reduced cardiac output during exercise; this the result of a reduction in stroke volume of 17 ml.beat-1 without adequate elevation in heart rate. the internal temperature (Tes) threshold for cutaneous vasodilation was elevated by 0.42 degree C in hypohydrated conditions; but once vasodilation occurred, the slope of the arm blood flow:Tes relation was unchanged from control. Maximal arm blood flow was reduced by nearly 50% in hypohydration. These restrictions in cutaneous blood flow served to maintain an already compromised venous return, but due to the limitation of core-to-skin heat transfer, forced Tes to nearly 39 degrees C, significantly higher than in euhydrated conditions.

To study the effect of hyperosmolality on thermoregulatory responses, five men [average maximal O2 consumption (VO2 max) = 48 ml X kg-1 X min-1] cycled at 65-75% VO2max for up to 30 min in a 30 degrees C, 40% relative humidity environment under three conditions. First, control tests (C) were performed where preexercise plasma volume (PV) and osmolality (Osm) averaged 3,800 ml and 282 mosmol X kg-1, respectively. Second, exercise tests (D) were performed following dehydration induced by fluid restriction and mild exercise (30% VO2max) in hot (40 degrees C) ambient conditions. Each subject then rested in cool surroundings 1 h before performing the exercise test. Preexercise PV and Osm averaged 3,606 ml and 293 mosmol X kg-1, respectively. Third, exercise tests (I) were performed following dehydration, but during the 1-h rest interval, 3% saline was infused so that PV was restored to 3,826 ml and Osm averaged 294 mosmol X kg-1 prior to exercise. During D, esophageal temperatures (Tes) were significantly higher than C, an avg 0.56 degrees C after 20 min exercise due to a 0.22 degrees C increase in Tes threshold for vasodilation, a 39% reduction in slope of the forearm blood flow (BF)-Tes relationship, a 32% average reduction in maximal exercise BF, and a 0.22 degrees C increase in Tes sweating threshold. During I, responses were similar to D, except the BF-Tes slope and the maximum BF were not significantly different from C. Thus hyperosmolality modifies thermoregulation by elevating thresholds for both vasodilation and sweating even without decreases in PV.

Five relatively fit men performed cycle ergometer exercise (65-70% VO2max) for up to 30 min at 30 degrees C, 40% rh. The data from control (normo-volemic), hypovolemic [8.7% reduction in blood volume (BV) induced by diuretics], and hypervolemic [7.9% expansion of BV induced by infusion if isotonic serum albumin] tests revealed significant effects of BV on body fluid and sweating responses. During control exercise, BV decreased an average (+/- SE) 370 +/- 64 ml at 20 min. A significantly smaller loss occurred after 20 min of hypovolemic exercise (270 +/- 29 ml). The decrease in BV during 30 min of hypervolemic exercise (541 +/- 43 ml) was significantly greater than during control (421 +/- 50 ml). Blood volume reduction also significantly altered the control of sweating rate independent of changes in plasma osmolality. The slope of the sweating rate-to-esophageal temperature relationship (SR/Tes) was significantly reduced from the mean value of 1.07 +/- 0.16 and 1.09 +/- 0.18 mg X min-1 X cm-2 X degrees C-1 during control tests, measured from the chest and arm, respectively, to 0.64 +/- 0.11 and 0.63 +/- 0.11 mg X min-1 X cm-2 X degrees C-1 during hypovolemia. The SR/Tes slope was unchanged in hypovolemia over active tissues (calf). Hypervolemia had no effect on the control of sweating at any site. Both the body fluid and sweating responses during hypovolemia act to conserve circulating blood volume during exercise.

Individuals greater than or equal to 60 yr of age are more susceptible to hyperthermia than younger people. However, the mechanisms involved remain unclear. To gain further insight, we examined the heat loss responses of 7 young (24-30 yr) and 13 older (58-74 yr) men during 20 min of cycle exercise [67.5% maximal O2 uptake (VO2max)] in a warm environment (30 degrees C, 55% relative humidity). Forearm blood flow (FBF) and chest sweat rate (SR) were plotted as a function of the weighted average of mean skin and esophageal temperatures [Tes(w)] during exercise. The sensitivity and threshold for each response were defined as the slope and Tes(w) at the onset of the response, respectively. When the young sedentary men were compared with a subgroup (n = 7) of the older physically active men with similar VO2max, the SR and FBF responses of the two groups did not differ significantly. However, when the young men were compared with a subgroup of older sedentary men with a similar maximal O2 pulse, the SR and FBF sensitivities were significantly reduced by 62 and 40%, respectively. These findings suggest that during a short exercise bout either 1) there is no primary effect of aging on heat loss responses but, rather, changes are associated with the age-related decrease in VO2max or 2) the decline in heat loss responses due to aging may be masked by repeated exercise training.