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   <subfield code="a">Intracellular calcium during fatigue of cane toad skeletal muscle in the absence of glucose</subfield>
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   <subfield code="a">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 &lt;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.</subfield>
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