Abstract
OBJECTIVE: Insulin sensitivity is lower in African American (AA) versus Caucasian American (CA). We tested the hypothesis that lower insulin sensitivity in AA could be explained by mitochondrial respiratory rates, coupling efficiency, myofiber composition, or H(2) O(2) emission. A secondary aim was to determine whether sex affected the results. METHODS: AA and CA men and women, 19-45 years, BMI 17-43 kg m(2) , were assessed for insulin sensitivity (SI(Clamp) ) using a euglycemic clamp at 120 mU/m(2) /min, muscle mitochondrial function using high-resolution respirometry, H(2) O(2) emission using amplex red, and % myofiber composition. RESULTS: SI(Clamp) was greater in CA (p < 0.01) and women (p < 0.01). Proportion of type I myofibers was lower in AA (p < 0.01). Mitochondrial respiratory rates, coupling efficiency, and H(2) O(2) production did not differ with race. Mitochondrial function was positively associated with insulin sensitivity in women but not men. Statistical adjustment for mitochondrial function, H(2) O(2) production, or fiber composition did not eliminate the race difference in SI(Clamp) . CONCLUSION: Neither mitochondrial respiratory rates, coupling efficiency, myofiber composition, nor mitochondrial reactive oxygen species production explained lower SI(Clamp) in AA compared to CA. The source of lower insulin sensitivity in AA may be due to other aspects of skeletal muscle that have yet to be identified.