| Effects of endurance training on mitochondrial ultrastructure and fiber type distribution in skeletal muscle of patients with stable chronic heart failure. | |
| | |
MedLine Citation:
|
PMID: 9120161 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
OBJECTIVES: The present study was designed to evaluate the effects of an ambulatory training program in patients with chronic heart failure (CHF) on the ultrastructural morphology of mitochondria and fiber type distribution of skeletal muscle and its relation to peripheral perfusion. BACKGROUND: Recent studies in patients with CHF have suggested that intrinsic abnormalities in skeletal muscle can contribute to the development of early lactic acidosis and fatigue during exercise. METHODS; Patients were prospectively randomized to either a training group (n = 9; mean [+/- SD] left ventricular ejection fraction [LVEF] 26 +/- 10) participating in an ambulatory training program or to a physically inactive control group (n = 9; LVEF 28 +/- 10%). At baseline and after 6 months, patients underwent symptom-limited bicycle exercise testing with measurement of central and peripheral hemodynamic variables as well as percutaneous needle biopsies of the vastus lateralis muscle. The mitochondrial ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry; cytochrome c oxidase activity was visualized by histochemistry and subsequently quantitated by morphometry. The fiber type distribution was determined by adenosine triphosphatase staining. RESULTS: After 6 months of exercise training there was a significant increase of 41% in the surface density of cytochrome c oxidase-positive mitochondria (SVMOcox+) (p < 0.05 vs. control) and of 43% in the surface density of mitochondrial cristae (SVMC) (p < 0.05 vs. control). Furthermore, exercise training induced a 92% increase in the surface density of the mitochondrial inner border membrane (p < 0.05 vs. control). In contrast, the total number of cytochrome c oxidase-positive mitochondria remained essentially unchanged. Exercise-induced improvement in peak oxygen uptake was closely linked to changes in SVMOcox+ (p < 0.01, r = 0.66). After exercise training, changes in submaximal femoral venous lactate levels were not related to changes in submaximal leg blood flow (r = -0.4), but were inversely related to changes in the volume density of mitochondria (p = 0.01; r = -0.6) as well as to changes in SVMC (p < 0.05; r = -0.5). After exercise training there was a "reshift" from type II to type I fibers (p < 0.05 vs. control). CONCLUSIONS: Patients with CHF who engage in regular physical exercise show enhanced oxidative enzyme activity in the working skeletal muscle and a concomitant reshift to type I fibers. These exercise-induced changes in oxidative capacity appear to be unrelated to changes in peripheral perfusion. |
| | |
Authors:
|
R Hambrecht; E Fiehn; J Yu; J Niebauer; C Weigl; L Hilbrich; V Adams; U Riede; G Schuler |
Publication Detail:
|
Type: Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: Journal of the American College of Cardiology Volume: 29 ISSN: 0735-1097 ISO Abbreviation: J. Am. Coll. Cardiol. Publication Date: 1997 Apr |
Date Detail:
|
Created Date: 1997-04-24 Completed Date: 1997-04-24 Revised Date: 2008-11-21 |
Medline Journal Info:
|
Nlm Unique ID: 8301365 Medline TA: J Am Coll Cardiol Country: UNITED STATES |
Other Details:
|
Languages: eng Pagination: 1067-73 Citation Subset: AIM; IM |
Affiliation:
|
Herzzentrum der Universitat Leipzig, Abteilung Kardiologie, Germany. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Electron Transport Complex IV
/
metabolism Exercise Test Exercise Therapy* Heart Failure / pathology*, rehabilitation Humans Leg / blood supply Middle Aged Mitochondria, Muscle / ultrastructure* Muscle Fibers, Skeletal* Myocardium / enzymology Oxygen Consumption Prospective Studies Pulmonary Gas Exchange Regional Blood Flow |
| Chemical | |
Reg. No./Substance:
|
EC 1.9.3.1/Electron Transport Complex IV |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Left ventricular remodeling with carvedilol in patients with congestive heart failure due to ischemi...
Next Document: Ejection fraction and risk of thromboembolic events in patients with systolic dysfunction and sinus ...