{'fraction_non_alphanumeric': 0.024603608529250958, 'fraction_numerical': 0.01366867140513942, 'mean_word_length': 5.398601398601398, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Fatigue pre‐conditioning increases fatigue resistance and protects muscle against the deleterious effects of no KATP channel activity

The objective of this study was to determine how one fatigue bout at 37°C after the kinetics of subsequent fatigue bout in CD‐1 mouse flexor digitorum brevis (FDB). All fatigue bouts were elicited with one tetanic contraction every sec for 3 min. The first fatigue bouts (FAT1) were all elicited under control conditions while the second fatigue bouts (FAT2) were elicited 60 min after FAT1 either under control conditions or in the presence of 10 μM glibenclamide, a KATP channel blocker. Another group of FDBs were fatigued only once but at the same time as FAT2, defined as delayed FAT1 (delFAT1), also under control conditions or in the presence of glibenclamide. Under both control and glibenclamide conditions, the rate of fatigue, measured from the decrease in tetanic intracellular Ca2+ ([Ca2+]i) and tetanic force, was significantly slower during FAT2 than during delFAT1; i.e., fatigue resistance increased after one fatigue bout. The presence of glibenclamide during delFAT1 resulted in several contractile dysfunctions including large increases in resting [Ca2+]i and resting tension, supercontracted single muscle fibers and diminished force recovery. During FAT2, none of these contractile dysfunctions was observed in the presence of glibenclamide. Furthermore, while during delFAT1 the rate of fatigue was faster in the presence than in the absence of glibenclamide, during FAT2 the rate of fatigue was the same for control and glibenclamide conditions. It is concluded that following one fatigue bout at 37°C fatigue resistance increases and the dependency on KATP channel to prevent contractile dysfunctions decreases. We define this new phenomenon as fatigue preconditioning.