Endogenous nitric oxide in the control of skeletal muscle oxygen extraction during exercise

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Abstract
Our previous studies uncovered an inhibitory effect of nitric oxide (NO) on leg skeletal muscle respiration in dogs at rest. The role of NO in the modulation of O2 consumption and O2 extraction in hindlimb muscle during elevated metabolic states was investigated in chronically instrumented dogs while walking and at three exercise intensities which markedly increased hindlimb blood flow. Walking resulted in increased O2 consumption by 17 ± 4 mL min−1 and O2 extraction from 24 ± 1 to 37 ± 8%, with no alteration in hindlimb blood flow (BFLeg) and vascular resistance (VRLeg). Running at the highest speed (9.1 mph) resulted in an increase in BFLeg from 0.67 ± 0.05 to 2.2 ± 0.1 L min−1, a reduction of VRLeg and elevation of hindlimb O2 consumption from 33 ± 3 to 226 ± 21 mL min−1 and O2 extraction from 29 ± 2 to 61 ± 5%, with a decrease in leg venous PO2 from 38 ± 1 to 25 ± 1 mmHg. After nitro‐L‐arginine (NLA) (35 mg kg−1, i.v.) to inhibit endogenous NO synthesis, walking caused greater increases in hindlimb O2 consumption (29 ± 5 mL min−1) and O2 extraction (43 ± 1 to 60 ± 3%) (both P < 0.05), with no significant change in BFLeg. During running at the highest speed, BFLeg was 1.9 ± 0.1 L min−1 (P < 0.05) and VRLeg was higher, accompanied by increases in hindlimb O2 consumption from 49 ± 7 to 318 ± 24 mL min−1 and O2 extraction from 41 ± 2 to 79 ± 4% (both P < 0.05), with a greater decrease in leg venous PO2 from 33 ± 1 to 20 ± 1 mmHg (P < 0.05). Similar results were found for intermediate levels of exercise. Our results indicate that NO modulates hindlimb skeletal muscle O2 extraction and O2 usage whether blood flow increased or not during exercise.