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Dihydropyridine effects on skeletal muscle fatigue
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
Summary
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.