Short-term exercise-heat acclimation enhances skin vasodilation but not hyperthermic hyperpnea in humans exercising in a hot environment

We tested the hypothesis that short-term exercise-heat acclimation (EHA) attenuates hyperthermia-induced hyperventilation in humans exercising in a hot environment. Twenty-one male subjects were divided into the two groups: control (C, n = 11) and EHA (n = 10). Subjects in C performed exercise-heat tests [cycle exercise for ~75 min at 58% \( \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} \) (37°C, 50% relative humidity)] before and after a 6-day interval with no training, while subjects in EHA performed the tests before and after exercise training in a hot environment (37°C). The training entailed four 20-min bouts of exercise at 50% \( \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} \) separated by 10 min of rest daily for 6 days. In C, comparison of the variables recorded before and after the no-training period revealed no changes. In EHA, the training increased resting plasma volume, while it reduced esophageal temperature (T _es), heart rate at rest and during exercise, and arterial blood pressure and oxygen uptake (\( \dot{V}_{{{\text{O}}_{2} }} \)) during exercise. The training lowered the T _es threshold for increasing forearm vascular conductance (FVC), while it increased the slope relating FVC to T _es and the peak FVC during exercise. It also lowered minute ventilation (\( \dot{V}_{\text{E}} \)) during exercise, but this effect disappeared after removing the influence of \( \dot{V}_{{{\text{O}}_{2} }} \) on \( \dot{V}_{\text{E}} \). The training did not change the slope relating ventilatory variables to T _es. We conclude that short-term EHA lowers ventilation largely by reducing metabolism, but it does not affect the sensitivity of hyperthermia-induced hyperventilation during submaximal, moderate-intensity exercise in humans.