Fat oxidation during whole body exercise appears to be a good example of regulation by the interaction of physiological systems

Abstract

A hallmark of metabolism during aerobic exercise such as walking, running or bicycling is a reduction in the absolute rate of fat oxidation when the intensity exceeds moderate levels (e.g. above approximately 60–75% maximal oxygen uptake). Running and bicycling are termed ‘whole body’ type exercise as they can recruit a large amount of skeletal muscle, involving both legs, several joints and numerous muscles while also triggering a strong neuroendocrine response, particularly when the intensity is high. This response includes a reduced rate of blood flow to each kilogram of exercising muscle, due presumably to central cardiovascular limitations (Andersen & Saltin, 1985) that restrict oxygen and plasma fatty acid delivery to muscle. In this issue of The Journal of Physiology, Helge et al. (2007) indicate that the hallmark reduction in fat oxidation during high intensity exercise does not occur when exercising a small muscle mass at a relatively high intensity of 85% of maximum aerobic power. It should be noted that the assumption of this paper is that the higher than expected rate of fat oxidation during exercise with a small compared to a large muscle mass (i.e. whole body) occurs without a reduction in the absolute amount of power or oxygen consumption per kilogram of active muscle. Although the authors present reasonable arguments to support this assumption it should be recognized that it is difficult to directly verify that the exercise load per kilogram of muscle under these conditions was identical to that during intense whole body exercise. Helge et al. (2007) indicate that unlike whole body exercise, small muscle mass exercise provides the working muscle tissue with high blood flow and oxygen supply while exposing it to only a small elevation in hormones such as adrenaline and noradrenaline. The implication is that ‘extra-muscular factors’, including but not limited to oxygen delivery, fatty acid delivery and catecholamines, play a functional role in regulating metabolism in general and in this case initiating the reduction in fat oxidation when whole body exercise becomes intense. The authors have employed several sophisticated cardiovascular and metabolic techniques to study fat metabolism directly across a limited amount of muscle mass during exercise. In a sense, the design shares similarities to studies that perfuse the isolated hindlimbs of animals during electrical muscle stimulation in that both preparations lack the strong potential influence of the neuroendocrine system. Furthermore, oxygen delivery could be maintained higher than what is typically observed during whole body exercise. Of course it is well known that muscle glycogenolysis or metabolic stress can be increased by reducing oxygen delivery or by increasing plasma adrenaline and that fat oxidation is subsequently attenuated (Wilson et al. 1977; Mora-Rodriguez & Coyle, 2000). Helge et al. (2007) currently recognize that increased glycolytic flux, muscle acidosis and lactate production are associated with the classic reduction in fat oxidation that typically accompanies high intensity whole body exercise. It seems that intense exercise at 85% of maximum aerobic power with a small muscle mass failed to attenuate fat oxidation, probably because it failed to markedly increase glycolytic flux and muscle lactate or venous lactate concentration. This agrees with the concept that carbohydrate metabolism regulates fat oxidation. It could be argued that fat oxidation was not reduced during intense small muscle mass exercise because glycolytic flux and lactate accumulation were not stimulated as much as would occur during large muscle mass exercise that places the same work-rate and oxygen cost on each kilogram of active muscle. If that is the case, then focus might again be placed on extramuscular factors, and their interactions, which increase glycolytic flux during whole body exercise as the intensity increases sufficiently to reduce fat oxidation. These observations beautifully exemplify systems physiology by suggesting that fat oxidation during exercise reflects a fine interplay between the cardiovascular, neurological, endocrine and muscle metabolic systems. These observations add strength to the possibility that the ‘functionally’ regulating factors that attenuate fat oxidation by muscle during high intensity exercise are extramuscular factors that stimulate muscle glycolytic flux (i.e. reduced oxygen delivery, muscle ATP/ADP ratio, catecholamines). This could imply that agents might be developed that allow the fat oxidation potential of skeletal muscle to be maintained even during exercise with a large muscle mass and thus under conditions of high total caloric expenditure and high total fat oxidation. Endurance exercise training has these benefits, yet the exact interplay between muscular adaptations (e.g. mitochondrial activity and capillarzation) and extramuscular factors (e.g.; oxygen and catecholamines) remains to be fully elucidated.