Hypoxia and Anaemia Produce Equivalent Effects on Maximal Oxygen Consumption

Abstract

In humans, oxygen flows from inspired air to the mitochondria against a resistance, which is overcome by an overall O2 pressure gradient. According to the O2 conductance equation, this resistance is provided by the sum of numerous in-series resistances, so that a progressive drop in O2 partial pressure from inspired air to the mitochondria takes place. This approach was applied to the study of the O2 transfer system at maximal exercise (22). In this case, at the steady-state, the flow of O2 is the same across each resistance and is equal to Vo2max. Afterwards, a multifactorial model of Vo2max limitation was developed, assuming that each of the resistances in-series (or their reciprocal, the conductances) provides a sizeable fraction of the overall limitation to Vo2max. Three major groups of conductances were identified, namely 1) the pulmonary conductances, related to alveolar ventilation and to alveolar-capillary O2 transfer, 2) the cardiovascular conductance (Gq), due to cardiovascular oxygen transport, and 3) the muscular conductances, related to tissue O2 diffusion and utilisation. The second turned out to provide 60-to-70% of the overall Vo2max limitation, at least during exercise with big muscle groups in normoxia (4, 5, 10).