Endurance exercise increases the protein levels of PGC-1α and respiratory chain complexes in mouse skeletal muscle during atorvastatin administration.
Kunihiko AnamiYutaka OzakiKenichi ItoMasahiro SakitaSatsuki UneJunichi AkiyamaPublished in: The journal of physiological sciences : JPS (2018)
Statins and exercise reduce cardiovascular disease incidence. We investigated whether endurance exercise in mice induces mitochondrial adaptation in skeletal muscle and muscle injury during administration of atorvastatin, a member of the statin medication class. Male C57BL mice were assigned to one of three groups: control (Con), statin (Statin), or statin and exercise (Statin + Ex). Atorvastatin was administered, and exercise performed on a treadmill for 8 weeks. The levels of mitochondria-associated proteins, PGC-1α, and respiratory chain complex, (COX) I-V, in the quadriceps femoris, and serum creatine kinase, a muscle injury marker, were measured. PGC-1α and COX I-V were upregulated in the Statin + Ex group compared to those in the Statin and Con groups; serum creatine kinase levels were similar. Endurance training in mice induced mitochondrial adaptation in skeletal muscle without causing muscle injury, during atorvastatin administration.
Keyphrases
- skeletal muscle
- cardiovascular disease
- high intensity
- insulin resistance
- coronary artery disease
- resistance training
- high fat diet induced
- physical activity
- low density lipoprotein
- oxidative stress
- healthcare
- risk factors
- cell death
- body composition
- high glucose
- high resolution
- protein kinase
- protein protein
- endothelial cells
- drug induced