有酸素運動は心不全の骨格筋萎縮を改善

有酸素運動は心不全の骨格筋萎縮を改善させるという研究（ラットと人）を紹介します。

Cunha TF, Bacurau AVN, Moreira JBN, Paixão NA, Campos JC, et al: Exercise Training Prevents Oxidative Stress and Ubiquitin-Proteasome System Overactivity and Reverse Skeletal Muscle Atrophy in Heart Failure. PLoS ONE 7(8): e41701. doi:10.1371/journal.pone.0041701


下記のHPで全文見ることができます。
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0041701


心不全では骨格筋萎縮と機能障害を生じることが知られていますが、そのメカニズムは十分理解されていません。そこで酸化ストレスとユビキチン・プロテアゾーム系を過活動にさせた心不全ラットに中等度の有酸素運動を行ったところ、これらが改善しました。

心不全の人での有酸素運動でも、骨格筋のキモトリプシン様プロテアゾームの活性が増加して、健常者と同等のレベルとなりました。これより心不全での有酸素運動は、酸化ストレスとユビキチン・プロテアゾーム系の過活動を改善させて、骨格筋萎縮を改善させるという結論です。

サルコペニア予防・治療には、レジスタンストレーニングだけでなく有酸素運動も有用と言われています。その根拠の1つとなるかもしれません。悪液質で積極的な運動が困難な場合でも、その方なりに可能な範囲での運動（それが立位保持程度であっても）を行うことが有用かもしれません。

Abstract

Background

Heart failure (HF) is known to lead to skeletal muscle atrophy and dysfunction. However, intracellular mechanisms underlying HF-induced myopathy are not fully understood. We hypothesized that HF would increase oxidative stress and ubiquitin-proteasome system (UPS) activation in skeletal muscle of sympathetic hyperactivity mouse model. We also tested the hypothesis that aerobic exercise training (AET) would reestablish UPS activation in mice and human HF.

Methods/Principal Findings

Time-course evaluation of plantaris muscle cross-sectional area, lipid hydroperoxidation, protein carbonylation and chymotrypsin-like proteasome activity was performed in a mouse model of sympathetic hyperactivity-induced HF. At the 7^th month of age, HF mice displayed skeletal muscle atrophy, increased oxidative stress and UPS overactivation. Moderate-intensity AET restored lipid hydroperoxides and carbonylated protein levels paralleled by reduced E3 ligases mRNA levels, and reestablished chymotrypsin-like proteasome activity and plantaris trophicity. In human HF (patients randomized to sedentary or moderate-intensity AET protocol), skeletal muscle chymotrypsin-like proteasome activity was also increased and AET restored it to healthy control subjects’ levels.

Conclusions

Collectively, our data provide evidence that AET effectively counteracts redox imbalance and UPS overactivation, preventing skeletal myopathy and exercise intolerance in sympathetic hyperactivity-induced HF in mice. Of particular interest, AET attenuates skeletal muscle proteasome activity paralleled by improved aerobic capacity in HF patients, which is not achieved by drug treatment itself. Altogether these findings strengthen the clinical relevance of AET in the treatment of HF.