Physical activity and metabolic cardiovascular syndrome.

Industrialization and computerization have provided comfort and well-being to communities living in industrialized countries but have also been responsible for a considerable decrease in daily energy needs. This issue has not been investigated in longitudinal studies but cross-sectional observations suggest that the transition from traditional to modern lifestyle may have induced a decrease in daily energy expenditure of 1–2 MJ/d, or even more (Singh et al. 1989). Since a regular participation in physical activity is known to facilitate the control of body weight, to reduce glycogen stores, and to increase sympathetic nervous system (SNS) activity, at least in skeletal muscle, a shift towards a sedentary lifestyle also necessarily involves a loss in the potential to regulate efficiently the energy–carbohydrate–lipid metabolism. This means that active people can maintain energy and macronutrient balance without excess plasma glucose and non-esterified fatty acid concentrations and their related mass-action effect to sustain substrate flux. In more clinical terms, regular physical activity thus reduces the likelihood to develop diseases associated with excess circulating substrates that are characterizing metabolic cardiovascular syndrome. In this month’s issue, Wareham and colleagues (Wareham et al. 1998) report a study that examined the relationship between physical activity participation and the risk to develop metabolic cardiovascular syndrome. As expected, the less-active, less-fit subjects were more prone to display the features of the syndrome, i.e. an increase in fasting and post-glucose glycaemia, hyperinsulinaemia and blood pressure. They were also more predisposed to dyslipidaemias. The original aspect of this study design was to allow a dissociation of the effects of fitness and energy expenditure in the aetiology of metabolic cardiovascular syndrome. The fitness component reflects long-term adaptations to exercise such as change in adiposity and the cumulative impact of exercise on mechanisms involved in biological work production. The energy expenditure component rather integrates the effect of variations in spontaneous movement (fidgeting) energy cost of activities, and voluntary participation in physical activities. This component also reflects the contribution of acute changes in variables involved in the regulation of energy and macronutrient balance such as glycogen stores, SNS activity, and other less-characterized factors. In addition, the two components are probably subjected to a different effect of heredity, sex, and measurement error. The calculation of univariate odds ratio revealed that the association with metabolic cardiovascular syndrome was stronger for the fitness component. However, after adjustment for obesity, sex, and exposure measurement error, results suggested that the syndrome was rather strongly related to reduced habitual energy expenditure. Beyond these specific conclusions, the question that arises from the Wareham et al. paper is ‘What is the biological meaning of their results?’ An attempt to answer this question is illustrated in Table 1 which first draws attention to the opposite effects of physical activity and metabolic syndrome on blood pressure, plasma glucose and insulin, and plasma lipids–lipoproteins. Table 1 also emphasizes that both physical activity and the syndrome can increase SNS activity and energy expenditure. Indeed, exercise has been shown to increase post-exercise resting energy expenditure via an increase in SNS activity (Poehlman & Danforth, 1991) mediated by b-adrenoreceptors (Tremblay et al. 1992). This effect seems to be tissuespecific since an increased concentration of b-adrenoreceptors was observed in skeletal muscle but not in heart of British Journal of Nutrition (1998), 80, 215–216 215