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. Author manuscript; available in PMC: 2015 Aug 22.
Published in final edited form as: Curr Top Dev Biol. 2011;96:231–271. doi: 10.1016/B978-0-12-385940-2.00009-7

Table 9.2.

Skeletal muscle abnormalities in circadian mutants

Mutation Circadian phenotype Skeletal muscle pathology Reference
Bmal1−/− Arrhythmic behavior and expression of clock genes in both SCN and peripheral tissues Sarcopenia age-associated decrease in muscle fiber number and fiber diameter
Reduced lifespan
Kondratov et al. (2006)
Muscle-rescued
Bmal1−/−
Arrhythmic wheel running behavior Normal body weight
Normal activity levels
Improved longevity
McDearmon et al. (2006)
Bmal1−/−
ClockΔ19
Arrhythmic wheel running behavior Decreased maximal force production
Myofilament disarrangement
Mitochondrial pathology
Andrews et al. (2010)
ClockΔ19 + Mel Liver and skeletal muscle-specific arrhythmic expression of clock genes Decreased GLUT4 expression
Possible skeletal muscle insulin resistance
Kennaway et al. (2007)
Per2−/− Short circadian period (tau = 22 h)
Arrhythmic in constant darkness
Reduced forced locomotor performance without alteration in skeletal muscle contractile function Bae et al. (2006)
RORb−/− Slightly longer circadian period, (tau = 24.3 h) Muscle weakness when young, gain strength with age
“Duck Like” gait
Locomotor difficulties
Andre et al. (1998)