Abstract
Physical activity is emerging as an alternative nonpharmaceutical strategy to prevent and treat a variety of cardiovascular diseases due to its cardiac and skeletal muscle beneficial effects. Oxidative stress occurs in skeletal muscle of chronic heart failure (CHF) patients with possible impact on muscle function decline. We determined the effect of voluntary‐free wheel running (VFWR) in preventing protein damage in Tgαq*44 transgenic mice (Tg) characterized by a delayed CHF progression. In the early (6 months) and transition (12 months) phase of CHF, VFWR increased the daily mean distance covered by Tg mice eliminating the difference between Tg and WT present before exercise at 12 months of age (WT Pre‐EX 3.62 ± 1.66 vs. Tg Pre‐EX 1.51 ± 1.09 km, P < 0.005; WT Post‐EX 5.72 ± 3.42 vs. Tg Post‐EX 4.17 ± 1.8 km, P > 0.005). This effect was concomitant with an improvement of in vivo cardiac performance [(Cardiac Index (mL/min/cm2): 6 months, untrained‐Tg 0.167 ± 0.005 vs. trained‐Tg 0.21 ± 0.003, P < 0.005; 12 months, untrained‐Tg 0.1 ± 0.009 vs. trained‐Tg 0.133 ± 0.005, P < 0.005]. Such effects were associated with a skeletal muscle antioxidant response effective in preventing oxidative damage induced by CHF at the transition phase (untrained‐Tg 0.438 ± 0.25 vs. trained‐Tg 0.114 ± 0.010, P < 0.05) and with an increased expression of protein control markers (MuRF‐1, untrained‐Tg 1.12 ± 0.29 vs. trained‐Tg 14.14 ± 3.04, P < 0.0001; Atrogin‐1, untrained‐Tg 0.9 ± 0.38 vs. trained‐Tg 7.79 ± 2.03, P < 0.01; Cathepsin L, untrained‐Tg 0.91 ± 0.27 vs. trained‐Tg 2.14 ± 0.55, P < 0.01). At the end‐stage of CHF (14 months), trained‐Tg mice showed a worsening of physical performance (decrease in daily activity and weekly distance and time of activity) compared to trained age‐matched WT in association with oxidative protein damage of a similar level to that of untrained‐Tg mice (untrained‐Tg 0.62 ± 0.24 vs. trained‐Tg 0.64 ± 0.13, P > 0.05). Prolonged voluntary physical activity performed before the onset of CHF end‐stage, appears to be a useful tool to increase cardiac function and to reduce skeletal muscle oxidative damage counteracting physical activity decline.
Highlights
Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society
Further deterioration was observed in 14 months-old mice as decreases in left atrial ejection fraction (LA EF), increases in end systolic volume (ESV), end diastolic volume (EDV), ejection rate (ER) and filling rate (FR), reduction of ejection time (ET), filling time (FT), and heart rate (HR) and further prolongation of IVCT
Tacking advantage of Tgaq*44 mouse model with protracted development of chronic heart failure (CHF), we investigated the effect of voluntary exercise in normalizing skeletal muscle oxidative stress during the progression of CHF
Summary
Patients with chronic heart failure (CHF) show exercise intolerance (Poole et al, 2012; Hirai et al, 2015), that affects the patients’ clinical picture, quality of life, and prognosis. Several evidences indicate that changes in cardiac function cannot fully explain the origin of exercise intolerance (Piepoli et al, 2010) and a key role of the periphery has emerged, indicating that changes in skeletal muscle can significantly limit exercise capacity in these patients. The impairment precludes these patients from obtaining the beneficial effects associated with exercise training (Hirai et al, 2015). To improve the quality of life of these patients the development of countermeasures that positively affect both cardiac and skeletal muscle is essential. Different training modalities are available to target the problems with which chronic heart failure patients are faced and low stress exercise is recommended for these patients (Aronow, 2003; Pin~a et al, 2003; Smart and Marwick, 2004)
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