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Articles in PresS, published online ahead of print January 16, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00490.2001
Submitted on October 12, 2001
Accepted on January 10, 2002
1 Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
* To whom correspondence should be addressed. E-mail: abram.katz{at}fyfa.ki.se.
The effects of glucose on muscle contractile function, free myoplasmic [Ca2+] ([Ca2+]i) and glycogen . Extensor digitorum longus muscles were stimulated to contract to fatigue and allowed to recover for 2 h in the absence or presence of 5.5 or 11 mM extracellular glucose. This was followed by a second fatigue run, which ended when the absolute force was the same as at the end of the first run. During the first fatigue run, the fluorescence ratio for indo-1 increased (reflecting an increase in [Ca2+]i)during the initial tetani, peaking at ~115% of the first tetanic value, followed by a continuous decrease to ~90% at fatigue. During the first fatigue run myofibrillar Ca2+-sensitivity was significantly decreased. During the second run, the number of tetani was 57±6% of initial in muscles that recovered in the absence of glucose, and 110±6% and 119±2% of initial in muscles that recovered in 5.5 and 11 mM glucose, respectively. Fluorescence ratios during the first, peak and last tetani did not differ significantly between the first and second fatigue runs during any of the three conditions. Glycogen decreased by almost 50% during the first fatigue run, and did not change further after recovery in the absence of glucose. After recovery in the presence of 5.5 and 11 mM glucose, glycogen increased 32 and 42% above the non-stimulated control value (P<0.01). These data demonstrate that extracellular glucose delays the decrease of tetanic force and [Ca2+]i during fatiguing stimulation and that glycogen supercompensation following contraction can occur in the absence of insulin.
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