Salminen A, Vihko V
Eur J Appl Physiol Occup Physiol. 1981;47(1):57-64. doi: 10.1007/BF00422483.
Acid hydrolase activities in skeletal and cardiac muscle were studied 5, 10 and 20 days after exhaustive intermittent running by untrained and endurance-trained mice. Exhaustion increased the activities of cathepsin D, beta-glucuronidase and ribonuclease, but not that of p-nitrophenylphosphatase in skeletal muscle of untrained mice. Activities were highest on the fifth day after exhaustion and decreased during the following two weeks. More intensive loading produced no changes in acid hydrolytic capacity in skeletal muscle of endurance-trained mice. Acid hydrolase activities in cardiac muscle of both untrained and trained mice were unaffected by exhaustive running. It is suggested that exhaustive running causes both lethal and sublethal hypoxic fiber injuries in the skeletal muscle of untrained mice but not in that of endurance-trained mice or in the cardiac muscle of animals of either group. These injuries manifest themselves as fiber necrosis (lethal) and as increased acid hydrolytic capacity in surviving fibers (sublethal).
对未经训练和经过耐力训练的小鼠进行力竭性间歇跑步后5天、10天和20天,研究其骨骼肌和心肌中的酸性水解酶活性。力竭增加了未经训练小鼠骨骼肌中组织蛋白酶D、β - 葡萄糖醛酸酶和核糖核酸酶的活性,但对对硝基苯磷酸酶的活性没有影响。力竭后第5天活性最高,随后两周内下降。更剧烈的负荷对经过耐力训练小鼠的骨骼肌酸性水解能力没有影响。未经训练和经过训练的小鼠心肌中的酸性水解酶活性均不受力竭性跑步的影响。提示力竭性跑步在未经训练小鼠的骨骼肌中会导致致死性和亚致死性缺氧性纤维损伤,但在经过耐力训练小鼠的骨骼肌或两组动物的心肌中则不会。这些损伤表现为纤维坏死(致死性)和存活纤维中酸性水解能力增加(亚致死性)。