Intensity of Resistance Exercise Determines Adipokine and Resting Energy Expenditure Responses in Overweight Elderly Individuals

OBJECTIVE

To evaluate the time course of leptin, adiponectin, and resting energy expenditure (REE) responses in overweight elderly males after acute resistance exercise protocols of various intensity configurations.

RESEARCH DESIGN AND METHODS

Forty inactive men (65–82 years) were randomly assigned to one of four groups (n = 10/group): control, low-intensity resistance exercise, moderate-intensity resistance exercise, and high-intensity resistance exercise. Exercise energy cost, REE, leptin, adiponectin, cortisol, insulin, lactate, glucose, nonesterified fatty acids (NEFAs), and glycerol were determined at baseline, immediately after exercise, and during a 72-h recovery period.

RESULTS

Exercise energy cost was lower in high-intensity than in low-intensity and moderate-intensity groups (221.6 ± 8.8 vs. 295.6 ± 10.7 and 281.6 ± 9.8 kcal, P < 0.001). Lactate, glucose, NEFAs, and glycerol concentrations increased (P < 0.001) after exercise and returned to baseline thereafter in all groups. REE increased (P < 0.001) in all groups at 12 h in an intensity-dependent manner (P < 0.05). REE reached baseline after 48 h in the low- and moderate-intensity groups and after 72 h in the high-intensity group. Cortisol peaked in all active groups after exercise (P < 0.001) and remained elevated (P < 0.001) for 12 h. After adjustment for plasma volume shifts, leptin remained unaltered. Adiponectin concentration increased after 12 h and remained elevated for 24 h only in the high-intensity group (P < 0.001).

CONCLUSIONS

Resistance exercise does not alter circulating leptin concentration but does increase REE and adiponectin in an intensity-dependent manner for as long as 48 and 24 h, respectively, in overweight elderly individuals. It appears that resistance exercise may represent an effective approach for weight management and metabolic control in overweight elderly individuals.Aging is characterized by progressive impairment of carbohydrate intolerance and is usually accompanied by physical inactivity and obesity, which may induce hyperinsulinemia, insulin resistance, and cardiovascular disease (1). Obesity, a growing health concern, is characterized by low-grade inflammation, which is associated with insulin resistance and metabolic diseases such as diabetes (2).Leptin and adiponectin, adipose tissue–derived cytokine proteins, are involved in insulin resistance and inflammation (3). Leptin improves fatty acid oxidation in muscle, regulates short-term carbohydrate intake, mediates energy balance and body weight, and upregulates resting energy expenditure (REE) (3). Adiponectin is inversely related to body fatness and type 2 diabetes risk in healthy adults (4), has an anti-inflammatory action, and is involved in substrate metabolism (5,6). Aging increases body fat and leptin levels probably owing to an upregulation of leptin gene expression and is characterized by a negative association between adiponectin and body fat distribution (4).Exercise is believed to extend life-span by reducing the incidence of cardiovascular and other degenerative diseases and increases functional performance in older individuals (7). Regular exercise seems to create energy deficits that help to regulate body weight and fat on a long-term basis in older individuals (1). Chronic resistance exercise increases muscle tissue, reduces aging-related sarcopenia (8), and alters adipokine responses in elderly individuals (7). Acute resistance exercise may elevate lipid mobilization in subcutaneous adipose tissue, energy expenditure, and neuroendocrine responses of obese subjects (9). Although the American Diabetes Association endorses resistance exercise as a means of improving body composition and metabolic control in obesity and diabetes (2), limited information exists regarding the acute effects of resistance exercise on adipokine and REE responses in aging. Therefore, the purpose of the present investigation was to explore 1) the time course of leptin, adiponectin, and REE responses after a single resistance exercise bout in elderly individuals and 2) whether resistance exercise intensity represents an important factor in adipokine and REE responses in elderly individuals.