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

PeerJ. 2016 Sep 15:4:e2447. doi: 10.7717/peerj.2447. eCollection 2016.

Abstract

Background: Alterations 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.

Methods: Passive SOL muscle force and size were obtained by means of a novel approach combining experimental data (dynamometry, electromyography, ultrasound imaging) with a musculoskeletal model.

Results: We 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.

Discussion: These findings suggest introducing exercise rehabilitation targeting muscle hypertrophy and, specifically for the calf muscles, exercise that promotes muscle lengthening.

Keywords: Heart failure; Passive force; Skeletal muscle; Soleus; Ultrasound.

Grants and funding

This work was supported by a Grant-in-Aid (G09P 4469) from the National Heart Foundation of Australia to JR, DJG, AJM and DGL, and a thesis dissertation grant from the International Society of Biomechanics to FAP. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.