Effects of reduced muscle glycogen concentration on force, Ca2+ release and contractile protein function in intact mouse skeletal muscle

E R Chin, D G Allen
Journal of Physiology 1997 January 1, 498 ( Pt 1): 17-29
1. The purpose of this study was to examine the effects of reduced glycogen concentration on force, Ca2+ release and myofibrillar protein function during fatigue in skeletal muscle. Force and intracellular free Ca2+ concentration ([Ca2+]i) were measured in single mammalian skeletal muscle fibres during fatigue and recovery. Glycogen was measured in bundles of 20-40 fibres from the same muscle under the same conditions. 2. Fatigue was induced by repeated maximum tetani until force was reduced to 30% of initial. This was associated with a reduction in muscle glycogen to 27 +/- 6% of control values. In fibres allowed to recover for 60 min in the presence of 5.5 mM glucose (n = 6), tetanic (100 Hz) force recovered fully but tetanic [Ca2+]i remained at 82 +/- 8% of initial values. This prolonged depression in Ca2+ release was not associated with decreased muscle glycogen since glycogen had recovered to pre-fatigue levels (157 +/- 42%). 3. To examine the responses under conditions of reduced muscle glycogen concentration, fibres recovered from fatigue for 60 min in the absence of glucose (n = 6). After glucose-free recovery, the decreases in tetanic force and [Ca2+]i were only partially reversed (to 64 +/- 8% and 57 +/- 7% of initial values, respectively). These alterations were associated with a sustained reduction in muscle glycogen concentration (27 +/- 4% of initial values). 4. In another set of fibres, fatigue was followed by 50 Hz intermittent stimulation for 22.6 +/- 4 min. With this protocol, tetanic force and [Ca2+]i partially recovered to 76 +/- 9% and 55 +/- 6% of initial levels, respectively. These changes were associated with a recovery of muscle glycogen (to 85 +/- 10%). 5. During fatigue, Ca2+ sensitivity and maximum Ca(2+)-activated force (Fmax) were depressed but these alterations were fully reversed when muscle glycogen recovered. When glycogen did not recover, Ca2+ sensitivity remained depressed but Fmax partially recovered. The altered myofibrillar protein function is probably due to alterations in inorganic phosphate levels or other metabolites associated with reduced levels of muscle glycogen. 6. These data indicate that the reductions in force, Ca2+ release and contractile protein inhibition observed during fatigue are closely associated with reduced muscle glycogen concentration. These findings also suggest that the changes in Ca2+ release associated with fatigue and recovery have two components-one which is glycogen dependent and another which is independent of glycogen but depends on previous activity.

Full Text Links

Find Full Text Links for this Article


You are not logged in. Sign Up or Log In to join the discussion.

Trending Papers

Remove bar
Read by QxMD icon Read

Save your favorite articles in one place with a free QxMD account.


Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"