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The hypothesis was tested that prolonged bed rest impairs O2 transport during exercise, which implies a lowering of cardiac output Qc and O2 delivery (QaO2). The following parameters were determined in five males at rest and at the steady-state of the 100-W exercise before (B) and after (A) 42-day bed rest with head-down tilt at -6 degrees: O2 consumption (VO2), by a standard open-circuit method; Qc, by the pressure pulse contour method, heart rate (fc), stroke volume (Qh), arterial O2 saturation, blood haemoglobin concentration ([Hb]), arterial O2 concentration (CaO2), and QaO2. The VO2 was the same in A and in B, as was the resting fc. The fc at 100 W was higher in A than in B (+17.5%). The Qh was markedly reduced (-27.7% and -22.2% at rest and 100 W, respectively). The Qc was lower in A than in B [-27.6% and -7.8% (NS) at rest and 100 W, respectively]. The CaO2 was lower in A than in B because of the reduction in [Hb]. Thus also QaO2 was lower in A than in B (-32.0% and -11.9% at rest and at 100 W, respectively). The present results would suggest a down-regulation of the O2 transport system after bed rest.

1. The hypothesis that the ventilatory resistance to O2 flow (RV) does limit maximal O2 consumption (VO2,max) in hypoxia, but not in normoxia, at least in non-athletic subjects, was tested. RV was reduced by using He-O2 mixtures. 2. VO2,max was measured during graded cyclo-ergometric exercise in eight men (aged 30 +/- 3 years) who breathed N2-O2 and He-O2 mixtures in normoxia (inspired oxygen fraction (FI,O2) = 0.21) and hypoxia (FI,O2 = 0.11). O2 consumption, expired and alveolar ventilations (VE and VA, respectively), blood lactate and haemoglobin concentrations, heart rate and arterial oxygen saturation (Sa,O2) were determined at the steady state of each work load. Arterial O2 and CO2 partial pressures (Pa,O2 and Pa,CO2, respectively) were measured at rest and at the end of the highest work load. 3. Maximal VE and VA were significantly increased by He-O2 breathing in normoxia (+27 and +18%, respectively), without significant changes in Pa,O2, Sa,O2 and VO2,max. In hypoxia, VE and VA increased (+31 and +24%, respectively), together with Pa,O2 (+17%), Sa,O2 (+6%) and VO2,max (+14%). 4. The results support the hypothesis that the role of RV in limiting VO2,max is negligible in normoxia. In hypoxia, the finding that higher VE and VA values during He-O2 breathing led to higher VO2,max values suggests a greater role of RV as a limiting factor. It is unclear whether the finding that the VO2,max values were the same during He-O2 and N2-O2 breathing in normoxia is due to a non-linear response of the O2 transfer system, as previously proposed.