As soon as the concept of maximal oxygen consumption \( (\dot{V}\,{\text{O}}_{{2{ \max }}} ) \) was created, it was clear that \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) was limited somewhere along the respiratory system. The quest for the single factor limiting \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) went on for long, with highly contradictory outcomes. The way of looking at \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) limitation, however, changed drastically some 30 years ago. The resumption of the oxygen cascade theory as a tool for a holistic description of the respiratory system led to the development of multifactorial models of \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) limitation. Two such models are currently available, one created by Pietro Enrico di Prampero and the other by Peter Wagner. These models are described in detail and criticized. The evidence supporting the predictions generated by the two models is presented. Demonstration is provided that the two models converge indeed on the same conclusion, namely that most of the limitation to \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) in normoxia is provided by cardiovascular oxygen transport. However, the same models show that the role of peripheral oxygen diffusion and utilization as limiting factors is such that it cannot be neglected. The special case of \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) in hypoxia is then presented, and the effects of a nonlinear oxygen equilibrium curve are discussed. It is acknowledged that as long as we operate on the flat portion of the oxygen equilibrium curve, the lungs do not limit \( \dot{V}\,{\text{O}}_{{2{ \max }}} \), but as soon as the steep part of the curve is attained, the lungs take over a significant fraction of \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) limitation. Finally, the case of prolonged bed rest is discussed as an example of \( \dot{V}\,{\text{O}}_{{2{ \max }}} \) changes induced by simultaneous multiple modifications occurring at various levels along the respiratory system.