title: Intracellular calcium during fatigue of cane toad skeletal muscle in the absence of glucose.
abstract: Mechanisms of fatigue were studied in single muscle fibres of the cane toad (Bufo marinus) in which force, intracellular calcium ([Ca2+]i), [Mg2+]i, glycogen and the rapidly releasable Ca2+ from the sarcoplasmic reticulum (SR) were measured. Fatigue was produced by repeated tetani continued until force had fallen to 50%. Two patterns of fatigue in the absence of glucose were studied. In the first fatigue run force fell to 50% in 8-10 min. Fatigue runs were then repeated until force fell to 50% in < 3 min in the final fatigue run. Addition of extracellular glucose after the final fatigue run prolonged a subsequent fatigue run. In the first fatigue run peak tetanic [Ca2+]i initially increased and then declined and at the time when force had fallen to 50% tetanic [Ca2+]i was 54+/-5% of initial value. In the final fatigue run force and peak tetanic [Ca2+]i declined more rapidly but to the same level as in first fatigue runs. At the end of the first fatigue run, the rapidly releasable SR Ca2+ store fell to 46+/-6% of the pre-fatigue value. At the end of the final fatigue run the rapidly releasable SR Ca2+ store was 109+/-16% of the pre-fatigue value. In unstimulated fibres the nonwashable glycogen content was 176+/-30 mmol glycosyl units/l fibre. After one fatigue run the glycogen content was 117+/-17 mmol glycosyl units/l fibre; at the end of the final fatigue run the glycogen content was reduced to 85+/-9 mmol glycosyl units/l fibre. [Mg2+]i did not change significantly at the end of fatigue in either the first or the final fatigue run suggesting that globally-averaged ATP does not decline substantially in either pattern of fatigue. These results suggest that different mechanisms are involved in the decline of tetanic [Ca2+]i in first compared to final fatigue runs. The SR Ca2+ store is reduced in first fatigue runs; this is not the case for the final fatigue run which is associated with a decline in glycogen and possibly related to either a non-metabolic effect of glycogen or a spatially-localised metabolic decline.
authors: Department of Phyisiology and Institute of Biomedical Science University of Sydney, Australia.
authors: A A
authors: AA
authors: Kabbara
authors: L T
authors: LT
authors: Nguyen
authors: G M
authors: GM
authors: Stephenson
authors: D G
authors: DG
authors: Allen
mesh_terms: D000818:Animals; D002024:Bufo marinus; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D004558:Electric Stimulation / Q000009:adverse effects; D005947:Glucose / Q000172:deficiency* / Q000494:pharmacology; D006003:Glycogen / Q000378:metabolism; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018763:Muscle Fatigue / Q000187:drug effects / Q000502:physiology*; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure
chemical_list: D006003:Glycogen; D008274:Magnesium; D005947:Glucose; D002118:Calcium