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Supplementation with vitamin E and vitamin C inversely alters mitochondrial copy number and mitochondrial protein in obese, exercising rats (1030.5)

Controversy exists as to whether supplementation with the antioxidants vitamin E (VE) and vitamin C (VC) blocks adaptation to exercise. Exercise is a first‐line means to treat obesity and its complications. While obesity alters mitochondrial (MT) function and induces insulin resistance (IR), no data exist as to whether supplementation with VE and VC modify responses to exercise in pre‐existing obesity. We tested the hypothesis that dietary supplementation with VE (0.4 g alpha‐tocopherol acetate/kg) and VC (0.5g/kg) blocks exercise‐induced effects on IR and MT content in obese rats maintained on a high‐fat diet. Obese, sedentary rats had a 2‐fold higher HOMA‐IR and insulin area under the curve following glucose tolerances test than rats fed a low‐fat (10% fat en), eucaloric diet. Exercising (12 wks) of obese rats normalized IR indices, an effect not modified by VE and VC. VE and VC supplementation with exercise elevated MT DNA content in adipose and skeletal muscle to a greater extent (20%) than exercise alone in a depot specific manner. On the other hand, VC and VE decreased MT protein content vs exercise for complex I (40%) and nicotinamide nucleotide transhydrogenase (35%) in a muscle‐dependent manner. These data indicate that VE and VC supplementation does not modify exercise‐induced insulin sensitivity but that MT biogenesis and MT protein expression may be separate events modified by antioxidant supplementation.