Intense exercise is associated with a reduction in cerebral blood flow (CBF), but regulation of CBF during strenuous exercise in the heat with dehydration is unclear. We assessed internal (ICA) and common carotid artery (CCA) haemodynamics (indicative of CBF and extra-cranial blood flow), middle cerebral artery velocity (MCA Vmean), arterial–venous differences and blood temperature in 10 trained males during incremental cycling to exhaustion in the heat (35°C) in control, dehydrated and rehydrated states. Dehydration reduced body mass (75.8 ± 3 vs. 78.2 ± 3 kg), increased internal temperature (38.3 ± 0.1 vs. 36.8 ± 0.1°C), impaired exercise capacity (269 ± 11 vs. 336 ± 14 W), and lowered ICA and MCA Vmean by 12–23% without compromising CCA blood flow. During euhydrated incremental exercise on a separate day, however, exercise capacity and ICA, MCA Vmean and CCA dynamics were preserved. The fast decline in cerebral perfusion with dehydration was accompanied by increased O2 extraction (P < 0.05), resulting in a maintained cerebral metabolic rate for oxygen (CMRO2). In all conditions, reductions in ICA and MCA Vmean were associated with declining cerebral vascular conductance, increasing jugular venous noradrenaline, and falling arterial carbon dioxide tension () (R2 ≥ 0.41, P ≤ 0.01) whereas CCA flow and conductance were related to elevated blood temperature. In conclusion, dehydration accelerated the decline in CBF by decreasing and enhancing vasoconstrictor activity. However, the circulatory strain on the human brain during maximal exercise does not compromise CMRO2 because of compensatory increases in O2 extraction.

Limb tissue and systemic blood flow increases with heat stress, but the underlying mechanisms remain poorly understood. Here, we tested the hypothesis that heat stress-induced increases in limb tissue perfusion are primarily mediated by local temperature-sensitive mechanisms. Leg and systemic temperatures and hemodynamics were measured at rest and during incremental single-legged knee extensor exercise in 15 males exposed to 1 h of either systemic passive heat-stress with simultaneous cooling of a single leg (n = 8) or isolated leg heating or cooling (n = 7). Systemic heat stress increased core, skin and heated leg blood temperatures (Tb), cardiac output, and heated leg blood flow (LBF; 0.6 ± 0.1 l/min; P < 0.05). In the cooled leg, however, LBF remained unchanged throughout (P > 0.05). Increased heated leg deep tissue blood flow was closely related to Tb (R2 = 0.50; P < 0.01), which is partly attributed to increases in tissue V̇O2 (R2 = 0.55; P < 0.01) accompanying elevations in total leg glucose uptake (P < 0.05). During isolated limb heating and cooling, LBFs were equivalent to those found during systemic heat stress (P > 0.05), despite unchanged systemic temperatures and hemodynamics. During incremental exercise, heated LBF was consistently maintained ∼0.6 l/min higher than that in the cooled leg (P < 0.01), with LBF and vascular conductance in both legs showing a strong correlation with their respective local Tb (R2 = 0.85 and 0.95, P < 0.05). We conclude that local temperature-sensitive mechanisms are important mediators in limb tissue perfusion regulation both at rest and during small-muscle mass exercise in hyperthermic humans.

Heat stress, leading to elevations in whole-body temperature, has a marked impact on both physical performance and cognition in ecological settings. Lab experiments confirm this for physically demanding activities, whereas observations are inconsistent for tasks involving cognitive processing of information or decision-making prior to responding. We hypothesized that divergences could relate to task complexity and developed a protocol consisting of 1) simple motor task [TARGET_pinch], 2) complex motor task [Visuo-motor tracking], 3) simple math task [MATH_type], 4) combined motor-math task [MATH_pinch]. Furthermore, visuo-motor tracking performance was assessed both in a separate- and a multipart protocol (complex motor tasks alternating with the three other tasks). Following familiarization, each of the 10 male subjects completed separate and multipart protocols in randomized order in the heat (40°C) or control condition (20°C) with testing at baseline (seated rest) and similar seated position, following exercise-induced hyperthermia (core temperature ∼ 39.5°C in the heat and 38.2°C in control condition). All task scores were unaffected by control exercise or passive heat exposure, but visuo-motor tracking performance was reduced by 10.7 ± 6.5% following exercise-induced hyperthermia when integrated in the multipart protocol and 4.4 ± 5.7% when tested separately (both P < 0.05). TARGET_pinch precision declined by 2.6 ± 1.3% (P < 0.05), while no significant changes were observed for the math tasks. These results indicate that heat per se has little impact on simple motor or cognitive test performance, but complex motor performance is impaired by hyperthermia and especially so when multiple tasks are combined.

The ability of direct heat stress to increase limb blood flow is well known, but the magnitude and profile of hemodynamic responses within the major vessels of the leg have not been explored. Here, we systematically characterize these responses through a wide range of heat stress levels and show that isolated leg heating confers potentially beneficial hemodynamic changes equivalent to those of moderate whole body hyperthermia, with these hemodynamic adjustments being predominantly driven by local temperature-sensitive mechanisms.

Reductions in cerebral blood flow and extracranial perfusion, induced by dehydration during prolonged exercise in the heat, may be coupled to fatigue. However, cerebral metabolism remains stable through enhanced O2 and glucose extraction. Thus, fatigue developed during prolonged exercise with dehydration is related to reductions in cerebral blood flow rather than to the cerebral metabolic rate for O2.