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1 Kinesiology, University of Waterloo, Waterloo, Canada
* To whom correspondence should be addressed. E-mail: green{at}healthy.uwaterloo.ca.
The hypothesis tested was that disturbances in the sarcoplasmic reticulum (SR) Ca2+-cycling responses to exercise would associate with muscle glycogen reserves. Ten untrained males (peak O2 consumption, VO2peak=3.41±0.20 L/min; mean±SE) performed a standardized cycle test (~70% VO2peak) on 2 occasions, namely, following 4 days of a high (Hi CHO) and 4 days of a low (Lo CHO) carbohydrate diet. Both Hi-CHO and Lo-CHO were preceded by a session of prolonged exercise designed to deplete muscle glycogen. SR Ca2+-cycling properties in crude homogenates prepared from vastus lateralis samples indicated higher (P<0.05) Ca2+-uptake (µM/g protein-1.min-1) in Hi CHO compared to Lo CHO at 30 min (2.93±0.10 vs 2.23±0.12) and at 67 min (2.77±0.16 vs 2.10±0.12) of exercise, the point of fatigue in Lo CHO. Similar effects (P<0.05) were noted between conditions for maximal Ca2+-ATPase (µM/g protein-1.min-1) at 30 min (142±8.5 vs 107±5.0) and at 67 min (130±4.5 vs 101±4.7). Both Phase One and Phase Two Ca2+-release were 23% and 37% higher (P<0.05) at 30 min of exercise and 15% and 34% higher (P<0.05), at 67 min during Hi CHO, compared to Lo CHO, respectively. No differences between conditions were observed at rest for any of these SR properties. Total muscle glycogen (mmol glucosyl units.kg dw) was higher (P<0.05) in Hi CHO compared to Lo CHO at rest (+36%), 30 min (+53%) and at 67 min (+44%) of cycling. These results indicate that exercise-induced reductions in SR Ca2+-cycling properties occur earlier in exercise during low glycogen states as compared to high glycogen states.
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