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Energy metabolism during fatigue in FDB muscle is impaired by the lack of K ATP channel activity
Author(s) -
Scott Kyle,
Renaud JeanMarc
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1058.2
Subject(s) - energy metabolism , muscle fatigue , metabolism , medicine , chemistry , endocrinology , biophysics , biology , physical medicine and rehabilitation , electromyography
The K ATP channel is crucial in preventing fiber damage during exercise and muscle fatigue. The channel is activated when energy levels fall and thus behaves as an energy sensor. Once activated, it directly reduces action potential amplitude lowering Ca 2+ release and force production in order to prevent damaging ATP depletion. So far, it remains unknown how the K ATP channel affects energy metabolism during muscle fatigue. The objective of this study was to determine whether K ATP channel deficient FDB muscle from Kir6.2 −/− mice have lower ATP levels and impaired ATP generation during fatigue compared to wild type FDB. The decreases in PCr was not different between W.T. and Kir6.2 −/− FDB while ATP levels were significantly lower in Kir6.2 −/− FDB. Glucose uptake was less and glycogen breakdown greater in Kir6.2 −/− FDB; but the amount of glucosyl units entering glycolysis was not different between the two muscle groups. Surprisingly, Kir6.2 −/− FDB produced less lactate and similar amount of 14 CO 2 when compared to wild type FDB, which suggests that the amount of unaccounted glucosyl units was greater in Kir6.2 −/− FDB; i.e., energy metabolism appeared impaired in FDB lacking K ATP channel activity.