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Pryor SL, Lewis SF, Haller RG, et al. Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease). J Clin Invest. 1990;85(5):1444-9doi: 10.1172/JCI114589.
Pryor, S. L., Lewis, S. F., Haller, R. G., Bertocci, L. A., & Victor, R. G. (1990). Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease). The Journal of clinical investigation, 85(5), 1444-9. https://doi.org/10.1172/JCI114589
Pryor, S L, et al. "Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease)." The Journal of clinical investigation vol. 85,5 (1990): 1444-9. doi: https://doi.org/10.1172/JCI114589
Pryor SL, Lewis SF, Haller RG, Bertocci LA, Victor RG. Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease). J Clin Invest. 1990 May;85(5):1444-9. doi: 10.1172/JCI114589. PMID: 2332499; PMCID: PMC296590.
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American Society for Clinical Investigation Free PMC Article

J Clin Invest. 1990 May;85(5):1444-9. doi: 10.1172/JCI114589.

Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease).

The Journal of clinical investigation

S L Pryor, S F Lewis, R G Haller, L A Bertocci, R G Victor

Affiliations

  1. Department of Internal Medicine Cardiology Division, Harry S. Moss Heart Center, Dallas, Texas.

PMID: 2332499 PMCID: PMC296590 DOI: 10.1172/JCI114589
Free PMC Article

Abstract

Static exercise in normal humans causes reflex increases in muscle sympathetic nerve activity (MSNA) that are closely coupled to the contraction-induced decrease in muscle cell pH, an index of glycogen degradation and glycolytic flux. To determine if sympathetic activation is attenuated when muscle glycogenolysis is blocked due to myophosphorylase deficiency (McArdle's disease), an inborn enzymatic defect localized to skeletal muscle, we now have performed microelectrode recordings of MSNA in four patients with McArdle's disease during static handgrip contraction. A level of static handgrip that more than doubled MSNA in normal humans had no effect on MSNA and caused an attenuated rise in blood pressure in the patients with myophosphorylase deficiency. In contrast, two nonexercise sympathetic stimuli, Valsalva's maneuver and cold pressor stimulation, evoked comparably large increases in MSNA in patients and normals. The principal new conclusion is that defective glycogen degradation in human skeletal muscle is associated with a specific reflex impairment in sympathetic activation during static exercise.

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