Muscle size explains low passive skeletal muscle force in heart failure patients

Author:

Panizzolo Fausto Antonio12,Maiorana Andrew J.34,Naylor Louise H.2,Dembo Lawrence G.5,Lloyd David G.6,Green Daniel J.27,Rubenson Jonas28

Affiliation:

1. John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, United States

2. The School of Sport Science, Exercise and Health, The University of Western Australia, Crawley, WA, Australia

3. Advanced Heart Failure and Cardiac Transplant Service, Royal Perth Hospital, Perth, WA, Australia

4. School of Physiotherapy and Exercise Science, Curtin University, Perth, WA, Australia

5. Envision Medical Imaging, Perth, WA, Australia

6. Centre for Musculoskeletal Research, Griffith Health Institute, Griffith University, Gold Coast, QLD, Australia

7. Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom

8. Biomechanics Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park, PA, United States

Abstract

BackgroundAlterations in skeletal muscle function and architecture have been linked to the compromised exercise capacity characterizing chronic heart failure (CHF). However, how passive skeletal muscle force is affected in CHF is not clear. Understanding passive force characteristics in CHF can help further elucidate the extent to which altered contractile properties and/or architecture might affect muscle and locomotor function. Therefore, the aim of this study was to investigate passive force in a single muscle for which non-invasive measures of muscle size and estimates of fiber force are possible, the soleus (SOL), both in CHF patients and age- and physical activity-matched control participants.MethodsPassive SOL muscle force and size were obtained by means of a novel approach combining experimental data (dynamometry, electromyography, ultrasound imaging) with a musculoskeletal model.ResultsWe found reduced passive SOL forces (∼30%) (at the same relative levels of muscle stretch) in CHF vs. healthy individuals. This difference was eliminated when force was normalized by physiological cross sectional area, indicating that reduced force output may be most strongly associated with muscle size. Nevertheless, passive force was significantly higher in CHF at a given absolute muscle length (non length-normalized) and likely explained by the shorter muscle slack lengths and optimal muscle lengths measured in CHF compared to the control participants. This later factor may lead to altered performance of the SOL in functional tasks such gait.DiscussionThese findings suggest introducing exercise rehabilitation targeting muscle hypertrophy and, specifically for the calf muscles, exercise that promotes muscle lengthening.

Funder

National Heart Foundation

International Society of Biomechanics

Publisher

PeerJ

Subject

General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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