Premium
Fatigue preconditioning increases fatigue resistance in mouse FDB using a different intracellular signalling pathway to ischemic preconditioning.
Author(s) -
Boudreault Louise,
Cifelli Carlo,
Bourassa Francois,
Renaud JeanMarc
Publication year - 2009
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.23.1_supplement.599.1
Subject(s) - intracellular , medicine , ischemic preconditioning , endocrinology , glibenclamide , muscle fatigue , chemistry , cardiology , pharmacology , ischemia , physical medicine and rehabilitation , biochemistry , electromyography , diabetes mellitus
The objective of this study was to determine the nature of the intracellular signalling pathway that regulates fatigue preconditioning (FPC) whereby one fatigue bout (FAT1) acutely increases the fatigue resistance of muscle during a second fatigue bout (FAT2). All fatigue bouts were elicited with one tetanic contraction every s for 3 min and FAT2 was elicited 60 min after FAT1. The decreases in peak tetanic Ca 2+ i and force were significantly slower while the increases in unstimulated Ca 2+ i and force were significantly less during FAT2 than during FAT1. The differences between FAT2 and FAT1 were even greater when KATP channels were blocked with 10 µM glibenclamide. Ischemic preconditioning (IPC) is a phenomenon in which short, non‐ damaging ischemic periods increase muscle resistance to the damaging effects of a long and damaging ischemic period. While adenosine, sarcolemmal and mitochondrial KATP channels, protein kinase C and reactive oxygen species have all been implicated in IPC, the addition of their specific blockers during FAT1 did not prevent the increased fatigue resistance during FAT2. We therefore conclude that IPC and FPC have different intracellular signalling pathways.