Maximal oxygen consumption in healthy humans: theories and facts

This article reviews the concept of maximal oxygen consumption ( $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max ) from the perspective of multifactorial models of $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation. First, I discuss procedural aspects of $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max measurement: the implications of ramp protocols are analysed within the theoretical work of Morton. Then I analyse the descriptive physiology of $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max , evidencing the path that led to the view of monofactorial cardiovascular or muscular $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation. Multifactorial models, generated by the theoretical work of di Prampero and Wagner around the oxygen conductance equation, represented a radical change of perspective. These models are presented in detail and criticized with respect to the ensuing experimental work. A synthesis between them is proposed, demonstrating how much these models coincide and converge on the same conclusions. Finally, I discuss the cases of hypoxia and bed rest, the former as an example of the pervasive effects of the shape of the oxygen equilibrium curve, the latter as a neat example of adaptive changes concerning the entire respiratory system. The conclusion is that the concept of cardiovascular $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation is reinforced by multifactorial models, since cardiovascular oxygen transport provides most of the $$\dot{V}\hbox{O}_{2\text{max} }$$ V ˙ O 2 max limitation, at least in normoxia. However, the same models show that the role of peripheral resistances is significant and cannot be neglected. The role of peripheral factors is greater the smaller is the active muscle mass. In hypoxia, the intervention of lung resistances as limiting factors restricts the role played by cardiovascular and peripheral factors