One direction of this research will be to study androgen regulation of muscle development. The proposed studies will investigate in detail the time course of androgen responses in normal, castrated, and hypophysectomized animals undergoing skeletal and cardiac muscle growth. A second objective is to determine which androgenic hormone (testosterone or 5Alpha-dihydrotestosterone) is primarily responsible for muscle growth. A third objective is to examine the androgen response to glucocorticoid-induced muscle atrophy. A fourth objective is to further study the possibility that elevated estrogen levels have an inhibitory effect on muscle development. Androgen receptor capacity, binding affinity, and binding speficity in muscle, as well as blood levels of testosterone, dihydrotestosterone, and testosterone - binding globulin (separation of bound from free) will be systematically measured in all studies to gain an understanding of androgen regulation in muscle. A second direction of this research is to gain insights into the regulatory mechanisms that limit the muscles capacity for aerobic metabolism. Using exercise-training as a model for study, we propose to show that skeletal muscle capillarity, myoglobin levels, and mitochondrial content are under independent control mechanisms. In addition, the neural, hormonal, and substrate level that are responsible for the separate turnover of myoglobin and mitochondrial proteins (cytochrome c) will be examined. The long-term objectives of the androgen research are to understand the mechanisms of muslce growth and the degradative processes associated with muscular-related disorders and dystrophies. There is also prevalent use of anabolic steroids (androgenic hormones) by athletes; thus, physiological and biochemical knowledge of their effects are needed. The primary long-term objectives of the exercise research are to provide a sound biochemical foundation for exercise prescription and toward understanding the role of exercise in the prevention and treatment of coronary heart disease and related disorders.
| Hickson, R C; Marone, J R (1993) Exercise and inhibition of glucocorticoid-induced muscle atrophy. Exerc Sport Sci Rev 21:135-67 |
| Czerwinski, S M; Kurowski, T T; McKee, E E et al. (1991) Myosin heavy chain turnover during cardiac mass changes by glucocorticoids. J Appl Physiol 70:300-5 |
| Czerwinski, S M; Hickson, R C (1990) Glucocorticoid receptor activation during exercise in muscle. J Appl Physiol 68:1615-20 |
| Falduto, M T; Czerwinski, S M; Hickson, R C (1990) Glucocorticoid-induced muscle atrophy prevention by exercise in fast-twitch fibers. J Appl Physiol 69:1058-62 |
| Hickson, R C; Czerwinski, S M; Falduto, M T et al. (1990) Glucocorticoid antagonism by exercise and androgenic-anabolic steroids. Med Sci Sports Exerc 22:331-40 |
| Czerwinski, S M; McKee, E E; Hickson, R C (1989) Glucocorticoid receptor activation in isolated perfused rat hearts. Am J Physiol 256:C219-25 |
| Czerwinski, S M; Zak, R; Kurowski, T T et al. (1989) Myosin heavy chain turnover and glucocorticoid deterrence by exercise in muscle. J Appl Physiol 67:2311-5 |
| Falduto, M T; Hickson, R C; Young, A P (1989) Antagonism by glucocorticoids and exercise on expression of glutamine synthetase in skeletal muscle. FASEB J 3:2623-8 |
| Miller, W C; Hickson, R C; Bass, N M (1988) Fatty acid binding proteins in the three types of rat skeletal muscle. Proc Soc Exp Biol Med 189:183-8 |
| Gorostiaga, E M; Czerwinski, S M; Hickson, R C (1988) Acute glucocorticoid effects on glycogen utilization, O2 uptake, and endurance. J Appl Physiol 64:1098-106 |
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