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Elevations in rat soleus muscle [Ca2+] with passive stretch

R B Armstrong1, C Duan, M D Delp

  • 1Exercise Biochemistry Laboratory, University of Georgia, Athens 30602.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 1, 1993
PubMed
Summary
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Passive muscle stretch increases calcium levels in rat soleus muscles, leading to reduced force production. This suggests stretch-induced calcium influx contributes to muscle injury during eccentric exercise.

Area of Science:

  • Skeletal Muscle Physiology
  • Cellular Biology
  • Exercise Physiology

Background:

  • Eccentric contractions (e.g., downhill walking) cause muscular injury and elevated mitochondrial calcium (MCC).
  • Cell membrane stretch is known to induce calcium influx in various tissues, including skeletal muscle.

Purpose of the Study:

  • To investigate if passive stretch of rat soleus muscles increases total muscle calcium (TCC) and MCC.
  • To determine the relationship between passive stretch, calcium levels, and force production.

Main Methods:

  • Isolated rat soleus muscles were incubated in vitro at resting length (Lo) or maximal length (S).
  • Measurements included total muscle calcium (TCC), mitochondrial calcium (MCC), twitch tension, ATP, phosphocreatine, and lactate release.
  • Experiments were conducted in normal and calcium-free buffers, with and without verapamil.

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Main Results:

  • Passive stretch (S) significantly increased TCC (+62%) and MCC (+56%) compared to resting length (Lo).
  • Maximal twitch tension was reduced by 63% in stretched muscles.
  • Metabolic markers (ATP, phosphocreatine, lactate) remained unchanged, ruling out impaired metabolism.
  • Calcium influx was confirmed by lack of increase in calcium-free buffer.
  • Verapamil partially blocked calcium increases, but at high concentrations.

Conclusions:

  • Passive muscle stretch induces calcium influx into skeletal muscle cells.
  • Stretch-induced calcium overload may contribute to the force deficits observed after eccentric contractions.
  • The mechanism of calcium influx during stretch warrants further investigation, potentially involving stretch-activated channels.