Metabolic control of cardiac output response to exercise in McArdle's disease

S. F. Lewis; R. G. Haller; J. D. Cook; C. G. Blomqvist

doi:10.1152/jappl.1984.57.6.1749

Metabolic control of cardiac output response to exercise in McArdle's disease

S. F. Lewis, R. G. Haller, J. D. Cook, C. G. Blomqvist

Research output: Contribution to journal › Article › peer-review

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Abstract

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)
Pages (from-to)	1749-1753
Number of pages	5
Journal	Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
Volume	57
Issue number	6
DOIs	https://doi.org/10.1152/jappl.1984.57.6.1749
State	Published - 1984

ASJC Scopus subject areas

Physiology
Endocrinology

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title = "Metabolic control of cardiac output response to exercise in McArdle's disease",

abstract = "During dynamic exercise cardiac output ({\.Q}) normally increases ~5 liters per liter of increase in O2 uptake ({\.V}(O2)) (i.e., Δ{\.Q}/Δ{\.V}(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 {\.Q} was normal at rest, but Δ{\.Q}/Δ{\.V}(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 Δ{\.Q}/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 Δ{\.Q}/Δ{\.V}(O2) (5.3 ± 0.4). Hyperglycemia (70% above control levels) partially normalized Δ{\.Q}/Δ{\.V}(O2). Nicotinic acid lowered plasma FFA concentration and dramatically increased Δ{\.Q}/Δ{\.V}(O2) (4.6 to 13.7) when administered after fasting plus prolonged exercise in one patient. Glucose infusion after nicotinic acid administration markedly lowered Δ{\.Q}/Δ{\.V}(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.",

author = "Lewis, {S. F.} and Haller, {R. G.} and Cook, {J. D.} and Blomqvist, {C. G.}",

year = "1984",

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T1 - Metabolic control of cardiac output response to exercise in McArdle's disease

AU - Lewis, S. F.

AU - Haller, R. G.

AU - Cook, J. D.

AU - Blomqvist, C. G.

PY - 1984

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N2 - 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.

AB - 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.

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Metabolic control of cardiac output response to exercise in McArdle's disease

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