Age-related apoptotic responses to stretch-induced hypertrophy in quail slow-tonic skeletal muscle.
In the present study, we examined the responses of apoptosis and apoptotic regulatory factors to muscle hypertrophy induced by stretch overload in quail slow-tonic muscles. The wings from one side of young and aged Japanese quails were loaded by attaching a tube weight corresponding to 12% of the bird's body weight for 7 or 21 days. Muscle from the contralateral side served as the intraanimal control. Relative to the intraanimal contralateral control side, the muscle wet weight increased by 96% in young birds, whereas the muscle weight gain in aged birds was not significant after 7 days of loading. After 21 days of loading, muscle weight significantly increased by 179% and 102% in young and aged birds, respectively. Heat shock protein (HSP)72 and HSP27 protein contents in the loaded sides were higher than on the control sides exclusively in young birds after 7 days of loading. Compared with the contralateral control muscle, the extent of apoptotic DNA fragmentation and the total cytosolic apoptosis-inducing factor protein content were reduced in all loaded muscles except for the 7-day-loaded muscles from the aged birds. Bax protein content was diminished in the loaded muscle relative to the control side from all groups, whereas Bcl-2 protein content was reduced in the young and aged muscles after 21 days of loading. The total cytosolic cytochrome c protein content was decreased and the X chromosome-linked inhibitor of apoptosis protein content was elevated in 7- and 21-day-loaded muscles relative to the intraanimal control muscle from young birds. Furthermore, after 7 days of loading the muscles of aged birds, H(2)O(2) content and the total cytosolic protein content of second mitochondrial activator of caspases/direct inhibitor of apoptosis-binding protein with low isoelectric point were elevated compared with the intraanimal control side. These data suggest that stretch overload-induced muscle hypertrophy is associated with changes in apoptosis in slow-tonic skeletal muscle. Moreover, discrepant apoptotic responses to muscle overload in young and aged muscles may account in part for the age-related decline in the capability for muscle hypertrophy.
Division of Exercise Physiology, School of Medicine, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26506-9227, USA.
Parco M
PM
Siu
Stephen E
SE
Alway
D000375:Aging; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D051033:Apoptosis Inducing Factor; D003370:Coturnix; D045304:Cytochromes c / Q000502:physiology; D053938:DNA Fragmentation / Q000502:physiology; D005420:Flavoproteins / Q000502:physiology; D006360:Heat-Shock Proteins / Q000502:physiology; D006861:Hydrogen Peroxide / Q000378:metabolism; D006984:Hypertrophy; D008565:Membrane Proteins / Q000502:physiology; D018657:Muscle Fibers, Slow-Twitch / Q000502:physiology*; D009124:Muscle Proteins / Q000502:physiology; D018482:Muscle, Skeletal / Q000502:physiology*; D011506:Proteins / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D051636:X-Linked Inhibitor of Apoptosis Protein; D051028:bcl-2-Associated X Protein
D051033:Apoptosis Inducing Factor; D005420:Flavoproteins; D006360:Heat-Shock Proteins; D008565:Membrane Proteins; D009124:Muscle Proteins; D011506:Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051636:X-Linked Inhibitor of Apoptosis Protein; D051028:bcl-2-Associated X Protein; D045304:Cytochromes c; D006861:Hydrogen Peroxide; D013482:Superoxide Dismutase