Maximal O₂ consumption (VO_2max) is a phenomenon where, during very intense exercise, O₂ uptake stops increasing despite the ability to further increase power output. Traditionally, physiologists have asked "What is the limiting factor to VO_2max?" In this presentation, it will be shown that every part of the pathway responsible for transporting O₂ from the air to the mitochondria contributes to setting VO_2max. The question should no longer be posed as above; it should be about the relative importance of each transport pathway step. Thus, the lungs, the heart, the vasculature and blood, and the muscles themselves all contribute to the limits to O₂ transport. While the role of the heart has been accepted for decades, inefficient pulmonary gas exchange also contribute, as do hemoglobin concentration and P₅₀. Perhaps least recognized is the role for transport of O₂ by diffusion between the muscle microcirculation and the mitochondria. In addition, interaction between physiological O₂ transport and subsequent biochemical utilization of O₂ can further affect VO_2max. In sum, O₂ transport and utilization occur via an in series system, and to understand their limits, it is important to consider the system as a whole and not just as a collection of individual parts. The presentation will develop these concepts in graphical form and use literature data to support them.