Exercise Training Prevents Diaphragm Contractile Dysfunction in HF

Study Questions:

Can aerobic exercise training prevent diaphragmatic contractile dysfunction in heart failure (HF), and can it attenuate the associated oxidative stress and proteolysis?

Methods:

A mouse model of HF induced by myocardial infarction and mice with sham surgery were randomized into three groups: sham, HF sedentary, or HF with aerobic exercise training. The HF with aerobic exercise training mice did treadmill exercise for a total of 9 weeks (1 hr x 5 d/wk at 15 m/min with a 15o incline) starting at 1 week post-surgery. All mice were sacrificed at 10 weeks. Heart function was assessed by echocardiogram and tissue analysis at 1 and 10 weeks, and diaphragmatic contractile function was assessed at 10 weeks by force transducer measurements and molecular analyses.

Results:

Cardiac dysfunction was well-matched in both HF mice at baseline. Compared with shams, sedentary HF mice developed significant diaphragm muscle weakness across a range of frequencies that was prevented by regular aerobic exercise training. Molecular analysis of diaphragm tissue revealed correlations with reductions in oxidative stress markers and activity of proteolytic pathways; however, it seems likely there are other pathways not revealed in this study.

Conclusions:

This novel study demonstrated that regular aerobic exercise training prevented diaphragm contractile dysfunction in HF mice and, when compared with sedentary HF mice, was associated with some reductions in markers of oxidative stress and proteolytic pathways that lead to muscle atrophy. It seems apparent that other mechanisms of diaphragm dysfunction are involved.

Perspective:

Many patient studies have demonstrated improvement of respiratory function in HF, such as improved inspiratory muscle strength, exercise capacity, and quality of life, due to aerobic exercise training. This appears to be the first study to show improvement of diaphragmatic dysfunction in HF and several of the mechanisms. Reductions in oxidative stress (which contributes to diaphragm dysfunction) and protein degradation (which leads to loss of muscle mass) were improved, though other mechanisms are likely involved. There is potential that in patients with HF, regular aerobic exercise training can protect against HF-induced diaphragmatic contractile dysfunction. Future studies using human subjects would beneficial.

Clinical Topics: Diabetes and Cardiometabolic Disease, Geriatric Cardiology, Heart Failure and Cardiomyopathies, Prevention, Acute Heart Failure, Exercise, Stress

Keywords: Diaphragm, Exercise, Exercise Therapy, Geriatrics, Heart Failure, Muscle Contraction, Muscle Strength, Muscle Weakness, Muscular Atrophy, Myocardial Infarction, Oxidative Stress, Proteolysis, Quality of Life, Secondary Prevention


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