Rapid weight gain in professional boxing and correlation with fight decisions: analysis from 71 title fights

Exercise in the heat can pose a severe challenge to human cardiovascular control, and thus the provision of oxygen to exercising muscles and vital organs, because of enhanced thermoregulatory demand for skin blood flow coupled with dehydration and hyperthermia. Cardiovascular strain, typified by reductions in cardiac output, skin and locomotor muscle blood flow and systemic and muscle oxygen delivery accompanies marked dehydration and hyperthermia during prolonged and intense exercise characteristic of many summer Olympic events. This review focuses on how the cardiovascular system is regulated when exercising in the heat and how restrictions in locomotor skeletal muscle and/or skin perfusion might limit athletic performance in hot environments.

This article presents a historical overview and an up-to-date review of hyperthermia-induced fatigue during exercise in the heat. Exercise in the heat is associated with a thermoregulatory burden which mediates cardiovascular challenges and influence the cerebral function, increase the pulmonary ventilation, and alter muscle metabolism; which all potentially may contribute to fatigue and impair the ability to sustain power output during aerobic exercise. For maximal intensity exercise, the performance impairment is clearly influenced by cardiovascular limitations to simultaneously support thermoregulation and oxygen delivery to the active skeletal muscle. In contrast, during submaximal intensity exercise at a fixed intensity, muscle blood flow and oxygen consumption remain unchanged and the potential influence from cardiovascular stressing and/or high skin temperature is not related to decreased oxygen delivery to the skeletal muscles. Regardless, performance is markedly deteriorated and exercise-induced hyperthermia is associated with central fatigue as indicated by impaired ability to sustain maximal muscle activation during sustained contractions. The central fatigue appears to be influenced by neurotransmitter activity of the dopaminergic system, but inhibitory signals from thermoreceptors arising secondary to the elevated core, muscle and skin temperatures and augmented afferent feedback from the increased ventilation and the cardiovascular stressing (perhaps baroreceptor sensing of blood pressure stability) and metabolic alterations within the skeletal muscles are likely all factors of importance for afferent feedback to mediate hyperthermia-induced fatigue during submaximal intensity exercise. Taking all the potential factors into account, we propose an integrative model that may help understanding the interplay among factors, but also acknowledging that the influence from a given factor depends on the exercise hyperthermia situation.

It has been proposed that self-paced exercise in the heat is regulated by an anticipatory reduction in work rate based on the rate of heat storage. However, performance may be impaired by the development of hyperthermia and concomitant rise in cardiovascular strain increasing relative exercise intensity. This study evaluated the influence of thermal strain on cardiovascular function and power output during self-paced exercise in the heat. Eight endurance-trained cyclists performed a 40 km simulated time trial in hot (35°C) and thermoneutral conditions (20°C), while power output, mean arterial pressure, heart rate, oxygen uptake and cardiac output were measured. Time trial duration was 64.3 ± 2.8 min (242.1 W) in the hot condition and 59.8 ± 2.6 min (279.4 W) in the thermoneutral condition (P < 0.01). Power output in the heat was depressed from 20 min onwards compared with exercise in the thermoneutral condition (P < 0.05). Rectal temperature reached 39.8 ± 0.3 (hot) and 38.9 ± 0.2°C (thermoneutral; P < 0.01). From 10 min onwards, mean skin temperature was ~7.5°C higher in the heat, and skin blood flow was significantly elevated (P < 0.01). Heart rate was ~8 beats min(-1) higher throughout hot exercise, while stroke volume, cardiac output and mean arterial pressure were significantly depressed compared with the thermoneutral condition (P < 0.05). Peak oxygen uptake measured during the final kilometre of exercise at maximal effort reached 77 (hot) and 95% (thermoneutral) of pre-experimental control values (P < 0.01). We conclude that a thermoregulatory-mediated rise in cardiovascular strain is associated with reductions in sustainable power output, peak oxygen uptake and maximal power output during prolonged, intense self-paced exercise in the heat.