Document Detail

Muscle mechanoreceptor sensitivity in heart failure.
MedLine Citation:
PMID:  15475527     Owner:  NLM     Status:  MEDLINE    
Prior work in animals suggests that muscle mechanoreceptor control of sympathetic activation (MSNA) during exercise in heart failure (HF) is heightened and that muscle mechanoreceptors are sensitized by metabolic by-products. We sought to determine whether 1) muscle mechanoreceptor control of MSNA is enhanced in HF patients and 2) lactic acid sensitizes muscle mechanoreceptors during rhythmic handgrip (RHG) exercise in healthy humans and patients with HF. Dichloroacetate (DCA), which reduces the production of lactic acid, or saline control was infused in 12 patients with HF and 13 controls during RHG. MSNA was recorded (microneurography). After saline was administered and during exercise thereafter, MSNA increased earlier in HF compared with controls, consistent with baseline-heightened mechanoreceptor sensitivity. In both HF and controls, MSNA increased during the 3-min exercise protocol, consistent with further sensitization of muscle mechanoreceptors by metabolic by-product(s). During posthandgrip circulatory arrest, MSNA returned rapidly to baseline levels, excluding the muscle metaboreceptors as mediators of the sympathetic excitation during RHG. To isolate muscle mechanoreceptors from central command, we utilized passive exercise in 8 HF and 11 controls, and MSNA was recorded. MSNA increased significantly during passive exercise in HF but not in controls. In conclusion, muscle mechanoreceptors mediate the increase in MSNA during low-level RHG exercise in healthy humans, and this muscle mechanoreceptor control is augmented further in HF. Neither lactate generation nor the fall in pH during RHG plays a central role in muscle mechanoreceptor sensitization. Finally, muscle mechanoreceptors in patients with HF have heightened basal sensitivity to mechanical stimuli resulting in exaggerated early increases in MSNA.
Holly R Middlekauff; Josephine Chiu; Michele A Hamilton; Gregg C Fonarow; W Robb Maclellan; Antoine Hage; Jaime Moriguchi; Jignash Patel
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Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  287     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-10-11     Completed Date:  2004-11-24     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1937-43     Citation Subset:  IM    
Div. of Cardiology, 47-123 CHS, UCLA Dept. of Medicine, 10833 Le Conte Ave., Los Angeles, CA 90095, USA.
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MeSH Terms
Cardiac Output, Low / physiopathology*
Dichloroacetate / pharmacology
Double-Blind Method
Hand Strength
Lactic Acid / antagonists & inhibitors,  metabolism*
Mechanoreceptors / physiopathology*
Middle Aged
Muscle, Skeletal / blood supply,  innervation*
Sympathetic Nervous System / physiopathology*
Grant Support
5 M01 RR-00865-25/RR/NCRR NIH HHS; R01-HL-67298/HL/NHLBI NIH HHS
Reg. No./Substance:
13425-80-4/Dichloroacetate; 50-21-5/Lactic Acid

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

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