Document Detail


Muscle high-energy metabolites and metabolic capacity in patients with heart failure.
MedLine Citation:
PMID:  11252072     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OKITA, K., K. YONEZAWA, H. NISHIJIMA, A. HANADA, T. NAGAI, T. MURAKAMI, and A. KITABATAKE. Muscle high-energy metabolites and metabolic capacity in patients with heart failure. Med Sci. Sports. Exerc., Vol. 33, No. 3, 2001, pp. 442-448. Background: Various abnormalities in skeletal muscle have been demonstrated by biopsy in patients with chronic heart failure (CHF). In mammalian muscles, high-energy metabolite composition at rest (HEMC) provides data on important metabolic characteristics; however, the significance of HEMC has not been clarified in patients with CHF. Therefore, we investigated HEMC in normal subjects and patients with CHF and examined its relation to muscle metabolic capacity and exercise tolerance. Methods: High-energy metabolites (phosphocreatine (PCr), inorganic phosphate (Pi), and ATP) in resting calf muscle were measured by 31P-magnetic resonance spectroscopy (31P-MRS), and ratios of Pi to PCr, Pi to ATP, and PCr to ATP were calculated in 34 patients with CHF and 13 age- and size-matched normal subjects. Muscle metabolism was evaluated during local exercise of unilateral plantar flexion by 31P-MRS. Metabolic capacity was estimated by the rate of PCr breakdown in relation to the workload. Systemic exercise capacity was evaluated by a bicycle ergometer. Results: The ratio of PCr to ATP was significantly increased in patients with CHF compared with controls (3.06 +/- 0.43 vs 2.72 +/- 0.36, P < 0.05) and was significantly correlated with metabolic capacity (r = -0.37, P < 0.01) and with peak oxygen uptake (r = -0.45, P < 0.01). There was a significant correlation between metabolic capacity and peak oxygen uptake (r = 0.53, P < 0.001). Conclusion: HEMC was altered in patients with CHF, and this change was related to metabolic capacity and exercise capacity. These findings provide new insight into the mechanism of impaired muscle metabolism in CHF.
Authors:
K Okita; K Yonezawa; H Nishijima; A Hanada; T Nagai; T Murakami; A Kitabatake
Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Medicine and science in sports and exercise     Volume:  33     ISSN:  0195-9131     ISO Abbreviation:  Med Sci Sports Exerc     Publication Date:  2001 Mar 
Date Detail:
Created Date:  2001-03-19     Completed Date:  2001-05-10     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8005433     Medline TA:  Med Sci Sports Exerc     Country:  United States    
Other Details:
Languages:  eng     Pagination:  442-8     Citation Subset:  IM; S    
Affiliation:
Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo 060-8638, Japan. cvext@med.hokudai.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Aged
Exercise / physiology*
Female
Heart Failure / complications*
Humans
Male
Middle Aged
Muscle, Skeletal / physiology*
Oxygen Consumption
Phosphates / metabolism
Phosphocreatine / analysis*,  metabolism
Physical Fitness
Chemical
Reg. No./Substance:
0/Phosphates; 56-65-5/Adenosine Triphosphate; 67-07-2/Phosphocreatine

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