Given that skeletal muscle contributes to a large proportion of resting energy expenditure due to its relative mass and its high oxidative capacity, the specific variation of the degree of mitochondrial coupling in skeletal muscle may play a considerable metabolic role at the whole-animal level. If we assume that skeletal muscle contributes up to 30% of the resting metabolic rate in birds (Duchamp and Barré, 1993), we can estimate that the observed 15% increase in mitochondrial oxidative phosphorylation efficiency contributes to a decrease of almost 5% in whole-body oxygen consumption of fasted chicks. This could represent up to 30% of the fasting-induced reduction in mass-specific metabolic rate. In penguins fasting onshore, pectoral muscles are little used and are therefore preferentially degraded to provide the blood with amino acids, whereas skeletal muscles involved in terrestrial locomotion are spared (Robin et al., 1988; Duchamp et al., 1991). Hence, because pectoralis muscles undergo a selective and progressive degradation during fasting, losing almost 15 g of fresh mass or 4.4 g of muscle protein per day in fasted chicks (Duchamp et al., 1991), the above calculated contribution of muscle mitochondrial efficiency to changes in chicks' metabolic rate might be overestimated. However, in contrast to total muscle proteins, mitochondrial proteins are spared during phase II of fasting and so is the specific oxidative activity of pectoralis muscles (Duchamp et al., 1991). By taking into account these data and the proportion of pectoralis muscle mass in winter chicks (Duchamp et al., 1991; Cherel et al., 1993a), the above calculated contribution of mitochondrial function might be overestimated by 5%. On the whole, the present data suggest that upregulation of the muscle mitochondrial energy efficiency may contribute to a lower metabolic rate by minimizing the metabolic need for oxygen and nutrients in cellular energy production.