Mathai Anila S, Bonen Arend, Benton Carley R, Robinson D L, Graham Terry E
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
J Appl Physiol (1985). 2008 Oct;105(4):1098-105. doi: 10.1152/japplphysiol.00847.2007. Epub 2008 Jul 24.
The mRNA of the nuclear coactivator peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) increases during prolonged exercise and is influenced by carbohydrate availability. It is unknown if the increases in mRNA reflect the PGC-1alpha protein or if glycogen stores are an important regulator. Seven male subjects [23 +/- 1.3 yr old, maximum oxygen uptake (Vo(2 max)) 48.4 +/- 0.8 ml.kg(-1).min(-1)] exercised to exhaustion ( approximately 2 h) at 65% Vo(2 max) followed by ingestion of either a high-carbohydrate (HC) or low-carbohydrate (LC) diet (7 or 2.9 g.kg(-1).day(-1), respectively) for 52 h of recovery. Glycogen remained depressed in LC (P < 0.05) while returning to resting levels by 24 h in HC. PGC-1alpha mRNA increased both at exhaustion (3-fold) and 2 h later (6.2-fold) (P < 0.05) but returned to rest levels by 24 h. PGC-1alpha protein increased (P < 0.05) 23% at exhaustion and remained elevated for at least 24 h (P < 0.05). While there was no direct treatment effect (HC vs. LC) for PGC-1alpha mRNA or protein, there was a linear relationship between the changes in glycogen and those in PGC-1alpha protein during exercise and recovery (r = -0.68, P < 0.05). In contrast, PGC-1beta did not increase with exercise but rather decreased (P < 0.05) below rest level at 24 and 52 h, and the decrease was greater (P < 0.05) in LC. PGC-1alpha protein content increased in prolonged exercise and remained upregulated for 24 h, but this could not have been predicted by the changes in mRNA. The beta-isoform declined rather than increasing, and this was greater when glycogen was not resynthesized to rest levels.
核共激活因子过氧化物酶体增殖物激活受体γ共激活因子-1α（PGC-1α）的信使核糖核酸（mRNA）在长时间运动期间会增加，并受碳水化合物可利用性的影响。目前尚不清楚mRNA的增加是否反映了PGC-1α蛋白，以及糖原储备是否是一个重要的调节因素。七名男性受试者[23±1.3岁，最大摄氧量（Vo₂max）48.4±0.8 ml·kg⁻¹·min⁻¹]在65%Vo₂max强度下运动至力竭（约2小时），随后分别摄入高碳水化合物（HC）或低碳水化合物（LC）饮食（分别为7或2.9 g·kg⁻¹·天⁻¹）进行52小时的恢复。在LC组中糖原水平持续降低（P<0.05），而在HC组中24小时后糖原水平恢复至静息水平。PGC-1α mRNA在运动力竭时增加了3倍，2小时后增加了6.2倍（P<0.05），但在24小时后恢复至静息水平。PGC-1α蛋白在运动力竭时增加了23%（P<0.05），并至少持续升高24小时（P<0.05）。虽然对于PGC-1α mRNA或蛋白没有直接的处理效应（HC组与LC组对比），但在运动和恢复期间，糖原变化与PGC-1α蛋白变化之间存在线性关系（r=-0.68，P<0.05）。相比之下，PGC-1β并不随运动增加，而是在24小时和52小时时降至静息水平以下（P<0.05），且在LC组中下降幅度更大（P<0.05）。在长时间运动中PGC-1α蛋白含量增加，并持续上调24小时，但这无法通过mRNA的变化来预测。β亚型下降而非增加，当糖原未重新合成至静息水平时下降幅度更大。
