The effect of heat acclimation on body-fluid regulation

Author

Mark J. Patterson, University of WollongongFollow

Year

1999

Degree Name

Doctor of Philosophy

Department

University of Wollongong. Dept. of Biomedical Science

Recommended Citation

Patterson, Mark J., The effect of heat acclimation on body-fluid regulation, Doctor of Philosophy thesis, University of Wollongong. Dept. of Biomedical Science, University of Wollongong, 1999. https://ro.uow.edu.au/theses/1098

Abstract

Following heat acclimation, a greater cardiac and thermal stability are reported regularly, during exercise in the heat. However, the mechanisms responsible for this greater stability are not completely understood. While a greater cardiac stability may result from an expanded resting plasma volume (PV), the mechanisms responsible for this expansion are contentious. Furthermore, an attenuated plasma loss during exercise in the heat may also improve cardiac stability, yet no investigation has adequately addressed this issue. Reductions in oesophageal temperature (T_es) during exercise in humid heat imply a greater thermal stability, which is possibly attributed to a greater evaporative heat loss. A redistribution of the sweating response may aid in elevating evaporation, however, methodological limitations have hindered interpretations of findings in previous investigations. This investigation was design to evaluate some of the underlying mechanisms responsible for a greater cardiac and thermal stability following heat acclimation.

Twelve male subjects completed a 22-d heat acclimation regimen. Heat acclimation exposures involved controlled hyperthermia (T_c = 38.5°C) during cycle ergometry for 90-min per day, six days a week (40°C, 60% RH ) . Resting body-fluid volumes and physiological responses to exercise in the heat were assessed on days 1, 8 and 22. Resting total body water (TBW; ³H ) , extracellular fluid (ECF; ⁸²Br and ⁵¹Cr-EDTA) and P V (T-1824) were determined, while intracellular fluid (ICF) and interstitial fluid (ISF) were derived. Local sweat rate responses were continuously measured (capacitance hygrometry; 3.16 cm² capsules) at the forehead, chest, scapula, forearm and thigh- Changes in bodyfluid volumes were determined using changes in body mass and urine loss (TBW), haematocrit and haemoglobin (PV), and chloride content (ECF). A number of plasma constituents were also measured: Na⁺, K⁺, CI^-, osmolality, total protein, albumin, arginine vasopressin, atrial natriuretic peptide and aldosterone.

Heat acclimation resulted in resting PV, ECF and TBW expansions on day 8. The relative PV expansion was similar to the ECF expansion, which probably implied that a greater retention of electrolytes was responsible for the PV expansion. However, on day 22 the elevated ECF could not solely account for the PV expansion, implying that plasma protein may have been responsible for the different elevations between PV and ECF.

Exercise-induced PV decrements indicated that PV was not preferentially defended after heat acclimation, and may even contribute to a greater proportion to the TBW loss. It was hypothesised that a reduced plasma albumin loss may aid in reducing the plasma loss, however, a trend for greater plasma albumin loss was observed after heat acclimation. The elevated resting PV accompanying heat acclimation may enable maintenance of venous return and cardiac filling pressures during exercise. This greater cardiac stability may result in a smaller decrement in splanchnic blood flow, which may have contributed to the loss of intravascular protein and fluid, following heat acclimation.

The previously reported trunk to limb redistribution of sweating was not observed in the current investigation. Large relative elevations in sweat rate were observed at the forearm and chest, in combination with smaller increments at the forehead and thigh. At any given site, the acclimationinduced sweating responses may simply be a function of differences in local sweat gland capacities, since the large variation observed prior to acclimation was reduced. Regions that possessed the lowest sweat gland capacities exhibited the greatest relative increases in sweat rate.

In conclusion, heat acclimation provided a greater cardiac stability during exercise in humid heat, although this was not associated with a greater maintenance of PV. The resting PV expansion was probably responsible for the greater cardiac stability and plasma loss during exercise. A lower T_es was evident during exercise in humid heat following acclimation, although this displacement seemed reliant on the reduced resting T_es, rather than greater heat dissipation. Therefore, it would seem that the major benefit of heat acclimation, during exercise in humid heat, is a greater cardiac stability, since the high ambient temperature and water vapour pressure hindered improvements in heat loss.