What governs skeletal muscle VO2max?: New evidence

Recent investigations into the determinants of skeletal muscle maximal oxygen consumption ((V) over dot O-2) have provided further evidence regarding the role of O-2 supply and demand in governing exercise metabolism. Specifically, four studies utilizing both animal and human exercise models are highlighted here: 1) the role of the diffusive O-2 component was examined in the exercising canine gastroenemius muscle by a rightward shift in the O-2 dissociation curve while maintaining O-2 delivery constant; 2) the role of peripheral and central components was examined by studying the human quadriceps muscle, already recognized to have a very high mass specific O-2 delivery, 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 highest recorded metabolic rates can be increased by increasing O-2 supply; 3) that a constant intracellular PO2 during graded exercise is therefore unrelated to increasing lactate efflux; and 4) that only in hyperoxia does trained human skeletal muscle approaching very high mitochondrial metabolic limits, as shown by a disproportionate increase in intracellular PO2 For the recorded change in (V) over dot O-2max.