Folland J, Leach B, Little T, Hawker K, Myerson S, Montgomery H, Jones D
Chelsea School Research Centre, University of Brighton, School of Sport and Exercise Sciences, University of Birmingham and Centre for Cardiovascular Genetics, University College London, UK.
Exp Physiol. 2000 Sep;85(5):575-9.
The response to strength training varies widely between individuals and is considerably influenced by genetic variables, which until now, have remained unidentified. The deletion (D), rather than the insertion (I), variant of the human angiotensin-converting enzyme (ACE) genotype is an important factor in the hypertrophic response of cardiac muscle to exercise and could also be involved in skeletal muscle hypertrophy - an important factor in the response to functional overload. Subjects were 33 healthy male volunteers with no experience of strength training. We examined the effect of ACE genotype upon changes in strength of quadriceps muscles in response to 9 weeks of specific strength training (isometric or dynamic). There was a significant interaction between ACE genotype and isometric training with greater strength gains shown by subjects with the D allele (mean +/- S.E.M.: II, 9.0+/-1.7 %; ID, 17.6 +/-2.2 %; DD, 14.9+/-1.3 %, ANOVA, P 0.05). A consistent genotype and training interaction (ID DD II) was observed across all of the strength measures, and both types of training. ACE genotype is the first genetic factor to be identified in the response of skeletal muscle to strength training. The association of the ACE I/D polymorphism with the responses of cardiac and skeletal muscle to functional overload indicates that they may share a common mechanism. These findings suggest a novel mechanism, involving the renin-angiotensin system, in the response of skeletal muscle to functional overload and may have implications for the management of conditions such as muscle wasting disorders, prolonged bed rest, ageing and rehabilitation, where muscle weakness may limit function.
力量训练的反应在个体之间差异很大，并且受到基因变量的显著影响，而这些基因变量至今仍未被确定。人类血管紧张素转换酶（ACE）基因型的缺失（D）而非插入（I）变体是心肌对运动肥大反应的一个重要因素，也可能与骨骼肌肥大有关——骨骼肌肥大是对功能性超负荷反应的一个重要因素。研究对象为33名无力量训练经验的健康男性志愿者。我们研究了ACE基因型对股四头肌力量变化的影响，这些变化是在进行9周特定力量训练（等长或动态）后出现的。ACE基因型与等长训练之间存在显著的交互作用，D等位基因的受试者力量增加更大（平均值±标准误：II型，9.0±1.7%；ID型，17.6±2.2%；DD型，14.9±1.3%，方差分析，P<0.05）。在所有力量测量指标和两种训练类型中均观察到一致的基因型与训练交互作用（ID>DD>II）。ACE基因型是在骨骼肌对力量训练反应中被确定的首个遗传因素。ACE I/D多态性与心脏和骨骼肌对功能性超负荷反应的关联表明它们可能共享一种共同机制。这些发现提示了一种涉及肾素-血管紧张素系统的新机制，参与骨骼肌对功能性超负荷的反应，并且可能对诸如肌肉萎缩性疾病、长期卧床休息、衰老和康复等情况的管理具有意义，在这些情况下肌肉无力可能会限制功能。
