EFFECT OF BODY FLUID REGULATION ON SWEATING

Prolonged exposure to hyperthermic conditions and/or prolonged exercise in the heat can induce water deficits due to profuse sweating, resulting in dehydration. This water deficit lowers both intracellular and extracellular volumes and results in plasma hyperosmolality and hypovolemia, both of which impair sweating. For example, Greenleaf and Castle proposed that the excessive rise in internal temperature in dehydrated subjects was due to inadequate sweating. Expanding this concept, Sawka observed that in progressively dehydrated subjects sweat rate was dramatically reduced despite greater elevations in rectal temperature. Later, Montain demonstrated that the threshold for the onset of sweating was elevated, whereas the slope of the relationship between the elevation in sweat rate relative to the elevation in internal temperature was attenuated, as a function of the level of dehydration, both of which are strongly suggestive of impaired sweating responsiveness.

Fortney conducted a study to identify the importance and independence of decreases in fluid volume (hypovolemia) from increases in plasma osmolality (hyperosmotic) on sweat rate.

Normovolemic subjects were exposed to heat stresses under hyperosmotic and isoosmotic conditions while sweat rate was assessed. During the ensuing exercise bout, the internal temperature threshold for the onset of sweating was significantly elevated relative to the response during exercise under isoosmotic conditions. The slope of the relationship between the elevation in sweating and the elevation in internal temperature was not affected by increased plasma osmolality.

Takamata extended these findings on assessing sweat rate in heat-stressed subjects who received an infusion of 0.9 or 3% saline.

They found that the threshold for sweating in the hyperosmotic condition (i.e., 3% saline infusion) was greatly shifted to a higher internal temperature relative to the isoosmotic condition. This hyperosmolality-induced suppres-sion of the sweating occurred regardless of heat acclimation status. In a follow-up study, Takamata found that when hyperosmotic subjects drink deionized water (38°C), sweat rate immediately increases without changes in plasma osmolality, although drinking deionized water in isoosmotic subjects did not alter sweat rate. These findings demonstrate that increased plasma osmolality, independent of plasma volume, impairs sweating responses and that an oral-pharyngeal reflex can modulate the sweating response in hyperosmotic individuals.

Fortney addressed the opposite question relative to that presented above, in that they investigated whether changes in blood volume, while keeping plasma osmolality constant, modulates the sweating response. They found that isoosmotic hypovolemia reduced the slope of the relationship between the change in sweating relative to the change in internal temperature, without altering the internal temperature threshold for the onset of sweating . Such a finding suggests that, once sweating has begun for the same elevation in internal temperature, there was less of an elevation in sweating. Conversely, isoosmotic hypervolemia does not change the internal temperature threshold for sweating or the aforementioned slope, unless plasma and blood volume expansion occurs via erythrocyte infusion. These observations suggest that sweating can be inhibited by isoosmotic hypovolemia, whereas hypervolemia in the absence of erythrocyte infusion does not alter sweating responses.