What is the physiological explanation for VO2max? This question has fascinated physiologists for over a century. As explained in Chapter 18, O2 consumption continues at maximum levels in isolated mitochondria until PO is much less than that found in venous blood (< 5 Torr; see Fig. 2 in Chapter 18). This suggests that the amount of mitochondria may determine VO2 max in an individual, and it is certainly true that well-trained athletes have higher mitochondrial densities in their muscles. However, there is also evidence for gas exchange limitations of maximal exercise. For example, increasing inspired O2 levels can increase VO2 max in well-trained athletes.
Recent evidence suggests that VO2 max occurs when venous PO2 reaches a minimum that represents the optimal match between cardiovascular O2 delivery and O2 diffusion in tissue. When researchers observed that
PvO2 during maximal exercise is lower at altitude than it is at sea level, they wondered why the muscles could not reach the same low PvO2 values at sea level because this would increase O2 extraction and increase VO2 max. However, further reductions in PvO2 would reduce the gradient for O2 diffusion into the muscle and decrease the O2 flux. Venous PO2 is the critical value because it defines the lower limit for the gradient driving diffusion of O2 out of the capillaries during maximal exercise. At VO2 max, the mitochondria consume every molecule of O2 so PO2 outside the capillaries is nearly zero. Increasing PvO2 to enhance O2 diffusion would only decrease O2 extraction and reduce VO2 because of the Fick principle.
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