Emerging evidence indicates that, besides
dyspnea relief, an improvement in locomotor muscle
oxygen delivery may also contribute to enhanced exercise tolerance following normoxic
heliox (replacement of inspired
nitrogen by
helium) administration in patients with
chronic obstructive pulmonary disease (
COPD). Whether blood flow redistribution from intercostal to locomotor muscles contributes to this improvement currently remains unknown. Accordingly, the objective of this study was to investigate whether such redistribution plays a role in improving locomotor muscle
oxygen delivery while breathing
heliox at near-maximal [75% peak work rate (WR(peak))], maximal (100%WR(peak)), and supramaximal (115%WR(peak)) exercise in
COPD. Intercostal and vastus lateralis muscle perfusion was measured in 10
COPD patients (FEV(1) = 50.5 ± 5.5% predicted) by near-infrared spectroscopy using
indocyanine green dye. Patients undertook exercise tests at 75 and 100%WR(peak) breathing either air or
heliox and at 115%WR(peak) breathing
heliox only. Patients did not exhibit exercise-induced hyperinflation. Normoxic
heliox reduced respiratory muscle work and relieved
dyspnea across all exercise intensities. During near-maximal exercise, quadriceps and intercostal muscle blood flows were greater, while breathing normoxic
heliox compared with air (35.8 ± 7.0 vs. 29.0 ± 6.5 and 6.0 ± 1.3 vs. 4.9 ± 1.2 ml·min(-1)·100 g(-1), respectively; P < 0.05; mean ± SE). In addition, compared with air, normoxic
heliox administration increased arterial
oxygen content, as well as
oxygen delivery to quadriceps and intercostal muscles (from 47 ± 9 to 60 ± 12, and from 8 ± 1 to 13 ± 3 mlO(2)·min(-1)·100 g(-1), respectively; P < 0.05). In contrast, normoxic
heliox had neither an effect on systemic nor an effect on quadriceps or intercostal muscle blood flow and
oxygen delivery during maximal or supramaximal exercise. Since intercostal muscle blood flow did not decrease by normoxic
heliox administration, blood flow redistribution from intercostal to locomotor muscles does not represent a likely mechanism of improvement in locomotor muscle
oxygen delivery. Our findings might not be applicable to patients who hyperinflate during exercise.