Challenging Traditional Paradigms of Exercise Performance
Traditionally it was believed that cardiac output, and more specifically stroke volume, is the primary limiting factor in improving an athletes VO2 max, and endurance performance. This point has been hammered by the like of A.V Hill, C. Lundby, JA Calbet, DR Basset, and ET Howley among dozens of others.
It's a view that has straightjacketed exercise physiology for 97 years at this point despite the fact that there is a ton of evidence to the contrary.
It's true that oxygen supply limitations are the most common in elite athletes, but that doesn't necessitate that cardiac output is the limiting factor for VO2max. In athletes with very high maximal cardiac outputs the decreased transit time of RBC's in the pulmonary capillaries can also lead to a pulmonary diffusion limitation, or respiratory limitation.
This is something I've observed countless times in elite CF athletes, who often experience significant arterial desaturation (as low as 86-90% SpO2) after maximal step tests, and it's also been confirmed by Dempsey et al who confirmed that arterial desaturation occurs in elite athletes as well as Powers et al who found that SaO2 can lower by 5% or greater after intense exercise in highly trained endurance athletes.
The NIRS trend above is from a CF games competitor doing a 5-1-5 step test. Note the THb trends set to set during the rest period, which indicate a vasodilation trend from CO2 build up, as well as the change in muscle oxygen saturation indicating a lack of oxygen reaching the working muscle. This athlete also has a change in SpO2 from 99% on set 1, down to 88% on the final work step of this test.
This finding, as well as the findings of other researchers, suggest that a healthy pulmonary system may in fact become a limiting factor in oxygen transport and utilization, as well as CO2 transport and elimination, during max effort exercise in well trained athletes.