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Potassium and caffeine contractures of mouse muscles before and after fatiguing stimulation
Author(s) -
Pagala Murali,
Ravindran Kadirimangalam,
Amaladevi Bellamakonda,
Namba Tatsuji,
Grob David
Publication year - 1994
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880170804
Subject(s) - caffeine , contracture , muscle contracture , contractility , chemistry , soleus muscle , medicine , endocrinology , muscle fatigue , muscle contraction , membrane potential , anatomy , skeletal muscle , electromyography , biochemistry , surgery , physical medicine and rehabilitation
To assess the impairment of muscle membrane excitation, excitation–contraction (E–C) coupling, and contractility during muscle fatigue, we monitored the contracture responses of resting and fatigued muscles on exposure to high potassium and caffeine. On exposure to 140 mmol/L potassium, mouse extensor digitorum longus (EDL) developed a contracture which was 15.7% of tetanic tension before fatigue and 31.7% after fatigue, while soleus developed 59.4% contracture before and 68.8% after fatigue. Potassium causes contractures by depolarizing the muscle fiber membrane. Hence, membrane excitation is reduced in fatigued EDL and soleus. On exposure to 32 mmol/L caffeine, the contracture was 7.1% in resting EDL, 8.5% in fatigued EDL, 50.1% in resting soleus, and 43.7% in fatigued soleus. On exposure to 1 mmol/L caffeine followed by rapid cooling, the contracture was 3.0% in resting EDL, 3.2% in fatigued EDL, 21.5% in resting soleus, and 10.3% in fatigued soleus. Caffeine causes contracture by releasing Ca + + from the sarcoplasmic reticulum. Our results indicate reduced E–C coupling attributable to reduced membrane excitation in fatigued EDL, and reduced contractility in fatigued soleus. © 1994 John Wiley & Sons, Inc.