摘要
While delayed structural alterations of muscles(DSAM) induced by strenuous exercises have always been one of the commoest findings in sports-related muscle injuries, its pathogenesis remains unidentified. And although acupuncture at Ashi points has proved its efficacy in halting the progress of DASM and speeding up its recovery, we know very little about the underlying mechanism. This paper presents our work on these problems by using amphibian DSAM models created by electrostimulation, and such research tools as electromicroscopy, enzymology, the fluores cence indicator, Fura 2, and electron probe microanalysis (EPMA). Our results indicate:1) As revealed by EPMA, cytoplasmic Ca continued to rbe,reaching 3.07 and 5. 33 mmol/kg dry wt. 3 and 6hrs afterelectrostimlation respectively. Analysis of regions with variousstructural alterations showed rise of Ca concentration inparallel with severity of myofibrillar injury. Testing with Fura 2also demonstrated obvious increase of free Ca++ in cytoplasm 3 hrs after electrostimulation. All these showed a positive correlation between DSAM and the increase of intracellular Ca++.2) Further study to explore the possible mechanisms underlying the increase of cytoplasmic Ca++ revealed two sources. During the initial rise of cytoplasmic Ca, a decline of sarcoplasmic reticulum Ca content was found, suggesting the contribution of sarcoplasmic reticulum Ca. However, no further decline was noted despite continued rise of cytoplasmic Ca, which, then, could only be accounted for by extracellular contribution.3) In skeletal muscles after long-term exhaustive stimulation and in those with delayed structural alterations,the inereased cytoplasmic Ca was quickly lowered by acupuncture, down to lpretest level 10 minutes after acupuncture. Meanwhile,no marked change in sarcoplasmic reticulum Ca content and in enzymic activity of Ca, Mg-ATPase was found, indicating no contribution on their part to the quick lowering of cytoplasmic Ca. But a rapid rise of cytoplasmic Na was found. And addition of Na-Ca exchange blocker, quinidine, or removal of Ca++ in Ringer’s solution greatly inhibited the Ca -lowering effect of acupuncture. Both these evidences support the view that Na -Ca exchange played the main role in restoring normal cytoplasmic Ca.4) As revealed by EPMA, along with the reduction of cytoplasmic Ca, structural alterations in muscles stimulated to exhaustion were reduced; and, in muscles with delayed structural injuries, Zband changes were markedly reduced, the contraction bands disappeared, and the recovery of disordered myofilament was quickened. The Ca-lowering effect of acupuncture is thus shown to be one of the important mechanisms underlying the alleviation of muscle structural injuries and the accelerated recovery of abnormal structures.
While delayed structural alterations of muscles(DSAM) induced by strenuous exercises have always been one of the commoest findings in sports-related muscle injuries, its pathogenesis remains unidentified. And although acupuncture at Ashi points has proved its efficacy in halting the progress of DASM and speeding up its recovery, we know very little about the underlying mechanism. This paper presents our work on these problems by using amphibian DSAM models created by electrostimulation, and such research tools as electromicroscopy, enzymology, the fluores cence indicator, Fura 2, and electron probe microanalysis (EPMA). Our results indicate:1) As revealed by EPMA, cytoplasmic Ca continued to rbe,reaching 3.07 and 5. 33 mmol/kg dry wt. 3 and 6hrs afterelectrostimlation respectively. Analysis of regions with variousstructural alterations showed rise of Ca concentration inparallel with severity of myofibrillar injury. Testing with Fura 2also demonstrated obvious increase of free Ca++ in cytoplasm 3 hrs after electrostimulation. All these showed a positive correlation between DSAM and the increase of intracellular Ca++.2) Further study to explore the possible mechanisms underlying the increase of cytoplasmic Ca++ revealed two sources. During the initial rise of cytoplasmic Ca, a decline of sarcoplasmic reticulum Ca content was found, suggesting the contribution of sarcoplasmic reticulum Ca. However, no further decline was noted despite continued rise of cytoplasmic Ca, which, then, could only be accounted for by extracellular contribution.3) In skeletal muscles after long-term exhaustive stimulation and in those with delayed structural alterations,the inereased cytoplasmic Ca was quickly lowered by acupuncture, down to lpretest level 10 minutes after acupuncture. Meanwhile,no marked change in sarcoplasmic reticulum Ca content and in enzymic activity of Ca, Mg-ATPase was found, indicating no contribution on their part to the quick lowering of cytoplasmic Ca. But a rapid rise of cytoplasmic Na was found. And addition of Na-Ca exchange blocker, quinidine, or removal of Ca++ in Ringer's solution greatly inhibited the Ca -lowering effect of acupuncture. Both these evidences support the view that Na -Ca exchange played the main role in restoring normal cytoplasmic Ca.4) As revealed by EPMA, along with the reduction of cytoplasmic Ca, structural alterations in muscles stimulated to exhaustion were reduced; and, in muscles with delayed structural injuries, Zband changes were markedly reduced, the contraction bands disappeared, and the recovery of disordered myofilament was quickened. The Ca-lowering effect of acupuncture is thus shown to be one of the important mechanisms underlying the alleviation of muscle structural injuries and the accelerated recovery of abnormal structures.
出处
《北京体育大学学报》
CSSCI
1995年第S2期35-42,共8页
Journal of Beijing Sport University
