MUSCLE MAXIMAL O-2 UPTAKE AT CONSTANT O-2 DELIVERY WITH AND WITHOUT CO IN THE BLOOD

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (V̇O2(max)) during hypoxia. O2 uptake (V̇O2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (Pa(O2)) and total hemoglobin concentration ([Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions Pa(O2) was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml· 100 g-1·min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. V̇O2(max) was 8.8 ± 0.6 (SE) ml·min-1·100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 ± 0.4 ml·min-1·100 g-1 when HbCO was present (n = 12; P<0.01). In both cases, mean muscle effluent venous PO2 (P(V(O2))) was the same (16 ± 1 Torr). Because Pa(O2) and P(V(O2)) were the same for both conditions, the mean capillary P(O2) (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO. Although the mechanism of this reduction cannot be identified by our data, they suggest that CO, even after shortlasting exposure at low P(CO), causes some impairment to the diffusion of O2 that appears to have a larger role in reducing V̇O2(max) than the CO-induced leftward shift of the O2 dissociation curve.