Document Detail

The exercise metaboreflex is maintained in the absence of muscle acidosis: insights from muscle microdialysis in humans with McArdle's disease.
MedLine Citation:
PMID:  11731594     Owner:  NLM     Status:  MEDLINE    
1. In McArdle's disease, muscle glycogenolysis is blocked, which results in absent lactate and enhanced ammonia production in working muscle. Using McArdle patients as an experimental model, we studied whether lactate and ammonia could be mediators of the exercise pressor reflex. 2. Changes in muscle interstitial ammonia and lactate were compared with changes in blood pressure and muscle sympathetic nerve activity (MSNA) during static arm flexor exercise at 30% of maximal contraction force. Muscle interstitial changes in lactate and ammonia were assessed by microdialysis of the biceps muscle, and MSNA by peroneal nerve microneurography, in six McArdle patients and 11 healthy, matched controls. One McArdle patient also had myoadenylate deaminase deficiency, a condition associated with abolished ammonia production in exercise. 3. Exercise-induced increases were higher in McArdle patients vs. controls for MSNA (change of 164 +/- 71 vs. 59 +/- 19%) and blood pressure (change of 47 +/- 7 vs. 38 +/- 4 mmHg). Interstitial lactate increased in controls (peak change 1.3 +/- 0.2 mmol x l(-1)) and decreased in McArdle patients (peak change -0.5 +/- 0.1 mmol x l(-1)) during and after exercise. Interstitial ammonia did not change during exercise in either group, but was higher post-exercise in McArdle patients, except in the patient with myoadenylate deaminase deficiency who had a flat ammonia response. This patient had an increase in MSNA and blood pressure comparable to other patients. MSNA and blood pressure responses were maintained during post-exercise ischaemia in both groups, indicating that sympathetic activation was caused, at least partly, by a metaboreflex. 4. In conclusion, changes in muscle interstitial lactate and ammonia concentrations during and after exercise are temporally dissociated from changes in MSNA and blood pressure in both patients with McArdle's disease and healthy control subjects. This suggests that muscle acidification and changes in interstitial ammonia concentration are not mediators of sympathetic activation during exercise.
J Vissing; D A MacLean; S F Vissing; M Sander; B Saltin; R G Haller
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The Journal of physiology     Volume:  537     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2001 Dec 
Date Detail:
Created Date:  2001-12-03     Completed Date:  2002-02-11     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  641-9     Citation Subset:  IM    
Copenhagen Muscle Research Centre, National University Hospital, Rigshospitalet, Copenhagen, Denmark.
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MeSH Terms
Acidosis / metabolism
Ammonia / metabolism
Cardiovascular System / physiopathology
Exercise / physiology*
Glycogen Storage Disease Type V / metabolism*
Lactic Acid / metabolism
Middle Aged
Muscle Contraction / physiology
Muscle, Skeletal / innervation,  metabolism*
Reference Values
Reflex / physiology*
Sympathetic Nervous System / physiopathology
Time Factors
Valsalva Maneuver
Reg. No./Substance:
50-21-5/Lactic Acid; 7664-41-7/Ammonia
Comment In:
J Physiol. 2001 Dec 1;537(Pt 2):331   [PMID:  11731567 ]

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