Evans William J
Nutrition, Metabolism, and Exercise Laboratory, Donald W. Reynolds Center on Aging, Slot 806, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Clin Orthop Relat Res. 2002 Oct(403 Suppl):S211-20. doi: 10.1097/00003086-200210001-00025.
Strength conditioning will result in an increase in muscle size and this increase in size is largely the result of increased contractile proteins. The mechanisms by which the mechanical events stimulate an increase in ribonucleic acid synthesis and subsequent protein synthesis are not well understood. Lifting weight requires that a muscle shorten as it produces force (concentric contraction). Lowering the weight, however, forces the muscle to lengthen as it produces force (eccentric contraction). These lengthening muscle contractions have been shown to produce ultrastructural damage (microscopic tears in contractile proteins muscle cells) that may stimulate increased muscle protein turnover. This muscle damage produces a cascade of metabolic events that is similar to an acute phase response and includes complement activation, mobilization of neutrophils, increased circulation of skeletal muscle interleukin-1, macrophage accumulation in muscle, and an increase in muscle protein synthesis and degradation. Although endurance exercise increases the oxidation of essential amino acids and increases the requirement for dietary protein, resistance exercise results in a decrease in nitrogen excretion, lowering dietary protein needs. This increased efficiency of protein use may be important for wasting diseases such as human immunodeficiency virus infection and cancer and particularly in elderly people suffering from sarcopenia. Research has indicated that increased dietary protein intake (as much as 1.6 g protein x kg x day ) may enhance the hypertrophic response to resistance exercise. It also has been shown that in very old men and women the use of a protein-calorie supplement was associated with greater strength and muscle mass gains than the use of placebo.
力量训练会导致肌肉尺寸增加，而这种尺寸的增加很大程度上是收缩蛋白增加的结果。机械性事件刺激核糖核酸合成及随后的蛋白质合成增加的机制尚未完全明确。举重时，肌肉在产生力量时会缩短（向心收缩）。然而，放下重物时，肌肉在产生力量时会被迫拉长（离心收缩）。这些肌肉拉长收缩已被证明会产生超微结构损伤（收缩蛋白肌肉细胞中的微观撕裂），这可能会刺激肌肉蛋白质更新增加。这种肌肉损伤会引发一系列类似于急性期反应的代谢事件，包括补体激活、中性粒细胞动员、骨骼肌白细胞介素 -1 循环增加、巨噬细胞在肌肉中的积聚，以及肌肉蛋白质合成和降解增加。虽然耐力运动增加必需氨基酸的氧化并增加对膳食蛋白质的需求，但抗阻运动导致氮排泄减少，从而降低膳食蛋白质需求。这种蛋白质利用效率的提高对于诸如人类免疫缺陷病毒感染和癌症等消耗性疾病可能很重要，尤其是对于患有肌肉减少症的老年人。研究表明，增加膳食蛋白质摄入量（高达 1.6 克蛋白质×千克×天）可能会增强对抗阻运动的肥大反应。研究还表明，在非常年长的男性和女性中，使用蛋白质 - 热量补充剂比使用安慰剂能带来更大的力量和肌肉量增加。
