Heat-producing thermoeffector plasticity in response to prolonged iterative exposure to a high-heat loss environment: no indication of thermoregulatory fatigue.

Previous studies have suggested that, during prolonged cold exposure, shivering thermogenesis may gradually be attenuated, supposedly reflecting a state of central fatigue (aka 'thermoregulatory fatigue') provoked by extended shivering activity, that precipitates hypothermia. The purpose of this study was to revisit the validity of this notion. Twelve noncold-acclimatized men participated in three ∼10-h sessions, during which they performed repeatedly three 120-min cold-water immersions. To induce discrete amounts of heat-producing thermoeffector output, presumptively leading to distinct levels of fatigue during each session, subjects were submersed, within each session, in either severely (15°C), moderately (20°C), or slightly (28°C) cold water. The cold-induced elevation in thermogenic rate was similar across the three repeated immersions performed within the 15°C (∼130 W·m²) and 20°C (∼100 W·m²) sessions (P ≥ 0.43). In the 28°C-session, the metabolic heat production was augmented by ∼7% in the second and third immersions compared with the first immersion (P = 0.01). No intrasession differences were noted with regards to the body-core cooling rate, the cold-induced drop in skin temperature and forearm cutaneous vascular conductance, or the stress-hormone (salivary α-amylase and cortisol concentrations) and thermoperceptual responses (P > 0.05). The present findings, therefore, demonstrate that the ability to generate heat remains intact during prolonged iterative exposure to a high-heat loss environment in a single day, regardless of the severity of cold stressor. The intermittent application of slight cold stress (i.e., 28°C water) appears to mediate metabolic sensitization, reflecting either the circadian rhythmicity of heat-producing thermoeffector activity, or perhaps the rapid induction of metabolic adaptation.NEW & NOTEWORTHY The study evaluated whether centrally mediated thermoregulatory fatigue is provoked by prolonged exposure to uncompensable cold. Regardless of the severity of cold stressor, the ability to produce endogenous heat remains intact during prolonged iterative exposure to a high-heat loss environment.