This work aims to highlight by VO₂ kinetics in constant load supra anaerobic threshold (AT) tests, the nitric oxide (NO) reversible direct inhibitory action on cytochromeC oxidase (cox). This results in decreased ability to oxidise electron flow (EF), by cytochromeC carried, in water, compensated by electron turnover (ET) increment via cox not yet NO bound, thus giving EF continuity along the respiratory chain O₂ ward. When NO production is increased and/or O₂ mitochondrial concentration decreased, as during intense effort, this compensation gradually weakened, owing to cox NO free oxidative capacity end limit, which approaches its saturation, but at the same time allows an O₂ saving and its diffusion deeper in tissues around vessels. O₂ saving effect is quantifiable in two bicycle constant load exercises by VO₂ kinetics supra AT, in previous triangular test identified, which describes two superimposed components, one rapid and one appreciably slower, allowing one to calculate area between them. After training, NO availability increasing, this area decreases in inverse ratio to treatment efficacy. Then the training is to seen as effective physiological means that allow one to reach the obtained enhanced functional capacity, by longer exercise owing to O₂ saving, so delaying the critical moment when effort is no longer sustainable from cardiovascular and pulmonary systems. In 10 untrained subjects, giving the NO donor isosorbide 5 mononitrate before second constant load test, the area is diminished on average of 46%. Therefore, all cardiopath subjects are to treat with organic nitrates in order to improve effort tolerance.