Reduced exercise tolerance in CHF may be related to factors other than impaired skeletal muscle oxidative capacity

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http://eprints.org/relation/isVersionOf https://vuir.vu.edu.au/id/document/990 http://eprints.org/relation/isVolatileVersionOf https://vuir.vu.edu.au/id/document/990 http://eprints.org/relation/isCoversheetVersionOf https://vuir.vu.edu.au/id/document/990 archive 292 disk0/00/00/14/05 2008-10-14 03:36:40 2021-08-27 13:58:34 2008-10-14 03:36:40 article show Williams Andrew D Williams, Andrew D Selig Steve E Selig, Steve E Hare David L Hayes Alan 0000-0003-1398-3694 Krum Henry Patterson Jeremy Geerling Ralph H Toia Deidre Carey Michael F Carey, Michael F Reduced exercise tolerance in CHF may be related to factors other than impaired skeletal muscle oxidative capacity pub 320000 BiomedicalSciences exercise capacity, skeletal muscle We sought to determine whether skeletal muscle oxidative capacity, fiber type proportions and fiber size, capillary density or muscle mass might explain the impaired exercise tolerance in chronic heart failure (CHF). Previous studies are equivocal regarding the maladaptations that occur in the skeletal muscle of patients with CHF and their role in the observed exercise intolerance. Total body O2 uptake (peak) was determined in 14 CHF patients and 8 healthy sedentary similarly-aged controls. Muscle samples were analysed for mitochondrial ATP production rate (MAPR), oxidative and glycolytic enzyme activity, fiber size and type, and capillary density. CHF patients demonstrated a lower peak (15.1 ± 1.1 vs. 28.1 ± 2.3 ml.kg&VO2&VO2-1.min-1, p<0.001) and capillary to fiber ratio (1.09 ± 0.05 vs. 1.40 ± 0.04; p<0.001) when compared to controls. However there was no difference in capillary density (capillaries per μm2) across any of the fiber types. Measurements of MAPR and oxidative enzyme activity indicated no difference in muscle oxidative capacity between the groups. We find that neither reduced muscle oxidative capacity nor capillary density are the cause of exercise limitation in CHF patients, so that the low VO2 peak observed in CHF patients is the result of muscle fiber atrophy and possibly impaired activation of oxidative phosphorylation. 2004 Elsevier 48573 2 2371712 dark_document 48573 HayesCorrespondence.pdf application/pdf 15c0cbdd4e54bb68f83c6f19f60e3a66 MD5 24468 2020-05-20 01:47:52 1405 3 3 application/pdf text Author Correspondence en staffonly

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other public Journal of Cardiac Failure 10 2 141-148 TRUE 1071-9164 Includes bibliographical references FALSE 53 2-s2.0-3042756374 2023-07-02 04:00:16