Cardiovascular Determinants Involved in Pacing Under Heat Stress

Abstract

I read with interest the review by Roelands et al. [1] regarding the ‘‘Neurophysiological Determinants of Theoretical Concepts and Mechanisms Involved in Pacing.’’ The manuscript explains much of the recently published literature pertaining to the novel mechanisms suggested to regulate or influence pacing and pacing strategy during time-trial exercise. As the authors highlight, the regulation of prolonged self-paced exercise is multifactorial and as such is influenced by a variety of factors, including the development of hyperthermia, brain neurotransmitters, the perception of effort, neuromuscular function, and metabolism. However, a particular mechanism that is conspicuously absent from the discussion, particularly when referring to prolonged efforts in the heat, is that of cardiovascular limitations. The first goal of the manuscript was to review the existing literature on pacing strategies in different climatic conditions [1]. Rightly, it is underscored that during exercise in the heat, a redistribution of blood from the core to the skin may decrease available blood flow to the exercising muscle. Yet, this potential influence on performance is not further discussed. Rather, the authors conclude that ‘‘recent literature showed that during exercise in the heat, a reduction in power output and muscle activation occurs before a critical core temperature is reached, indicating that subjects can anticipate the exercise intensity and heat stress they will be exposed to; thereby preventing catastrophic outcomes’’ [1]. Although the concept of cardiovascular limitations during prolonged exercise in the heat dates from the early work of Rowell [2–4], it is in itself not dated. The premise of this mechanism lies with the redistribution of blood flow from the central to the peripheral circulation for the purposes of thermoregulation. During exercise in the heat, core and skin temperature increase. This increase narrows the core-to-skin temperature gradient, which in turn increases the skin blood flow requirement for heat dissipation [5]. The rise in cutaneous blood volume and a temperature-mediated increase in intrinsic heart rate result in a decrease in cardiac filling, which ultimately leads to the reduction in stroke volume [3, 6–9]. Consequently, when exercise is performed in the heat, maximum cardiac output decreases [10, 11] and the cardiovascular system is forced toward a functional limit at submaximal workloads and oxygen uptake (i.e., maximal aerobic capacity is reduced) [12–15]. This reduction in cardiovascular reserve is purported to be the primary factor limiting constant rate aerobic exercise in the heat, and is manifested as an increase in relative exercise intensity [% maximum oxygen uptake (%VO2max)] and perceived exertion [10, 11, 16]. While the previous observations pertain to constant-rate exercise and have been reported outside the literature search range (2004–2012) defined by the authors, two selfpaced studies that fall within the literature search parameters were not included. Indeed, Ely et al. [17] examined well-trained runners performing an 8-km time trial in warm (*30 C) and cool (*17 C) environments. As with most studies, it was observed that time to completion was longer in warm conditions. However, the authors provided evidence against both the attainment of a critical core temperature and changes in heat storage regulating pacing in Please link with doi:10.1007/s40279-013-0051-z, the reply to this letter.