The effects of heat acclimatization on intravascular volume and protein responses to acute heat stress and exercise were studied in six male subjects. Absolute values for hematocrit and hemoglobin concentration were lower after, than before, acclimatization, indicating hemodilution. Also, after acclimatization, the magnitude of the hemoconcentration response to exercise in the heat was significantly increased. There ws no change in the concentration of plasma protein during or after acclimatization compared with before acclimatization, but there was a net increase in the total intravascular protein content. It is suggested that the hemodilution associated with heat acclimatization may be explained in terms of an increase in the intravascular oncotic pressure following an exercise-induced augmentation of protein, occurring at the expense of the interstitial compartment. It is concluded that this hemodilution is unlikely to be primarily responsible for the cardiovascular adjustment accompanying heat acclimatization and that it should be regarded as a secondary feature of adaptation to heat.
The effects of alterations in skin temperature on intravascular volume and protein content have been investigated in resting subjects. With a normal core temperature (Tac) both skin cooling and skin heating caused hemoconcentration, and heating was associated with an increased rate of protein loss from the intravascular space. Raising of the skin temperature after cooling, with Tac depressed, and cooling of the skin after heating, with Tac raised, were associated with an immediate reversal of the hemoconcentration, and gain of protein by the intravascular space. It is concluded that intravascular volume responses to thermal stress are dependent on the skin and core temperatures obtaining immediately prior to imposition of the stress and that, in particular, a low skin temperature predisposes toward hemodilution on subsequent exposure to heat; sweating per se does not necessarily result in hemoconcentration. The association of hemodilution with augmentation of intravascular protein, and the rapidity with which extravascular protein can apparently gain entry to the intravascular space, is taken as indicating a possible direct return of protein through capillary walls.
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