Effects of Endurance Training on Detrimental Structural, Cellular, and Functional Alterations in Skeletal Muscles of Heart Failure With Preserved Ejection Fraction
Effects of Endurance Training on Detrimental Structural, Cellular, and Functional Alterations in Skeletal Muscles of Heart Failure With Preserved Ejection Fraction
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DOI：
10.1016/j.cardfail.2018.08.009
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发表时间：
2018-09-01
影响因子：
6
通讯作者：
Adams, Volker
中科院分区：
文献类型：
--
作者：
Bowen, T. Scott;Herz, Christian;Adams, Volker
背景资料：射血分数保留性心力衰竭（HFpEF）的基础是导致疾病严重程度的有害骨骼肌改变，但其潜在机制和治疗方法仍不明确。本研究使用非人类动物模型HFpEF，以更好地了解骨骼肌异常是否（1）纤维类型的具体和（2）可逆的各种运动training regimes.Methods和Results：瘦对照组大鼠与肥胖的HFpEF 1大鼠在20周，然后8周后久坐，高强度的间歇训练，或适度的连续跑步机运动。评估氧化比目鱼肌和糖酵解趾长伸肌（EDL）的纤维大小，毛细血管，糖酵解代谢，自噬和收缩功能。HFpEF使比目鱼肌和趾长伸肌的纤维尺寸和毛细血管减少了20%-50%（P <0.05），但耐力训练不能逆转这些作用。相比之下，HFpEF中的两种耐力训练方案都减弱了比目鱼肌中观察到的乳酸脱氢酶活性升高。自噬在趾长伸肌中下调，在比目鱼肌中上调（P <0.05），耐力训练对自噬无影响。HFpEF损害收缩力的两块肌肉的20%（P <0.05），这些都没有被逆转的training.Conclusions：肥胖相关的HFpEF与有害的结构，细胞和功能的改变，慢氧化和快速糖酵解骨骼肌，不能逆转的耐力训练。
Background: Heart failure with preserved ejection fraction (HFpEF) is underpinned by detrimental skeletal muscle alterations that contribute to disease severity, yet underlying mechanisms and therapeutic treatments remain poorly established. This study used a nonhuman animal model of HFpEF to better understand whether skeletal muscle abnormalities were (1) fiber-type specific and (2) reversible by various exercise training regimes.Methods and Results: Lean control rats were compared with obese ZSF1 rats at 20 weeks and then 8 weeks after sedentary, high-intensity interval training, or moderate continuous treadmill exercise. Oxidative soleus and glycolytic extensor digitorum longus (EDL) muscles were assessed for fiber size, capillarity, glycolytic metabolism, autophagy, and contractile function. HFpEF reduced fiber size and capillarity by 20%-50% (P < .05) in both soleus and EDL, but these effects were not reversed by endurance training. In contrast, both endurance training regimes in HFpEF attenuated the elevated lactate dehydrogenase activity observed in the soleus. Autophagy was down-regulated in EDL and up-regulated in soleus (P < .05), with no influence of endurance training. HFpEF impaired contractile forces of both muscles by 20% (P < .05), and these were not reversed by training.Conclusions: Obesity-related HFpEF was associated with detrimental structural, cellular, and functional alterations to both slow-oxidative and fast-glycolytic skeletal muscles that could not be reversed by endurance training.