cellular lipid (IMCL) has been associated with insulin resistance. However, an association between IMCL and insulin resistance might be modulated by oxidative capacity in skeletal muscle. We examined the hypothesis that 12 wk of exercise training would increase both IMCL and the oxidative capacity of skeletal muscle in older (67.3 Ϯ 0.7 yr), previously sedentary subjects (n ϭ 13; 5 men and 8 women). Maximal aerobic capacity (V O2 max) increased from 1.65 Ϯ 0.20 to 1.85 Ϯ 0.14 l/min (P Ͻ 0.05), and systemic fat oxidation induced by 1 h of cycle exercise at 45% of V O2 max increased (P Ͻ 0.05) from 15.03 Ϯ 40 to 19.29 Ϯ 0.80 (mol ⅐ min Ϫ1 ⅐ kg fat-free mass Ϫ1 ). IMCL, determined by quantitative histological staining in vastus lateralis biopsies, increased (P Ͻ 0.05) from 22.9 Ϯ 1.9 to 25.9 Ϯ 2.6 arbitrary units (AU). The oxidative capacity of muscle, determined by succinate dehydrogenase staining intensity, significantly increased (P Ͻ 0.05) from 75.2 Ϯ 5.2 to 83.9 Ϯ 3.6 AU. The percentage of type I fibers significantly increased (P Ͻ 0.05) from 35.4 Ϯ 2.1 to 40.1 Ϯ 2.3%. In conclusion, exercise training increases IMCL in older persons in parallel with an enhanced capacity for fat oxidation. skeletal muscle; physical activity; fiber type; triacylglycerol ELEVATED INTRAMYOCELLULAR LIPID (IMCL), consisting primarily of triglyceride (TG), has been associated with insulin resistance (17,40,43,46) and type 2 diabetes (18, 30) in middleaged adults. It has recently been speculated that higher IMCL content is also linked to an impaired mitochondrial capacity for fatty acid oxidation within muscle (42). This is also consistent with reports that insulin-resistant skeletal muscle is characterized by lower oxidative capacity (50, 51) and lower postabsorptive rates of fatty acid oxidation (29). Other studies, however, suggest that muscle TGs are not invariably associated with insulin resistance. Endurance-trained athletes, who are markedly insulin sensitive, have similar IMCL to those with type 2 diabetes, suggesting that IMCL itself may not promote insulin resistance in the context of a high oxidative capacity in muscle (16). There have been few intervention-based human studies to examine whether exercise training might actually increase IMCL in populations at risk for the development of insulin resistance and type 2 diabetes.Aging is also associated with metabolic dysregulation, including insulin resistance (8, 10), a higher prevalence of type 2 diabetes (21), and lower capacity for oxidative metabolism in muscle (4), although many of these defects can be attributed to age-related physical inactivity (5). Petersen et al. (41) recently reported that a reduced capacity for oxidative metabolism and higher IMCL are associated with insulin resistance of aging (41). Although this (41) and other (16, 26) cross-sectional studies highlight the interaction between IMCL and reduced oxidative capacity in insulin resistance, intervention-based studies are needed to further elucidate these associations. The effects of exercise training o...

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