Reduced reflex sensitivity persists several days after long-lasting stretch-shortening cycle exercise
Reduced reflex sensitivity persists several days after long-lasting stretch-shortening cycle exercise
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DOI：
10.1152/jappl.1999.86.4.1292
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发表时间：
1999-04-01
影响因子：
3.3
通讯作者：
Rama, D
中科院分区：
文献类型：
--
作者：
Avela, J;Kyröläinen, H;Rama, D
本研究探讨了长时间牵张缩短周期运动后牵张反射功能急性和迟发性继发性损害的相关机制。结果表明，疲劳后肌肉功能立即明显恶化，同时主动和被动反射灵敏度明显降低。对于主动和被动牵张反射，这种减少是双相的（P < 0.05至P < 0.001）。而电刺激诱发的最大Hoffmann反射与最大质量复合动作电位的比值仅在疲劳后即刻有一次显著降低（71.2%，P < 0.01）。肌肉的抗牵张力也有类似的显著性降低（P < 0.01）。肌肉损伤的间接标志物（血清肌酸激酶活性和骨骼肌钙蛋白I）明显增加，这可能意味着超微结构肌肉损伤的发生。这表明，反射敏感性的急性降低是反射的起源，由于两个积极的机制，障碍和突触前抑制。然而，延迟的第二次下降的敏感性的一些反射参数可能是由于继发性损伤，因为一些炎症反应的肌肉损伤。这可能强调了通过第III和IV组肌肉传入的突触前抑制的作用。
The mechanisms related to the acute and delayed secondary impairment of the stretch reflex function were investigated after long-lasting stretch-shortening cycle exercise. The results demonstrated a clear deterioration in muscle function immediately after fatigue, which was accompanied by a clear reduction in active and passive reflex sensitivity. For active and passive stretch reflexes, this reduction was biphasic (P < 0.05 to P < 0.001). However, for the ratio of the electrically induced maximal Hoffmann reflex to the maximal mass compound action potential, only one significant reduction was seen immediately after fatigue (71.2%, P < 0.01). A similar significant (P < 0.01) decrease in the stretch-resisting force of the muscle was also detected. Clear increases were found in the indirect markers of muscle damage (serum creatine kinese activity and skeletal troponin I), which could imply the occurrence of ultrastructural muscle damage. It is suggested that the acute reduction in reflex sensitivity is of reflex origin and due to two active mechanisms, disfacilitation and presynaptic inhibition. However, the delayed second decline in the sensitivity of some reflex parameters may be attributable to the secondary injury, because of some inflammatory response to the muscle damage. This might emphasize the role of presynaptic inhibition via group III and IV muscle afferents.