The influence of thermal factors on post‐exercise haemodynamics in endurance exercise‐trained men

Recovery from exercise is associated with significant cardiovascular adjustments. Studies have shown that a single bout of dynamic exercise elicits a persistent reduction in mean arterial pressure lasting nearly 2 h in healthy normotensive individuals (Halliwill, 2001). It occurs in response to either aerobic or resistance exercise (MacDonald et al. 1999) although the magnitude of the decrease in mean arterial pressure is more pronounced and longer following exercise of increasing intensity (Forjaz et al. 2004). The removal of the skeletal muscle pump is thought to promote venous blood pooling which in turn reduces cardiac filling and unloads cardiopulmonary baroreceptors (Halliwill, 2001). The baroreflex is reset to defend a lower blood pressure following exercise and sympathetic vasoconstrictor outflow is consequently reduced (Halliwill et al. 1996). Furthermore, vascular responsiveness to sympathetic vasoconstrictor outflow is impaired so that vascular resistance is attenuated for a given level of sympathetic nerve stimuli (Halliwill et al. 2003). Other factors contributing to the post-exercise hyperaemia include a sustained histamine receptor-dependent vasodilatation (McCord & Halliwill, 2006). The vasodilatation that underlies post-exercise hypotension is not restricted to active skeletal muscles but also involves inactive muscle regions as forearm and calf vascular resistances are decreased in parallel with systemic vascular resistance (Senitko et al. 2002). Recent interpretation of data suggests that post-exercise hypotension in healthy sedentary and normally active individuals is due to a persistent rise in systemic vascular conductance that is not completely offset by increases in cardiac output (Halliwill, 2001). However, endurance-trained men appear to be an exception as systemic vascular conductance remains unchanged or decreases relative to pre-exercise and cardiac output falls during recovery from exercise (Senitko et al. 2002; Dujic et al. 2006). Differences in myocardial contractility and/or central venous pressure (associated with sweating-induced plasma volume losses) response have been proposed as possible factors underlining the post-exercise reduction in cardiac output. Lynn et al. (2009) demonstrate in this issue of The Journal of Physiology that ‘in the absence of either superimposed orthostatic stress or hypervolaemia, oral fluid replacement that restores normal plasma volume does not attenuate post-exercise hypotension’ but does mitigate the reduction in cardiac output (and stroke volume) typically seen in endurance-trained individuals. While it is suggested that factors related to plasma volume changes that affect preload and/or cardiac dimension and function may explain the underlying cause for the reduced cardiac output observed post-exercise in endurance-trained men, Lynn et al. (2009) propose a novel perspective that the cause may be of thermal rather non-thermal origin. An unexpected finding of their study was the observed similarity in the pattern of response in cardiac output following exercise performed in the heat without fluid replacement compared to exercise at normal ambient temperature with fluid replacement. One would expect that exercise performed in the heat would exacerbate the post-exercise reductions in cardiac output due to exercise-induced decreases in central blood volume associated with a greater sweating response (loss of plasma volume) and a parallel elevated skin blood flow response (redistribution of blood to compliant cutaneous vasculature). What are the implications of a possible thermal influence on altering post-exercise haemodynamics? An earlier study by Senitko et al. (2002) compared responses between sedentary and endurance-trained individuals following exercise performed at the same relative peak oxygen consumption . A greater rate of metabolic heat production elicited by workloads based on equal percentages of a different will require substantially greater rates of sweating and skin blood flow to maintain heat balance in endurance-trained individuals. Thus, one cannot discount the possibility that the post-exercise reduction in cardiac output in trained men observed by Senitko et al. (2002) is the result of a greater sweating-related fluid loss leading to greater reductions in plasma volume and therefore central venous pressure. While Lynn et al. (2009) did not compare responses with sedentary or recreationally active individuals, their observation that exercise in the heat without fluid replacement attenuated the post-exercise reduction in cardiac output also suggests an important role for thermal factors. The notion that thermal factors might modulate the post-exercise cardiac output response is certainly an interesting one. Exercise in the heat is associated with significant cardiovascular and thermoregulatory disturbances which can persist for a prolonged period post-exercise. Thus, it is not inconceivable to suggest a possible role of thermal input in the control of cardiac output. Lynn et al. (2009) surmised that the post-exercise elevated cardiac output under warm ambient conditions may be linked to a temperature-dependent increase in myocardiac contractility (Johnson & Proppe, 1996) and/or cardiac function (Brothers et al. 2009). This was shown by the fact that the increase in cardiac output was parallelled by a concomitant increase in heart rate and occurred during a state of elevated hyperthermia (∼0.2°C above baseline resting) for the duration of recovery. In evaluating the effects of fluid replacement and heat stress on post-exercise haemodynamics, the present contribution by Lynn et al. (2009) provides a more comprehensive understanding of the mechanisms governing the post-exercise reduction in cardiac output in highly fit individuals. Further, their work establishes a strong methodological framework from which future investigations may be conducted to examine this response under conditions of increasing levels of cardiovascular (i.e. higher levels of dehydration) and thermal (i.e. elevated levels of hyperthermia) strain. While their findings show that thermal factors have an influence on post-exercise haemodynamics, the precise physiological relationship is an important area of future study.

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