Anthony J C, Anthony T G, Layman D K
Division of Nutritional Sciences and the Department of Food Science and Human Nutrition, University of Illinois, Urbana, IL 61801, USA.
J Nutr. 1999 Jun;129(6):1102-6. doi: 10.1093/jn/129.6.1102.
This study was designed to determine the ability of leucine to enhance muscle recovery after exercise. Male rats (200 g) were divided into five groups: sedentary, food-deprived (SF); exercised, food-deprived (EF); exercised, fed a carbohydrate meal (EC); exercised, fed a leucine meal (EL); and exercised, fed a combination of carbohydrate and leucine (ECL). All meals were administered by oral gavage immediately following exercise. EC and ECL meals were isocaloric and provided 15% of daily energy intake. EL and ECL meals each provided 270 mg leucine. Rats ran on a motor-driven treadmill for 2 h at 36 m/min and were killed 1 h postexercise. Plasma glucose and insulin were measured, and the gastrocnemius and plantaris muscles were excised as a unit to determine glycogen levels and the fractional rate of skeletal muscle protein synthesis (Ks). Exercise did not alter plasma glucose or insulin. In contrast, prolonged exercise reduced muscle glycogen (-51%) and Ks (-18%). Refeeding a combination of carbohydrate and leucine increased plasma insulin relative to the EF and SF groups and produced complete recovery of muscle Ks and glycogen to values not different from those in SF rats. Feeding leucine alone restored Ks to that in the SF group without affecting plasma glucose or insulin concentrations. Feeding carbohydrate alone enhanced the rate of glycogen repletion compared to the EF group, concomitant with increases in plasma glucose and insulin. The degree of glycogen recovery correlated with plasma insulin concentrations (r = 0.58, P < 0.05). These data suggest that leucine stimulates muscle protein synthesis following exercise, independent of increased plasma insulin. This is the first demonstration that orally administered leucine stimulates recovery of skeletal muscle protein synthesis after exercise.
本研究旨在确定亮氨酸增强运动后肌肉恢复的能力。将雄性大鼠(200克)分为五组:久坐不动、禁食(SF);运动、禁食(EF);运动、给予碳水化合物餐(EC);运动、给予亮氨酸餐(EL);运动、给予碳水化合物和亮氨酸组合餐(ECL)。所有餐食均在运动后立即通过灌胃给予。EC餐和ECL餐热量相等,提供每日能量摄入的15%。EL餐和ECL餐各提供270毫克亮氨酸。大鼠在电动跑步机上以36米/分钟的速度跑2小时,并在运动后1小时处死。测量血浆葡萄糖和胰岛素水平,并将腓肠肌和比目鱼肌作为一个整体切除以测定糖原水平和骨骼肌蛋白质合成分数率(Ks)。运动未改变血浆葡萄糖或胰岛素水平。相比之下,长时间运动降低了肌肉糖原(-51%)和Ks(-18%)。与EF组和SF组相比,给予碳水化合物和亮氨酸组合餐使血浆胰岛素增加,并使肌肉Ks和糖原完全恢复至与SF大鼠无差异的值。单独给予亮氨酸可使Ks恢复至SF组水平,而不影响血浆葡萄糖或胰岛素浓度。与EF组相比,单独给予碳水化合物可提高糖原补充率,同时血浆葡萄糖和胰岛素增加。糖原恢复程度与血浆胰岛素浓度相关(r = 0.58,P < 0.05)。这些数据表明,亮氨酸在运动后刺激肌肉蛋白质合成,与血浆胰岛素增加无关。这是首次证明口服亮氨酸可刺激运动后骨骼肌蛋白质合成的恢复。