The cardiovascular system has frequently been hypothesized to be the limiting step for O2 transport that determines VO2 max in many species of mammals. Careful analysis of the factors that determine how O2 is transported by the circulation demonstrate that such a single-step limitation cannot exist. Evaluation of the results of experiments in which circulatory O2 transport capacity was experimentally altered demonstrates no direct or absolute relationship between changes in O2 transport capacity and changes in VO2 max. Furthermore, experimental evidence collected during maximal exercise in hypoxia and hyperoxia supports the concept that multiple components of the O2 transport system contribute to limiting O2 flux at VO2 max. Consideration of the basic equations that describe O2 transport through the respiratory system shows that changes in PO2 at each step of the system required to increase O2 flux through that step conflict with the changes in PO2 required to increase flux through adjacent steps. Changes in convection, capacitance, or conductance at one step affect gas transport through the adjacent steps. Hence, no single-step limitation to O2 transport is possible, because the convective and diffusive gas exchangers are interdependent. Increasing QT at VO2 max always increases O2 flux (although not necessarily in proportion to the increase in QT), unless VO2 max is limited by mitochondrial oxidative capacity, as in goats. Cardiovascular structure and function in mammals reflects allometric, adaptive and induced variation. Maximal heart rate is determined strictly by body size, thus maximal QT/Mb is inevitably lower in larger mammals. Adaptive and induced variation elicit hypertrophy of muscle, capillaries, and mitochondria, increasing circulatory capacity and VO2 max. When selection for maximal respiratory function is weak, as in most species of mammals, any component(s) of the respiratory system may be underdeveloped, relative to other structures in the system, and contribute disproportionately to limiting O2 flux. When selection for aerobic capacity is strong, as in racehorses, malleable elements of the respiratory system, including the cardiovascular structures, may hypertrophy until their capacities for O2 transport match that of the least malleable structure, the lung. Amplifying circulatory function so greatly in a large animal may lead to functional demand exceeding structural capacity, resulting in the nearly ubiquitous occurrence of exercise-induced pulmonary hemorrhage in racehorses.
|Original language||English (US)|
|Number of pages||35|
|Journal||Advances in Veterinary Science and Comparative Medicine|
|State||Published - 1994|
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