Vøllestad N K, Sejersted O M, Bahr R, Woods J J, Bigland-Ritchie B
Department of Physiology, National Institute of Occupational Health, Oslo, Norway.
J Appl Physiol (1985). 1988 Apr;64(4):1421-7. doi: 10.1152/jappl.1988.64.4.1421.
Contractile failure during various types of exercise has been attributed to intramuscular metabolic changes. We examined the temporal changes in force-generating capacity and metabolic state during intermittent isometric contractions in humans. One-legged quadriceps contractions at 30% maximum voluntary contraction (MVC) were executed for 6 s, with 4 s of rest between. The decrease in force-generating capacity was tested from brief MVC's and short bursts of 50-Hz stimulation applied at 5-min intervals. After 1 min of exercise, the MVC force declined linearly and in parallel to the 50-Hz stimulation force, indicating that the contractile failure was due to intramuscular processes. After 30 min of exercise the MVC force had declined by approximately 40% compared with the value obtained after 1 min. In separate experiments the same contraction protocol was followed, but two-legged contractions were used. Muscle biopsies taken after 5, 15, and 30 min of exercise showed only minor changes in the concentrations of glycogen, lactate, creatine phosphate (CrP), and ATP. However, at exhaustion, defined as loss of ability to sustain the target force, the concentrations of CrP and glycogen were reduced by 73 and 32%, and muscle lactate concentration had increased to 4.8 mmol/kg wet wt. Thus the gradual decline in force-generating capacity was not due to lactacidosis or lack of substrates for ATP resynthesis and must have resulted from excitation/contraction coupling failure, whereas exhaustion was closely related to phosphagen depletion, without significant lactacidosis.
各种类型运动期间的收缩功能衰竭被归因于肌肉内代谢变化。我们研究了人体间歇性等长收缩过程中力量产生能力和代谢状态的时间变化。以最大自主收缩(MVC)的30%进行单腿股四头肌收缩6秒,中间休息4秒。通过每隔5分钟进行的短暂MVC和50赫兹刺激短脉冲来测试力量产生能力的下降情况。运动1分钟后,MVC力量呈线性下降且与50赫兹刺激力量平行下降,表明收缩功能衰竭是由于肌肉内过程所致。运动30分钟后,MVC力量与1分钟后获得的值相比下降了约40%。在单独的实验中,遵循相同的收缩方案,但采用双腿收缩。在运动5、15和30分钟后采集的肌肉活检样本显示,糖原、乳酸、磷酸肌酸(CrP)和ATP的浓度仅有轻微变化。然而,在定义为无法维持目标力量的疲劳状态下,CrP和糖原的浓度分别降低了73%和32%,肌肉乳酸浓度增加到4.8 mmol/kg湿重。因此,力量产生能力的逐渐下降并非由于乳酸酸中毒或缺乏用于ATP再合成的底物,而必定是由兴奋/收缩偶联失败导致的,而疲劳与磷酸原耗尽密切相关,并无明显的乳酸酸中毒。