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Creatine ingestion augments dietary carbohydrate mediated muscle glycogen supercompensation during the initial 24 h of recovery following prolonged exhaustive exercise in humans

机译:人体进行长时间的力竭运动后恢复的最初24小时内肌酸的摄入会增强饮食中碳水化合物介导的肌肉糖原的超补偿作用

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摘要

Muscle glycogen availability can limit endurance exercise performance. We previously demonstrated 5 days of creatine (Cr) and carbohydrate (CHO) ingestion augmented post-exercise muscle glycogen storage compared to CHO feeding alone in healthy volunteers. Here, we aimed to characterise the time-course of this Cr-induced response under more stringent and controlled experimental conditions and identify potential mechanisms underpinning this phenomenon. Fourteen healthy, male volunteers cycled to exhaustion at 70 % VO2peak. Muscle biopsies were obtained at rest immediately post-exercise and after 1, 3 and 6 days of recovery, during which Cr or placebo supplements (20 g day−1) were ingested along with a prescribed high CHO diet (37.5 kcal kg body mass−1 day−1, >80 % calories CHO). Oral-glucose tolerance tests (oral-GTT) were performed pre-exercise and after 1, 3 and 6 days of Cr and placebo supplementation. Exercise depleted muscle glycogen content to the same extent in both treatment groups. Creatine supplementation increased muscle total-Cr, free-Cr and phosphocreatine (PCr) content above placebo following 1, 3 and 6 days of supplementation (all P < 0.05). Creatine supplementation also increased muscle glycogen content noticeably above placebo after 1 day of supplementation (P < 0.05), which was sustained thereafter. This study confirmed dietary Cr augments post-exercise muscle glycogen super-compensation, and demonstrates this occurred during the initial 24 h of post-exercise recovery (when muscle total-Cr had increased by <10 %). This marked response ensued without apparent treatment differences in muscle insulin sensitivity (oral-GTT, muscle GLUT4 mRNA), osmotic stress (muscle c-fos and HSP72 mRNA) or muscle cell volume (muscle water content) responses, such that another mechanism must be causative.
机译:肌肉糖原的可用性会限制耐力运动表现。先前我们证明,与健康志愿者中单独CHO喂养相比,肌酸(Cr)和碳水化合物(CHO)摄入5天可增加运动后肌肉糖原的存储。在这里,我们旨在表征在更严格和受控的实验条件下这种Cr诱导的响应的时间过程,并确定支撑这种现象的潜在机制。 14名健康的男性志愿者以70%的VO2peak循环衰竭。运动后和休息后1、3、6天休息后进行肌肉活检,在此期间摄入铬或安慰剂补充剂(20 g day -1 )以及高CHO饮食(37.5 kcal公斤体重 -1 -1 ,> 80%卡路里的CHO)。运动前和补充铬,安慰剂1、3和6天后进行口服葡萄糖耐量试验(oral-GTT)。在两个治疗组中,运动消耗的肌肉糖原含量相同。补充肌酸后1、3和6天,肌肉总Cr,游离Cr和磷酸肌酸(PCr)含量高于安慰剂(所有P <0.05)。补充肌酸在补充1天后也比安慰剂明显增加了肌肉糖原含量(P <0.05),此后持续存在。这项研究证实饮食中的Cr会增加运动后肌肉糖原的超补偿,并证明这是在运动后恢复的最初24小时内发生的(当肌肉总Cr增加了<10%时)。随后在没有明显治疗差异的肌肉胰岛素敏感性(口服GTT,肌肉GLUT4 mRNA),渗透压(肌肉c-fos和HSP72 mRNA)或肌肉细胞体积(肌肉含水量)响应方面没有明显的治疗差异,因此必须采用另一种机制原因。

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