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Am J Physiol Regul Integr Comp Physiol 283: R1131-R1139, 2002. First published July 11, 2002; doi:10.1152/ajpregu.00226.2002
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Vol. 283, Issue 5, R1131-R1139, November 2002

Effect of mild carboxy-hemoglobin on exercising skeletal muscle: intravascular and intracellular evidence

R. S. Richardson1, E. A. Noyszewski2, B. Saltin3, and J. González-Alonso3

1 Deparmement of Medicine University of California, San Diego, La Jolla, California 92093; 2 Department of Radiology University of Pennsylvania, Philadelphia, Pennsylvania 19104; and 3 Copenhagen Muscle Research Centre, Rigshopitalet, Copenhagen, Denmark

We studied muscle blood flow, muscle oxygen uptake (VO2), net muscle CO uptake, Mb saturation, and intracellular bioenergetics during incremental single leg knee-extensor exercise in five healthy young subjects in conditions of normoxia, hypoxia (H; 11% O2), normoxia + CO (COnorm), and 100% O2 + CO (COhyper). Maximum work rates and maximal oxygen uptake (VO2 max) were equally reduced by approx 14% in H, COnorm, and COhyper. The reduction in arterial oxygen content (CaO2) (approx 20%) resulted in an elevated blood flow (Q) in the CO and H trials. Net muscle CO uptake was attenuated in the CO trials. Suprasystolic cuff measurements of the deoxy-Mb signal were not different in terms of the rate of signal rise or maximum signal attained with and without CO. At maximal exercise, calculated mean capillary PO2 was most reduced in H and resulted in the lowest Mb-associated PO2. Reductions in ATP, PCr, and pH during H, COnorm, and COhyper occurred earlier during progressive exercise than in normoxia. Thus the effects of reduced CaO2 due to mild CO poisoning are similar to H.

exercise; metabolism; CO toxicity; magnetic resonance spectroscopy; 31P; maximal O2 consumption; intracellular partial pressure of O2


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