Vitamin E reduces rat liver oxidative damage without modifying metabolic response to experimental and functional hyperthyroidism. We investigated whether vitamin E has similar effects in skeletal muscle from rats made hyperthyroid by exposure to low environmental temperature. The vitamin maintained cold-induced increases in aerobic capacity and O2 consumption of homogenates and mitochondria, and muscle content of mitochondrial proteins. Conversely, vitamin limited oxidative damage of muscle preparations as shown by the reduced hydroperoxide and protein-bound carbonyl levels and enhanced glutathione content in muscle homogenates. Vitamin E protects muscle from oxidative damage not only by direct action on lipids and proteins component of cellular membranes, but also through a modulation of rates of reactive oxygen species generation by muscle mitochondria. Indeed, during basal and stimulated respiration, succinate-supported H2O2 release rates increased in all cold exposed rats, but in smaller measure in vitamin-treated rats, whereas pyruvate/malate supported H2O2 release rates were not modified by cold exposure and vitamin E treatment. Finally, it was also found that vitamin E treatment offers further protection to skeletal muscle reducing its susceptibility to oxidative challenge. In the whole, our results show that vitamin E preserves the high aerobic capacity, reducing the high oxidative damage and susceptibility to oxidants, elicited in the muscle as a response to cold stress.