Skeletal muscle: microcirculatory adaptation to metabolic demand

Abstract

The issue of whether skeletal muscle is master or slave of the cardiovascular system depends on frame of reference. Acute manipulations of convective O2 delivery clearly show that O2 supply sets the upper limit of muscle VO2max. However, studies of adaptation to chronic conditions such as training and hypoxia show that skeletal muscle has a remarkable capacity to meet changes in metabolic demand. Moreover, there are several lines of evidence that these adaptations are essential to changes in VO2max. Studies show that with training, electrical stimulation, and chronic hypoxia, the ratio of capillary surface per fiber surface and fiber mitochondrial volume/fiber length is preserved, suggesting a primary regulated feature in skeletal muscle is matching the structural capacity for O2 flux to mitochondrial metabolic demand. Adaptations in both capillarity and mitochondrial respiratory capacity have also been shown to be important components in the adaptive increase in VO2max with training. Collectively, this evidence argues against skeletal muscle being simply a slave to the cardiovascular system.