Older people are prone to develop glucose intolerance, hyperinsulinemia, hyperlipidemia, and obesity, all of which are metabolic risk factors for atherosclerosis. These declines in metabolic function with aging may not be due to biological aging process per se, but may be related more to lifestyle changes of increasing sedentariness and overeating with resultant deconditioning and obesity. The effects of physical conditioning on metabolic function in older men are examined in this project by controlling for factor, such as disease, age, cigarette smoking and alcohol, which affect function and by measuring other confounding variables such as body composition (% body fat and its distribution), diet, and aerobic capacity (V02max). The mechanisms by which physical conditioning and body composition affect glucose, lipid and adipose tissue metabolism are studied in selected disease-free lean and obese older men with a spectrum of V02max (20-60 ml/kg.min). Sixty-four men, 55-75 years of age have been carefully screened for disease. A subset have undergone measurements of: (a) glucose tolerance, insulin sensitivity and secretion (glucose clamp); (b) insulin binding and autophosphorylation; (c) fasting and postprandial lipoprotein lipids and HDL subspecies; (d) postheparin plasma lipoprotein lipase (LDL) and hepatic lipase activities, and (e) adipose tissue LPL activity and the regulation of lipolysis by adrenergic agonists. Results suggest that obesity and V02max interact to regulate metabolic function in older men. Longitudinal interventions are in progress to determine mechanisms by which differences in V02max and body composition affect glucose, lipid, and adipose tissue metabolism. Reevaluation in a few subjects suggests that convergence of lean men to similar V02max and obese men to V02max and % body fat equivalent to the leaner men, narrows differences in metabolic function. This suggests that lifestyle habits, not aging Per se, are major determinants of certain metabolic functions in older men.
