Recent investigations into the determinants of skeletal muscle maximal oxyg
en consumption ((V) over dot O-2) have provided further evidence regarding
the role of O-2 supply and demand in governing exercise metabolism. Specifi
cally, four studies utilizing both animal and human exercise models are hig
hlighted here: 1) the role of the diffusive O-2 component was examined in t
he exercising canine gastroenemius muscle by a rightward shift in the O-2 d
issociation curve while maintaining O-2 delivery constant; 2) the role of p
eripheral and central components was examined by studying the human quadric
eps muscle, already recognized to have a very high mass specific O-2 delive
ry, under conditions of increased (hyperoxia) and reduced O-2 availability
(hypoxia); 3) the role of intracellular PO2 in the progressive increase in
lactate efflux from skeletal muscle from submaximal to maximal effort; and
finally 4) the role of intracellular PO2 itself as a determinant of maximal
mitochondrial O-2 consumption. In summary, these investigations illustrate
1) the importance of the diffusion gradient from blood to muscle cell; 2)
illustrate that even in functionally isolated trained skeletal muscle the h
ighest recorded metabolic rates can be increased by increasing O-2 supply;
3) that a constant intracellular PO2 during graded exercise is therefore un
related to increasing lactate efflux; and 4) that only in hyperoxia does tr
ained human skeletal muscle approaching very high mitochondrial metabolic l
imits, as shown by a disproportionate increase in intracellular PO2 For the
recorded change in (V) over dot O-2max.