THERMAL CONTROL OF SWEATING

In the late 19th and early 20th centuries, the existence of a thermoregulatory center within the hypothalamic region of the brain was identified. Studies demonstrated that elevated brain temperature engaged heat loss mechanisms in animals. Reports from early investigators were somewhat mixed with respect to the location of the primary controller of sweating. Before the middle of the 20th century, it was thought that skin temperature was more important in the control of sweating relative to internal temperature. For example, in 1923, Adolph reported that, in nonexercising subjects, sweat rate was proportional to the effective environmental temperature above 90°F (32°C) and suggested a close correlation between sweating and superficial body temperature.

Kuno later suggested that central thermoregulatory centers were more important for temperature control, because sweating responses were delayed despite increasing skin temperature when exposed to elevated environmental temperatures. Kuno proposed that, if skin temperature was the primary controller of sweating, then sweating should have occurred immediately on exposure to the elevated environmental conditions. Nevertheless, Kuno did not evaluate sweating as a function of internal temperature in those studies.

In 1959, Benzinger proposed that, under steady-state conditions the increased sweat rate caused by exercise and/or variations in the environmental temperature were very closely correlated to rises in tympanic temperature and that this relationship was stronger than the relationship between skin temperature and sweating. His proposition was later supported by Nielsen and Nielsen, although they observed that rapid decreases in mean skin temperature reduced sweat rate when internal temperature remained stable.

Given findings that internal and mean skin temperatures can control sweating, researchers began to assess the relationship between sweating and various combinations of internal and skin temperatures. This resulted in the concept of mean body temperature, which represents the sum of a fraction of internal and skin temperatures, and it is now frequently used when expressing sweating responses during exercise and during exposure to elevated ambient air temperatures.

Although alluded to by others, Nadel and colleagues were among the first to directly access the relationship between the increase in sweat rate relative to dynamic increases in internal temperature in humans. Later, this concept was confirmed in monkeys in which direct measures of brain temperature were obtained while sweating was assessed by Smiles. They concluded that sweating is primarily controlled by central brain temperature and secondarily affected by mean skin temperature. Given these findings, sweating responses are now commonly characterized by the internal or mean body temperature threshold for the onset of sweating, as well as the slope of the relationship between the elevation in sweating and the elevation in internal or mean body temperature, as eloquently outlined in the reviews by Gisolfi and Wenger. An increase in the internal or mean body temperature threshold for the onset of sweating and/or an attenuation of the elevation in sweating relative to the elevation in internal or mean body temperature is recognized as impaired sweating responsiveness.

Whereas mean skin temperature alters sweating via central mechanisms, sweat rate is also influenced by local temperature of the sweat gland via peripheral mechanisms. For example, local heating accentuates sweat rate while local cooling attenuates sweat rate. Possible mechanisms by which local temperature alters sweating may be an effect of temperature on neurotransmitter release or sensitization or desensitization of the receptors on sweat glands by temperature. It remains unclear which of these mechanisms, or whether both, are responsible for these observations.