During dynamic exercise cardiac output (Q̇) normally increases ~5 liters per liter of increase in O2 uptake (V̇(O2)) (i.e., ΔQ̇/ΔV̇(O2) ≃5), indicative of a tight coupling between systemic O2 transport and utilization. We studied four patients with muscle phosphorylase deficiency (McArdle's disease) in whom Q̇ was normal at rest, but ΔQ̇/ΔV̇(O2) was 14.1 ± 1.3 during bicycle exercise. Procedures designed to alter the availability of substrates were employed to test the hypothesis that the increased ΔQ̇/ΔVΔ(O2) is linked to the abnormal metabolic state of skeletal muscle. Fasting plus prolonged moderate exercise was used to increase the availability of plasma free fatty acid (FFA) and resulted in a normalization of ΔQ̇/ΔV̇(O2) (5.3 ± 0.4). Hyperglycemia (70% above control levels) partially normalized ΔQ̇/ΔV̇(O2). Nicotinic acid lowered plasma FFA concentration and dramatically increased ΔQ̇/ΔV̇(O2) (4.6 to 13.7) when administered after fasting plus prolonged exercise in one patient. Glucose infusion after nicotinic acid administration markedly lowered ΔQ̇/ΔV̇(O2). The results support the hypothesis and suggest that the metabolic state of skeletal muscle, possibly via activation of muscle afferents, participates in the regulation of systemic O2 transport.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Applied Physiology Respiratory Environmental and Exercise Physiology|
|State||Published - 1984|
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