TESTOSTERONE, CORTISOL AND CATECHOLAMINE RESPONSES TO EXERCISE STRESSAND AUTONOMIC DYSREFLEXIA IN ELITE QUADRIPLEGIC ATHLETES

Citation
G. Wheeler et al., TESTOSTERONE, CORTISOL AND CATECHOLAMINE RESPONSES TO EXERCISE STRESSAND AUTONOMIC DYSREFLEXIA IN ELITE QUADRIPLEGIC ATHLETES, Paraplegia, 32(5), 1994, pp. 292-299
Citations number
NO
Categorie Soggetti
Neurosciences,Surgery,Orthopedics
Journal title
ISSN journal
00311758
Volume
32
Issue
5
Year of publication
1994
Pages
292 - 299
Database
ISI
SICI code
0031-1758(1994)32:5<292:TCACRT>2.0.ZU;2-1
Abstract
Episodes of short high intensity exercise are associated with an incre ase in circulating total testosterone (T) in men. Mechanisms may inclu de hemoconcentration, decreased metabolic clearance and/or increased s ynthesis. Beta-blockade abolishes the T response suggesting a direct b eta-adrenergic effect on the testes. Some spinal cord injured (SCI) at hletes deliberately induce autonomic dysreflexia (boosting) to enhance performance. Associated with this practice are elevated catecholamine (CA) levels and exaggerated responses to serum catecholamine levels. Since basal T levels are reported to be normal in the SCI male, the T response to acute high intensity exercise might be expected to be exag gerated by boosting and associated elevated CA levels. The acute exerc ise T response has not been examined in SCI men to date. To determine whether the increased CA values associated with boosting enhanced the exercise-induced T elevation we measured circulating levels of T, cort isol (C), norepinephrine (NE) and epinephrine (E) before and' after ma ximal exertion and a simulated 7.5 km race with and without boosting i n eight elite quadriplegic athletes. Maximal incremental exercise and a simulated 7.5 km race resulted in a rise in T similar to able bodied men under normal exercise conditions. Under boosted conditions the ri se in T was eliminated while NE levels were significantly elevated abo ve unboosted levels. The data may suggest an inhibitory role for CA on T. production or release under conditions of extreme stress. Other po ssible mechanisms include C induced suppression, impaired gonadotropin stimulation of the Leydig cell and CA mediated alterations in gonadal blood supply.