van Breda E, Keizer H, Kuipers H, Kranenburg G
Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Maastricht University, Maastricht, The Netherlands.
Br J Sports Med. 2003 Aug;37(4):345-50. doi: 10.1136/bjsm.37.4.345.
To investigate in glycolytic and oxidative muscles of trained (nine weeks) and untrained hyperglycaemic female rats the effect of hyperandrogenicity and/or endurance training on energy metabolic properties.
Glycogen content and activity of muscle enzymes with regulatory functions in glycogen synthesis were examined.
Testosterone treatment increased glycogen content of extensor digitorum longus (EDL) and soleus muscles of hyperglycaemic sedentary (18% and 84% respectively) and hyperglycaemic trained (7% and 16% respectively) rats. In both types of muscle of the hyperglycaemic testosterone treated exercised subgroup, less depletion of glycogen was found than in the untreated group (38% and 87% for EDL and soleus respectively).
The mechanisms by which training and/or hyperandrogenism alone or in combination elicits their specific effects are complex. Differences in sex, surgery, levels of hormones administered, and exercise model used may be the main reasons for the observed discrepancies. Conclusions from the results: (a) hyperandrogenism is not a primary cause of the development of insulin resistance; (b) glycogen content of slow and fast twitch muscle is increased by training through increased glycogen synthase activity. The most plausible explanation for differences between different muscle fibre types is the different levels of expression of androgen receptors in these fibres. Hyperandrogenicity therefore acts on energy metabolic variables of hyperglycaemic animals by different mechanisms in glycolytic and oxidative muscle fibres.
研究训练(9周)和未训练的高血糖雌性大鼠的糖酵解肌和氧化肌中,高雄激素血症和/或耐力训练对能量代谢特性的影响。
检测糖原含量以及在糖原合成中具有调节功能的肌肉酶的活性。
睾酮处理使久坐不动的高血糖大鼠(分别为18%和84%)和训练后的高血糖大鼠(分别为7%和16%)的趾长伸肌(EDL)和比目鱼肌的糖原含量增加。在高血糖睾酮处理的运动亚组的两种类型肌肉中,发现糖原消耗均少于未处理组(EDL和比目鱼肌分别为38%和87%)。
训练和/或高雄激素血症单独或联合产生其特定作用的机制很复杂。性别、手术、给予的激素水平和使用的运动模型的差异可能是观察到差异的主要原因。结果得出的结论:(a)高雄激素血症不是胰岛素抵抗发展的主要原因;(b)通过增加糖原合酶活性,训练可增加慢肌和快肌的糖原含量。不同肌纤维类型之间差异最合理的解释是这些纤维中雄激素受体的表达水平不同。因此,高雄激素血症通过不同机制作用于高血糖动物糖酵解肌纤维和氧化肌纤维的能量代谢变量。