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Dehydration, the process of losing body water through thermoregulatory sweating, can lead to marked alterations in physiological function and decrements in athletic performance during training and competition in temperate-to-hot environments. Impaired endurance capacity in the dehydrated athlete is often associated with significant cardiovascular strain, typified by gradual reductions in cardiac output, mean arterial pressure and blood flow to exercising limb muscle and skin during prolonged exercise in temperate and warm environments (Sawka et al. 1979; Hamilton et al 1991; Montain & Coyle, 1992; González-Alonso et al. 1995, 1998, 2008). Blood flow to the brain might also decline with dehydration since reductions in blood flow to active muscle and skin only account for two-thirds of the fall in cardiac output during prolonged exercise in the heat (González-Alonso et al. 1998). The first study of this project systematically investigated the responses of the cerebral circulation and metabolism to progressive dehydration during submaximal and maximal aerobic exercise in the heat and the benefits of maintaining a normal hydration status (euhydration) via fluid ingestion.

A widely held concept in cardiovascular physiology is that blood flow to the muscles of the arm and legs remain unchanged in humans exposed to severe environmental heat stress, despite cardiac output increasing by up to 5-6 L/min compared to control resting conditions (Rowell 1974). This has been interpreted to mean that muscle blood flow regulation is insensitive to increases in tissue temperature. Findings from our laboratory, however, challenge this long-standing view by showing that the heat stress-mediated increases in leg blood flow (up to 1.1 L/min above baseline) are accompanied by proportional reductions in muscle blood oxygenation indicative of significant increases in leg muscle blood flow with elevations in temperature (Pearson et al. 2011). Because both blood and muscle temperatures increase rapidly at onset of exercise (González-Alonso et al., 1999; González-Alonso & Calbet 2003), our recent observations raise important questions regarding the role of blood and tissue temperature on the regulation of muscle, brain and systemic blood flow in exercising humans. A second aim of this project was therefore to further investigate the responses and temperature-sensitive mechanisms controlling limb tissue hyperaemia in the heat stressed human.

Research Studies

This project consisted of three different studies. The two major aims of these studies were (1) to characterise the impact of hydration and heat stress on brain and active muscle blood flow and metabolism during submaximal and maximal aerobic exercise and (2) to provide insight into the temperature-sensitive mechanisms controlling local tissue blood flow with hyperthermia. Detailed information about the experimental designs employed for each of the studies can be found in the research outputs reported below.

Ã÷ÐÇ°ËØÔ 1: Brain circulation and metabolism during prolonged submaximal and incremental maximal aerobic exercise with exercise-induced dehydration and hydration.

Ã÷ÐÇ°ËØÔ 2: Brain and muscle blood flow and metabolism during incremental cycling exercise with and without heat stress

Ã÷ÐÇ°ËØÔ 3: Temperature-sensitive mechanism controlling limb tissue hyperthermia in the heat stressed-human.

Knowledge of how vital organs such as the brain, heart and active muscles respond to strenuous exercise is paramount to advance our understanding of exercise fatigue mechanisms and thus optimise human performance. This project characterized the brain, muscle and systemic blood flow and metabolic responses to strenuous submaximal and maximal aerobic exercise in conditions commonly experienced by elite and recreational athletes in warm and hot environments. A close association between the development of fatigue and reductions in cerebral and muscle blood flow and oxygen delivery was observed, particularly when fatiguing sooner whilst experiencing significant dehydration and hyperthermia.

Whilst the development of dehydration and hyperthermia exacerbates the cerebrovascular strain and accentuates the fall in cerebral blood flow, the global brain aerobic metabolism is preserved due to compensatory elevations in oxygen and substrate extraction from the circulation. Thus, reduced brain aerobic metabolism is unlikely to contribute to the fall in maximal aerobic power and endurance performance in the dehydrated and hyperthermic athlete. Rather, the early fatigue experienced by the dehydrated athlete in these conditions is coupled to high levels of core hyperthermia and alterations in muscle substrate, glycogen and oxygen utilization and increases in muscle anaerobic metabolism and neural activation, possibly reflecting a mismatch between energy demand and production.

These findings provide physiologists, sport scientists, coaches and athletes with evidence to explain how dehydration and/or hyperthermia impact brain and muscle blood perfusion and metabolism during exercise and heat stress and ultimately human performance. The data further substantiate the use of fluid replacement during exercise as a means of delaying the reductions in brain, skeletal muscle and systemic circulation during exhaustive exercise in temperate to hot environments and thus optimise performance in the endurance athlete. 

Research Outputs

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