Testosterone, cortisol and catecholamine responses to exercise stress and autonomic dysreflexia in elite quadriplegic athletes.

Abstract

Episodes of short high intensity exercise are associated with an increase in circulating total testosterone (T) in men. Mechanisms may include hemoconcentration, decreased metabolic clearance and/or increased synthesis. Beta-blockade abolishes the T response suggesting a direct beta-adrenergic effect on the testes. Some spinal cord injured (SCI) athletes 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 exaggerated by boosting and associated elevated CA levels. The acute exercise 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, cortisol (C), norepinephrine (NE) and epinephrine (E) before and after maximal exertion and a simulated 7.5 km race with and without boosting in 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 rise in T was eliminated while NE levels were significantly elevated above unboosted levels. The data may suggest an inhibitory role for CA on T production or release under conditions of extreme stress. Other possible mechanisms include C induced suppression, impaired gonadotropin stimulation of the Leydig cell and CA mediated alterations in gonadal blood supply.