Muscle mitochondrial oxidative phosphorylation activity, but not content, is altered with abdominal obesity in sedentary men: synergism with changes in insulin sensitivity.

CONTEXT: Abdominal obesity is a major risk factor for muscle insulin resistance. Mitochondria may play a key role in this etiology. OBJECTIVE: Changes in muscle mitochondrial content and function were examined according to abdominal obesity and insulin sensitivity in men. STUDY DESIGN AND SETTING: The descriptive MitHyCal study was conducted on the general population of Clermont-Ferrand, France. PARTICIPANTS: Forty-two healthy sedentary men (41.7 +/- 4.3 yr) were divided into four groups according to waist circumference: 87 cm or less (group 1, n = 10); 88-93 cm (group 2, n = 12); 94-101 cm (group 3, n = 10); and 102 cm or greater (group 4, n = 10). INTERVENTION: Plasma metabolic check-up was performed, and insulin sensitivity index was calculated from glucose and insulin responses to a 3-h oral glucose tolerance test. Muscle biopsies were obtained to assess mitochondrial content, oxidative phosphorylation activity, and superoxide anion (reactive oxygen species) production. MAIN OUTCOME MEASURES: Assessment of muscle mitochondrial content and function was planned before data collection began. RESULTS: Abdominal obesity was negatively correlated to insulin sensitivity index (r = -0.39; P < 0.01), and only group 4 was insulin-resistant (P < 0.05). There were no between-group differences in muscle mitochondrial content and maximal activity of key oxidative enzymes. In contrast, muscle mitochondrial ADP-stimulated respiration rate was 24% higher in groups 2 and 3 compared to groups 1 and 4 (P < 0.05). Mitochondrial ATP and reactive oxygen species production rates were 27 and 48% lower in group 4 than in group 1 (P < 0.05). CONCLUSION: Abdominal obesity is associated with alterations in intrinsic muscle mitochondrial function but not content. These adaptations mainly result in reduced mitochondrial ATP production rate in response to insulin resistance.