The response of the O2 transport system to acute changes in alveolar ventilation (VA) was analysed. The fractional limitations to maximal O2 consumption (VO2max) imposed by the lungs (ventilation, FV, and lung-blood transfer, FL), the cardiovascular system (FQ), and peripheral O2 diffusion (Fp) were calculated according to a multifactorial model. A reference set of data, describing the status of O2 transport at maximal exercise in normoxia was used. The effects of VA on VO2max were assessed on the assumption of a constant reference O2 flow in mixed venous blood (QVO2). The changes in reference data after given independent changes in VA were calculated by an iterative procedure, until the VO2max value compatible with the constant reference QVO2 was found, at PIO2 values of 150 (normoxia), 130, 110 and 90 Torr. The VO2max changes in normoxia were less than expected assuming a linear O2 transport system, because of the flatness of the O2 dissociation curve around normoxic PO2. This affected the cardiovascular resistance to O2 flow, and its changes counterbalanced the effects on VO2max of induced changes in VA. This phenomenon was reversed in hypoxia, as the steep part of the O2 dissociation curve was approached. The fractional limitations to VO2max in normoxia resulted as follows: FV and FL provided between 5 and 12%, FQ between 59 and 78%, and Fp between 13 and 19% of the overall VO2max limitation. In hypoxia, FV and FL increased and FQ decreased. At PIO2 = 90 Torr, when VA was halved, FV, FL, FQ and Fp amounted to 0.35, 0.31, 0.20 and 0.14, respectively.