Date of Graduation


Document Type


Degree Type



College of Physical Activity and Sport Sciences


Sport and Exercise Psychology

Committee Chair

Stephen E Alway


Apoptosis has been implicated in mediating the process of muscle loss during muscle disuse and with aging. However, the physiologic role of apoptosis in muscle remodeling is largely unknown. The purposes of this dissertation were to examine the role of apoptosis in different muscle remodeling conditions including muscle denervation, hindlimb suspension, muscle unloading following overload, endurance treadmill training, and muscle overload in mice, rats, or quails. Apoptotic signaling components and cellular stress markers including Bax, Bcl-2, Apaf-1, cytochrome c, caspases, Smac/DIABLO, XIAP, ARC, FLIP, AIF, p53, Id2, p21, c-Myc, PARP, HSP70, HSP27, HSP60, MnSOD, CuZnSOD, catalase, H2O2, MDA/4-HAE, nitrotyrosine or 8-OHdG were assessed. The incidence of apoptosis, activation of the pro-apoptotic signaling, and elevation of oxidative stress were generally evident in the skeletal muscles following denervation, hindlimb suspension, and unloading following overload in mice, rats, or quails. Moreover, p53 and Id2 were responsive to muscle unloading or overload in a subcellular compartmentalized manner. Furthermore, anti-apoptotic alterations were found in the muscles following endurance training or muscle overloading. These findings are consistent with the hypotheses that apoptosis has a role in regulating muscle loss and exercise training is able to alter the apoptotic signaling in skeletal muscle.