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Few studies have investigated the influence of body composition, abdominal obesity, age and fitness on coronary risk factors in populations of patients with coronary heart disease (CHD). We investigated whether abdominal obesity or generalized adiposity is a better predictor of cardiovascular risk in men with coronary artery disease (CAD), and the effects of exercise training on coronary risk factors in younger and older patients with CAD.The study population consisted of 81 male patients aged 33-83 years (mean +/- SD 60.0 +/- 13.3 years) with established CAD. We studied the relationships among body composition, body fat distribution, dietary intake, peak aerobic capacity, lipid concentrations, and plasma glucose and insulin concentrations. We subsequently measured the influence of exercise training on these components.The study population was characterized by a high prevalence of obesity, particularly in younger patients. Body mass index, rather than body fat distribution, was the best anthropometric predictor of plasma triglyceride concentrations (r2 = 0.11, P0.05) and cholesterol/high-density lipoprotein cholesterol (HDL-C) ratio (r2 = 0.13, P0.01). Body weight, rather than body fat distribution, was the best predictor of plasma HDL-C concentration (r2 = 0.14, P0.01) and fasting glucose concentrations (r2 = 0.10, P0.05). Fat mass was the best anthropometric predictor of fasting plasma insulin concentrations (r2 = 0.38, P0.0001) and for the glucose-insulin ratio (r2 = 0.39, P0.0001) in men with CAD. Younger patients tended to have greater improvements in HDL-C concentrations and the cholesterol:HDL-C ratio than did older individuals, as a result of exercise training.In men with CAD, general measures of obesity, such as body weight, body mass index, and fat mass are better predictors of coronary risk factors than body fat distribution. Younger and older men with CAD experienced similar improvements in body composition and body fat distribution after an exercise training program.

In addition to being associated with termination of reproductive life in women, the menopause coincides with an increase in several comorbidities including cardiovascular disease. This increase in the prevalence of cardiovascular disease in the postmenopausal years has been partially attributed to adverse effects of estrogen deficiency on plasma lipid-lipoprotein levels and on the cardiovascular system, although other factors are contributing. Central body fatness and insulin resistance are components of a cluster of metabolic abnormalities which also increases the risk of cardiovascular disease. This review summarizes studies that have examined the effects of the menopause transition and of estrogen-replacement therapy on central body fatness and insulin resistance. Review of cross-sectional studies suggests that the menopause transition is associated with an increase in abdominal and visceral adipose tissue accumulation, as measured either with dual X-ray absorptiometry or computed tomography. These results appear to be independent of the aging process and total body fatness. In general, cross-sectional studies using circumference measurements did not find any significant effect of the menopause. Longitudinal studies also support that accumulation of central body fatness accelerates with menopause. The effects of the menopause on insulin resistance appear to be moderate, if any, although available studies are clearly insufficient to draw firm conclusions. The majority of interventional studies support the notion that hormone-replacement therapy attenuates the accumulation of central fat in postmenopausal women, compared with control or placebo-treated women. Retrospective comparisons of hormone users and nonusers also support a protective effect of hormone replacement on fat distribution. Moderate effects of estrogen therapy were found on insulin resistance in postmenopausal women, although long-term, controlled trials using accurate measurements of insulin sensitivity are lacking. Treatment with progestins exerts moderate deleterious effects on insulin sensitivity, which may be attributable to the partial androgenicity of progestins used. It is concluded that part of the increased incidence of cardiovascular disease in postmenopausal women may be attributable to increased central body fatness. Therapies aiming at preventing these changes in fat distribution such as hormone-replacement therapy, diet or exercise are likely to provide long-term cardiovascular and metabolic benefits for women's health.

The menopause transition is associated with several physiological changes that may impact women's health outcome. Among the changes associated with the loss of ovarian function is an increased risk of metabolic and cardiovascular disease. The present review focuses on changes in energy expenditure, body composition and body fat distribution during the postmenopausal transition. Previous work indicates that the most important component of total daily expenditure, resting metabolic rate, may be reduced by the menopause, independently of the effects of the normal aging process. This effect is mainly attributable to a decrease in fat-free mass. The energy expenditure associated with physical activity is the most variable component of total daily energy expenditure. However, small changes in this component may have a substantial impact on body composition. Longitudinal data from our laboratory indicate that the menopause transition also leads to significant decreases in physical activity energy expenditure. The changes in body composition that accompany the menopause transition have been studied by several groups and, although some studies suggested increases in body mass index or total body fat mass with the menopause, currently available cross-sectional data preclude a firm conclusion. Nevertheless, results from our longitudinal study showed significant increases in fat mass with the menopause. The accumulation of abdominal fat, which may be a better correlate of the comorbidities associated with obesity, has also been shown to be accelerated by the menopause transition. In this regard, it has been shown that treatment with hormone replacement therapy prevents the increase in the rate of abdominal adipose tissue accumulation that was noted with the menopause. Thus, it appears that the loss of ovarian function induces a reduction in resting metabolic rate, physical activity energy expenditure, fat-free mass, and an increase in fat mass and abdominal adipose tissue accumulation. These modifications probably contribute to the increased risk of cardiovascular disease of postmenopausal women.