Limitations to aerobic performance in mammals: interaction of structure and demand

In this paper we have explored the linked series of structures that collectively comprise the respiratory system. In examining each of these structural resistors, some seem to be primarily fixed, for example, the trachea, while others must be primarily variable or adaptable, for example, the cardiovascular system. Those structures that are truly variable will not be maintained with structural capacity in excess of their functional demand. As a consequence, these structures are the ones that may most often appear to be limiting O₂ uptake. However, we question under which in vivo circumstances the most plastic steps in the cascade of resistances will impart the single-step limitation to O₂ uptake. When reviewed in this context, available experimental evidence suggests that among the most athletic animals (those with the greatest weight-specific VO₂), the respiratory resistors are likely tuned rather than dominated by a single-step limitation. Skeletal muscle must set the demand for O₂ in exercising animals; hence, the relationship between total skeletal muscle mitochondria and maximum O₂ consumption is quantitatively consistent, spanning broad differences in body size and aerobic capacity. Those respiratory structures that are primarily nonadaptable must be built with enough 'excess structure' to accommodate potential adaptation in an animal's aerobic capacity during its lifetime. Consequently, the least aerobic animals will always appear to experience a limitation to VO(2max) in one of the most plastic or adaptable structures. We suggest that the adaptable structures upstream to the muscle mitochondria are built and maintained at a cost-benefit maximum ('structural efficiency') in all species. This differs from the concept of optimal structural design or symmorphosis.