Description:
<jats:p> The aim was to determine the mechanisms facilitating exercise performance in hot conditions following heat training. In a counter-balanced order, seven males (V̇o<jats:sub>2max</jats:sub> 61.2 ± 4.4 ml·min<jats:sup>−1</jats:sup>·kg<jats:sup>−1</jats:sup>) were assigned to either 10 days of 90-min exercise training in 18 or 38°C ambient temperature (30% relative humidity) applying a cross-over design. Participants were tested for V̇o<jats:sub>2max</jats:sub> and 30-min time trial performance in 18 (T18) and 38°C (T38) before and after training. Blood volume parameters, sweat output, cardiac output (Q̇), cerebral perfusion (i.e., middle cerebral artery velocity [MCAv<jats:sub>mean</jats:sub>]), and other variables were determined. Before one set of exercise tests in T38, blood volume was acutely expanded by 538 ± 16 ml with an albumin solution (T38<jats:sub>A</jats:sub>) to determine the role of acclimatization induced hypervolemia on exercise performance. We furthermore hypothesized that heat training would restore MCAv<jats:sub>mean</jats:sub> and thereby limit centrally mediated fatigue. V̇o<jats:sub>2max</jats:sub> and time trial performance were equally reduced in T38 and T38<jats:sub>A</jats:sub> (7.2 ± 1.6 and 9.3 ± 2.5% for V̇o<jats:sub>2max</jats:sub>; 12.8 ± 2.8 and 12.9 ± 2.8% for time trial). Following heat training both were increased in T38 (9.6 ± 2.1 and 10.4 ± 3.1%, respectively), whereas both V̇o<jats:sub>2max</jats:sub> and time trial performance remained unchanged in T18. As expected, heat training augmented plasma volume (6 ± 2%) and mean sweat output (26 ± 6%), whereas sweat [Na<jats:sup>+</jats:sup>] became reduced by 19 ± 7%. In T38 Q̇<jats:sub>max</jats:sub> remained unchanged before (21.3 ± 0.6 l/min) to after (21.7 ± 0.5 l/min) training, whereas MCAv<jats:sub>mean</jats:sub> was increased by 13 ± 10%. However, none of the observed adaptations correlated with the concomitant observed changes in exercise performance. </jats:p>