Document Detail


Reflex sympathetic activation during static exercise is severely impaired in patients with myophosphorylase deficiency.
MedLine Citation:
PMID:  12640006     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During static exercise, metabolites accumulate in the muscle interstitium where they stimulate chemosensitive afferent nerves that reflexly increase efferent muscle sympathetic nerve activity (MSNA) and blood pressure. In experimental animals, lactic acid potently stimulates the muscle metaboreflex, but its role in humans is more controversial. To determine if lactic acid is a critical mediator of metaboreflex activation in humans, we performed microelectrode recordings of MSNA in eight patients with myophosphorylase deficiency (McArdle's disease) who cannot metabolize intramuscular glycogen and do not generate lactic acid in exercising muscles. Each patient was matched with three healthy control subjects to maximize statistical power. In controls, 2 min of static handgrip performed at 33 % or 45 % of maximal voluntary contraction (MVC) produced intensity-dependent increases in MSNA (171 +/- 22 % and 379 +/- 95 %, respectively). In the patients, MSNA responses to static handgrip were markedly attenuated (33 +/- 14 % at 33 % MVC; 32 +/- 19 % at 45 % MVC; P < 0.05 vs. controls). Likewise, when static handgrip (30 % MVC) was performed to fatigue, MSNA increased by 366 +/- 73 % in controls but only by 51 +/- 14 % in patients (P < 0.05). Pressor responses to static handgrip were also attenuated in patients compared to controls, whereas heart rate responses were identical. In contrast to exercise, the MSNA responses to other reflex stimuli (the cold pressor test or Valsalva's manoeuvre) were similar in patients and controls. Together these data indicate that appropriate activation of glycogenolytic pathways is obligatory for normal metaboreflex-mediated sympathoexcitation during static exercise in humans.
Authors:
Paul J Fadel; Zhongyun Wang; Meryem Tuncel; Hitoshi Watanabe; Aamer Abbas; Debbie Arbique; Wanpen Vongpatanasin; Robert W Haley; Ronald G Victor; Gail D Thomas
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Publication Detail:
Type:  Comment; Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2003-03-14
Journal Detail:
Title:  The Journal of physiology     Volume:  548     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-05-01     Completed Date:  2004-08-19     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  983-93     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Division of Hypertension, University of Texas Southwestern Medical Center, Dallas, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Body Mass Index
Exercise / physiology*
Female
Glycogen Phosphorylase, Muscle Form / deficiency*,  physiology
Glycogen Storage Disease Type V / physiopathology*
Hand Strength / physiology*
Humans
Male
Middle Aged
Muscle, Skeletal / innervation*
Reference Values
Reflex / physiology*
Sympathetic Nervous System / physiopathology*
Grant Support
ID/Acronym/Agency:
HL06296/HL/NHLBI NIH HHS; HL07360/HL/NHLBI NIH HHS; HL64784/HL/NHLBI NIH HHS; HL69648/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
EC 2.4.1.-/Glycogen Phosphorylase, Muscle Form
Comments/Corrections
Comment On:
J Physiol. 2003 May 1;548(Pt 3):666   [PMID:  12640003 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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