摘要
用电镜和免疫电镜观察超过习惯负荷后人骨骼肌收缩结构和收缩蛋白定位延迟性变化的结果提示：超过习惯负荷后延迟发生的骨骼肌收缩蛋白的降解优势导致收缩结构的改变或解体。这种收缩结构的改变构成了后继负荷工作的背景，如后继负荷能促进收缩蛋白的合成则可促进收缩结构的恢复和增强；如后继负荷导致收缩蛋白降解优势的积累和稳定，则将引起收缩结构变化的积累和稳定而导致骨骼肌的慢性或急性损伤。这种变化的一过性和两向发展的可能性提示：在未形成稳定的变化之前，其变化性质是生理的或是生理—病理双向变化的过渡的性质。
Alterations of contractile structure resulted from predominant degradation of contractile protien after excessive work load constitute the background of the succeeding load. In the event of the optimal arrangement,the contractile structue can be resumed and strengthened. But,if the succeeding load results in the accumulation and stabilization of alterations of the contractile structure,the chronic injuries of muscles wiil happen or predispose to acute injuies in case of sudden violent stress. Since the changes of contractile protiens and structures after excessive load are reversible and transient, no permanant pathological changes are formed,these changes may regarded as being physiological or at most on the transitional zone between physiological and pathological ranges. It is thus clear that rational scheduling of work loads is crucial to the prevention of injuries of skeletal muscles.
出处
《北京体育大学学报》
CSSCI
1994年第2期23-29,共7页
Journal of Beijing Sport University
基金
国家自然科学基金
关键词
骨骼肌损伤
收缩结构
肌损伤
病理
injuries of skeletal muscles, degradation of contractile protein, change of contractile structure
