Higher skeletal muscle α2AMPK activation and lower energy charge and fat oxidation in men than in women during submaximal exercise
Higher skeletal muscle α2AMPK activation and lower energy charge and fat oxidation in men than in women during submaximal exercise
复制标题
DOI：
10.1113/jphysiol.2006.108720
复制
发表时间：
2006-07-01
影响因子：
5.5
通讯作者：
Kiens, Bente
中科院分区：
文献类型：
--
作者：
Roepstorff, Carsten;Thiele, Maja;Kiens, Bente
5 'AMP活化蛋白激酶（AMPK）是一种能量传感器，可在肌肉收缩时被细胞能量状态扰动激活。活化的AMPK被认为调节几个关键的代谢途径。我们使用性别比较来研究运动过程中骨骼肌中AMPK信号是否调节脂肪氧化。受过中等训练的女性和男性完成90分钟的自行车运动在60%（O2峰值）。AMPK Thr（172）磷酸化和α（2）AMPK活性在男性运动中增加（接近200%，P < 0.001），但在女性中不显着。运动时肌肉AMPK激活的性别差异伴随着肌肉游离AMP的增加（与164%相似，P < 0.01），游离AMP/ATP比值（159%，P < 0.05），肌酸（与42%相似，P < 0.001），男性，但女性（NS），这表明女性缺乏AMPK激活是由于与男性相比更好地维持了肌肉细胞能量平衡。运动时，女性每kg瘦体重的脂肪氧化量高于男性（P < 0.05）。回归分析显示，1型肌纤维的比例较高，（与23%相似，P < 0.01）和较高的毛细血管化女性比男性高23%（P < 0.05），这可以部分解释a2 AMPK活性的性别差异（r =-0.54，P < 0.05）和脂肪氧化（r = 0.64，P < 0.05）。另一方面，脂肪氧化似乎不通过AMPK调节。总之，在60%（O2 peak）的长时间亚极量运动期间，女性较高的脂肪氧化不能用较高的AMPK信号来解释，但伴随着女性肌肉细胞能量平衡的改善，这可能是由于性别特异性肌肉形态。
5'AMP-activated protein kinase (AMPK) is an energy sensor activated by perturbed cellular energy status such as during muscle contraction. Activated AMPK is thought to regulate several key metabolic pathways. We used sex comparison to investigate whether AMPK signalling in skeletal muscle regulates fat oxidation during exercise. Moderately trained women and men completed 90 min bicycle exercise at 60% (O2peak). Both AMPK Thr(172) phosphorylation and alpha(2)AMPK activity were increased by exercise in men (similar to 200%, P < 0.001) but not significantly in women. The sex difference in muscle AMPK activation with exercise was accompanied by an increase in muscle free AMP (similar to 164%, P < 0.01), free AMP/ATP ratio (159%, P < 0.05), and creatine (similar to 42%, P < 0.001) in men but not in women (NS), suggesting that lack of AMPK activation in women was due to better maintenance of muscle cellular energy balance compared with men. During exercise, fat oxidation per kg lean body mass was higher in women than in men ( P < 0.05). Regression analysis revealed that a higher proportion of type 1 muscle fibres (similar to 23%, P < 0.01) and a higher capillarization (similar to 23%, P < 0.05) in women than in men could partly explain the sex difference in a2AMPK activity (r = -0.54, P < 0.05) and fat oxidation (r = 0.64, P < 0.05) during exercise. On the other hand, fat oxidation appeared not to be regulated via AMPK. In conclusion, during prolonged submaximal exercise at 60% (O2peak), higher fat oxidation in women cannot be explained by higher AMPK signalling but is accompanied by improved muscle cellular energy balance in women probably due to sex specific muscle morphology.