The issue of whether skeletal muscle is master or slave of the cardiovascul
ar system depends on frame of reference. Acute manipulations of convective
O-2 delivery clearly show that O-2 supply sets the upper limit of muscle (V
) over dot O-2max. However, studies of adaptation to chronic conditions suc
h as training and hypoxia show that skeletal muscle has a remarkable capaci
ty to meet changes in metabolic demand. Moreover, there are several lines o
f evidence that these adaptations are essential to changes in (V) over dot
O-2max. Studies show that with training, electrical stimulation, and chroni
c hypoxia, the ratio of capillary surface per fiber surface and fiber mitoc
hondrial volume/fiber length is preserved, suggesting a primary regulated f
eature in skeletal muscle is matching the structural capacity for O-2 flux
to mitochondrial metabolic demand. Adaptations in both capillarity and mito
chondrial respiratory capacity have also been shown to be important compone
nts in the adaptive increase in (V) over dot O-2max. With training. Collect
ively, this evidence argues against skeletal muscle being simply a slave to
the cardiovascular system.