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Oxidants and skeletal muscle function: physiologic and pathophysiologic implications.

T L Clanton1, L Zuo, P Klawitter

  • 1Department of Internal Medicine, Pulmonary and Critical Medicine, Biophysics Program, The Ohio State Unviersity, Columbus 43210, USA. clanton.1@osu.edu

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
|December 22, 1999
PubMed
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Skeletal muscles produce reactive oxygen species during contraction, influencing muscle function. While normally physiological, excessive production can cause muscle injury under certain conditions.

Area of Science:

  • Muscle Physiology
  • Cellular Redox Biology

Background:

  • Skeletal muscles generate reactive oxygen species (ROS) during intense contractions.
  • The physiological role and pathological implications of ROS in muscle function are not fully understood.

Purpose of the Study:

  • To investigate the significance of ROS production in skeletal muscle physiology.
  • To determine if ROS contribute to normal muscle function or pathological states.

Main Methods:

  • Analysis of studies involving exogenous antioxidant treatments during muscle contraction.
  • Review of evidence linking muscle conditioning to antioxidant defense upregulation.
  • Examination of conditions associated with intense exercise that may increase ROS production.

Main Results:

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  • Exogenous antioxidants influence contractile function, suggesting ROS are involved in normal muscle physiology.
  • Redox tone appears to affect excitation-contraction coupling and metabolic enzymes.
  • Muscle conditioning enhances antioxidant defenses, indicating a link between ROS and contractile activity.

Conclusions:

  • Reactive oxygen species play a significant role in normal skeletal muscle physiology.
  • Imbalances in ROS production and antioxidant defenses can lead to oxidant stress and myocyte injury.
  • Conditions like ischemia-reperfusion, hypoxia, heat stress, and injury can cause ROS-mediated muscle dysfunction.