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Dihydropyridine effects on skeletal muscle fatigue

J H Williams1, C W Ward

  • 1Division of Health and Physical Education, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg 24061-0326.

Journal De Physiologie
|January 1, 1991
PubMed

Insights

Altering calcium (Ca2+) influx with dihydropyridine derivatives significantly increased skeletal muscle fatigue in frog sartorius muscles, suggesting a role for sarcolemmal Ca2+ exchange in muscle fatigue.

Area of Science:

  • Physiology
  • Muscle Physiology
  • Calcium Signaling

Background:

  • Skeletal muscle fatigue is a complex physiological process.
  • Extracellular calcium influx is crucial for muscle contraction.
  • Dihydropyridine derivatives are known modulators of calcium channels.

Purpose of the Study:

  • To investigate the effect of altered extracellular calcium (Ca2+) influx on skeletal muscle fatigue.
  • To determine if dihydropyridine derivatives (Bay K 8644, nifedipine) influence muscle fatigue rates and magnitudes.

Main Methods:

  • Frog sartorius muscles underwent tetanic contractions (80 Hz, 100 msec) every second for 3 minutes.
  • Muscles were fatigued in normal Ringer's solution (NR), or NR with nifedipine, Bay K 8644, or low Ca2+.
  • Fatigue rate constants and end-stimulation tetanic forces were measured.

Main Results:

  • Bay K 8644, nifedipine, and low Ca2+ conditions significantly increased the rate and magnitude of skeletal muscle fatigue compared to NR.
  • Fatigue rate constants were significantly greater under experimental conditions (p < .05).
  • Tetanic forces at the end of stimulation were significantly reduced under experimental conditions (p < .05).

Conclusions:

  • Alterations in sarcolemmal calcium (Ca2+) exchange influence the process of skeletal muscle fatigue.
  • Dihydropyridine derivatives and modified extracellular calcium levels can exacerbate muscle fatigue.

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