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Aging is characterized by deleterious changes in body composition and in fat distribution. The mechanisms that determine the aging-associated changes in body composition are not well defined, but the evidence suggests that the loss of fat-free mass is at least partially attributable to physical inactivity. The increase in fat mass may be the result of alterations in fatty acid metabolism. Indeed, fat oxidation is decreased in elderly individuals in several physiological conditions: a) at rest, b) during exercise, and c) in response to meal ingestion (after weight loss). These defects are related in part to loss of fat-free mass, but may also be the consequence of estrogen loss (in women) and/or a decrease in the intrinsic capacity of muscle for fat oxidation, and are amenable to partial correction by exercise training. Special emphasis should be placed in future studies upon the role of steroid hormone in the regulation of fatty acid metabolism in elderly individuals (especially women), as well as therapeutic interventions that may increase the quantity of the fat-free mass and/or fat oxidation.

The hypothesis that exercise increases fat oxidation at rest independently of changes in energy balance, body composition, and/or lipolysis was tested in 21 volunteers. After a period of energy balance, volunteers were randomly allocated to one of four groups: control, overfed (OF), overfed and exercised (OF-EX), and exercised (EX). OF and OF-EX were overfed 50% excess of energy balance calories; OF-EX and EX spent 50% excess of energy balance calories during daily exercise sessions. Exercise increased fat oxidation at rest independently of dietary intake (OF-EX = + 22 +/- 2.4, EX = + 23 +/- 1.5 mg/min) and reduced carbohydrate oxidation (OF-EX = - 49 +/- 6.2, EX = - 46 +/- 5.4 mg/min). Volunteers in the OF group had an increase in carbohydrate oxidation (85 +/- 5.9 mg/min) and a decline in fat oxidation (- 33 +/- 1.4 mg/min). Protein oxidation did not change in any group. These changes occurred without a direct relation with changes in lipolysis and persisted even when expressed as a percentage or as an absolute equivalent of resting metabolic rate in calories. Thus exercise, independent of changes in energy intake and body composition and not related to changes in lipolysis, increases fat oxidation at rest, which may explain the beneficial effects of exercise in weight loss programs.

The impact of aerobic fitness level on the production and disposal of serum free fatty acids was investigated in 26 normal young volunteers. The fitness level was ascertained by history and confirmed by determination of maximal aerobic capacity. Energy expenditure and substrate oxidation at rest were measured with indirect calorimetry. Free fatty acid turnover was measured with an infusion of [14C]palmitic acid. All tests were done > or = 48 h after the last bout of exercise. The sedentary (SED) volunteers had higher rates of systemic delivery of fatty acids than aerobically fit (FIT) individuals (532 +/- 53.4 vs. 353 +/- 62.3 mumol/min; P = 0.05). This difference was accentuated when the values were normalized to fat-free mass (9.2 +/- 0.8 and 5.9 +/- 0.98 mumol.kg-1.min-1 for SED and FIT, respectively). Fatty acid oxidation was similar between FIT and SED volunteers in absolute numbers (209 +/- 25 vs. 202 +/- 21 mumol/min, respectively; NS) as well as when normalized to fat-free mass (3.8 +/- 0.9 vs. 3.6 +/- 1.4 mumol.kg-1.min-1, respectively; NS). In contrast, the nonoxidative disposal of serum fatty acids was higher in SED (330 +/- 46.1 mumol/min) than in FIT individuals (144 +/- 52 mumol/min; P = 0.026). Thus, the ratio of nonoxidative to oxidative disposal rates of fatty acids was higher in SED than in FIT individuals (1.65 +/- 0.29 vs. 0.75 +/- 0.17; P = 0.021). The data support the hypothesis that high aerobic fitness level is associated with a low rate of systemic delivery of fatty acids at rest. Nevertheless, subjects with high aerobic fitness levels have fat oxidation at the same rate as unfit individuals.

Exercise induces negative energy balance either directly or by enhancing meal thermogenesis, increasing resting metabolic rate, and/or decreasing food intake. A quantitative evaluation of these effects in programs of weight control led to the following conclusions: 1) energy cost of exercise per se is minimal, 2) effects on thermic of food are negligible, and 3) exercise training may be advantageous in conjunction with low-calorie diet programs because it helps to maintain resting metabolic rate and fat-free mass. However, exercise may not prevent, and may even accentuate, the fall in metabolic rate in programs of severe calorie restriction, thus hampering weight reduction. Overall, exercise should not be envisioned as a sole agent to induce negative energy balance, but it is an essential element in comprehensive programs for morbidly obese patients due to its effects on lipids, carbohydrate metabolism, and cardiovascular system.