Muscle & nerve · 2012
Oxidative capacity and fatigability in run-trained malignant hyperthermia-susceptible mice.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Rouviere Clement, Corona Benjamin T, Ingalls Christopher P
Аннотация
INTRODUCTION: The purpose of this study was to test the hypothesis that malignant hyperthermia model mice (RyR1Y522S/wt) are more vulnerable to exercise-induced muscle injury and fatigability and adapt less to run training.
METHODS: After 6 weeks of voluntary wheel running, we measured anterior crural muscle fatigability, muscle injury, and cytochrome oxidase (COX) and citrate synthase (CS).
RESULTS: Although RyR1Y522S/wt mice ran without undergoing MH episodes, they ran 42% less distance than wild-type (WT) mice. Muscles from WT mice exhibited increased fatigue resistance and COX content after training. Muscles from RyR1Y522S/wt mice demonstrated no significant change in fatigability or COX and CS after training. However, muscles from RyR1Y522S/wt mice displayed less intrinsic fatigability and greater COX/CS content and muscle damage than WT mice.
CONCLUSIONS: RyR1Y522S/wt mice can run without having rhabdomyolysis, and their inability to adapt to training appears to stem from intrinsic enhancement of mitochondrial enzymes and fatigue resistance.
METHODS: After 6 weeks of voluntary wheel running, we measured anterior crural muscle fatigability, muscle injury, and cytochrome oxidase (COX) and citrate synthase (CS).
RESULTS: Although RyR1Y522S/wt mice ran without undergoing MH episodes, they ran 42% less distance than wild-type (WT) mice. Muscles from WT mice exhibited increased fatigue resistance and COX content after training. Muscles from RyR1Y522S/wt mice demonstrated no significant change in fatigability or COX and CS after training. However, muscles from RyR1Y522S/wt mice displayed less intrinsic fatigability and greater COX/CS content and muscle damage than WT mice.
CONCLUSIONS: RyR1Y522S/wt mice can run without having rhabdomyolysis, and their inability to adapt to training appears to stem from intrinsic enhancement of mitochondrial enzymes and fatigue resistance.
Предметные рубрики MeSH
AerobiosisAnimalsBlotting, WesternCitrate (si)-SynthaseDisease SusceptibilityElectron Transport Complex IVFemaleHypertension, MalignantIsometric ContractionMaleMiceMice, Inbred C57BLMitochondria, MuscleMuscle FatigueMuscle Fibers, SkeletalMuscle StrengthMuscle, SkeletalMyosin Heavy ChainsOrgan SizeOxidation-ReductionPhysical Conditioning, AnimalPhysical EndurancePolymerase Chain ReactionRunningRyanodine Receptor Calcium Release Channel