PGC-1alpha is required for training-induced prevention of age-associated decline in mitochondrial enzymes in mouse skeletal muscle
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PGC-1alpha is required for training-induced prevention of age-associated decline in mitochondrial enzymes in mouse skeletal muscle. / Leick, Lotte; Lyngby, Stine Secher; Wojtaszewski, Jørgen; Wojtasewski, Jørgen F P; Pilegaard, Henriette.
In: Experimental Gerontology, Vol. 45, No. 5, 2010, p. 336-342.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - PGC-1alpha is required for training-induced prevention of age-associated decline in mitochondrial enzymes in mouse skeletal muscle
AU - Leick, Lotte
AU - Lyngby, Stine Secher
AU - Wojtaszewski, Jørgen
AU - Wojtasewski, Jørgen F P
AU - Pilegaard, Henriette
N1 - CURIS 2010 5200 141
PY - 2010
Y1 - 2010
N2 - The aim of the present study was to test the hypothesis that exercise training prevents an age-associated decline in skeletal muscle mitochondrial enzymes through a PGC-1alpha dependent mechanism. Whole body PGC-1alpha knock-out (KO) and littermate wildtype (WT) mice were submitted to long term running wheel exercise training or a sedentary lifestyle from 2 to 13 month of age. Furthermore, a group of approximately 4-month-old mice was used as young untrained controls. There was in both genotypes an age-associated approximately 30% decrease in citrate synthase (CS) activity and superoxide dismutase (SOD)2 protein content in 13-month-old untrained mice compared with young untrained mice. However, training prevented the age-associated decrease in CS activity and SOD2 protein content only in WT mice, but long term exercise training did increase HKII protein content in both genotypes. In addition, while CS activity and protein expression of cytc and SOD2 were 50-150% lower in skeletal muscle of PGC-1alpha mice than WT mice, the expression of the pro-apoptotic protein Bax and the anti-apoptotic Bcl2 was approximately 30% elevated in PGC-1alpha KO mice. In conclusion, the present findings indicate that PGC-1alpha is required for training-induced prevention of an age-associated decline in CS activity and SOD2 protein expression in skeletal muscle.
AB - The aim of the present study was to test the hypothesis that exercise training prevents an age-associated decline in skeletal muscle mitochondrial enzymes through a PGC-1alpha dependent mechanism. Whole body PGC-1alpha knock-out (KO) and littermate wildtype (WT) mice were submitted to long term running wheel exercise training or a sedentary lifestyle from 2 to 13 month of age. Furthermore, a group of approximately 4-month-old mice was used as young untrained controls. There was in both genotypes an age-associated approximately 30% decrease in citrate synthase (CS) activity and superoxide dismutase (SOD)2 protein content in 13-month-old untrained mice compared with young untrained mice. However, training prevented the age-associated decrease in CS activity and SOD2 protein content only in WT mice, but long term exercise training did increase HKII protein content in both genotypes. In addition, while CS activity and protein expression of cytc and SOD2 were 50-150% lower in skeletal muscle of PGC-1alpha mice than WT mice, the expression of the pro-apoptotic protein Bax and the anti-apoptotic Bcl2 was approximately 30% elevated in PGC-1alpha KO mice. In conclusion, the present findings indicate that PGC-1alpha is required for training-induced prevention of an age-associated decline in CS activity and SOD2 protein expression in skeletal muscle.
KW - 3-Hydroxyacyl CoA Dehydrogenases
KW - Aging
KW - Animals
KW - Citrate (si)-Synthase
KW - Cytochromes c
KW - Female
KW - Glucose Transporter Type 4
KW - Hexokinase
KW - Mice
KW - Mitochondria, Muscle
KW - Muscle, Skeletal
KW - Physical Conditioning, Animal
KW - Superoxide Dismutase
KW - Trans-Activators
KW - bcl-2-Associated X Protein
U2 - 10.1016/j.exger.2010.01.011
DO - 10.1016/j.exger.2010.01.011
M3 - Journal article
C2 - 20085804
VL - 45
SP - 336
EP - 342
JO - Experimental Gerontology
JF - Experimental Gerontology
SN - 0531-5565
IS - 5
ER -
ID: 33717124