Effect of exercise on erythrocyte beta-adrenergic receptors and plasma concentrations of catecholamines and thyroid hormones in Thoroughbred horses.

The effects of exercise stress on erythrocyte beta-adrenergic receptor characteristics and plasma concentrations of adrenaline, noradrenaline and thyroid hormones were studied in Thoroughbred racehorses during rest and after exercise. Five minutes after a maximal speed race of 1200 +/- 200 m (mean +/- s.d.), both plasma adrenaline and noradrenaline concentrations increased with respect to basal values (from 2.48 +/- 0.15 to 3.83 +/- 0.27 and from 2.13 +/- 0.11 to 3.53 +/- 0.27 nmol/l respectively). The increment of adrenaline was greater in high performance (HP) as compared to low performance (LP) horses (76.9 vs. 43.5%), in accordance with the contribution of the adrenal medulla in the sympathoadrenal response to exercise. Triiodothyronine (T3), but not thyroxine (T4) levels increased 5 min after exercise (from 55.6 +/- 2.9 to 81 +/- 3.7 ng/dl and from 0.67 +/- 0.04 to 0.70 +/- 0.05 micrograms/dl respectively). No differences were observed in basal values of thyroid hormones or in the percentage of T3 increment, when comparing HP vs. LP horses. Erythrocyte membranes obtained 5 min after racing showed decreased concentrations of beta-adrenergic receptors (beta-AR) and dissociation constant as compared to basal values (50.1 +/- 7.0 vs. 95.7 +/- 12.0 fmol/mg protein and 0.97 +/- 0.24 vs. 2.04 +/- 0.3 nmol/l respectively). This temporal pattern suggest that the observed changes in beta-AR characteristics could be mediated by catecholamines, but not by thyroid hormones, in this model. This down regulation of beta-AR may act as a protecting mechanism preventing the erythrocytes from the decrease in membrane fluidity known to be provoked by adrenergic agonists. The accomplished study showed that, in the Thoroughbred horse, there is a homeostatic response to race stress, characterised by a sudden increase in plasma catecholamines and T3 and a parallel decrease in beta-AR concentration on the erythrocyte membrane. In this way the racing horse could rapidly adjust its metabolism to the exercise stress, but at the same time override one possible undesirable side-effect caused by these hormonal changes. Further studies will be required to establish performance-related differences occurring in endocrine changes.

Role of exercise and ascorbate on plasma antioxidant capacity in thoroughbred race horses.

During exercise, the oxygen consumption and the production of free radicals increase and can lead to oxidative stress with a deleterious effect on cellular structures involved in physical activity. To evaluate the oxidative stress produced by exercise and the role of ascorbate as an antioxidant, venous blood samples were obtained from 44 thoroughbred racehorses, before and after a 1000+/-200-m race at maximum velocity. Fourteen of these horses were treated intravenously with 5 g of ascorbate before running. Antioxidant capacity (PAOC), endogenous and exogenous ascorbate concentration, total antioxidant reactivity (TAR), urate concentration, creatine kinase activity, protein concentration and thiobarbiturate reactive substances (TBAR) as oxidative stress indicators were measured in the plasma of some of these horses. PAOC, TAR and TBAR increased after the race, while plasma ascorbate and urate concentrations remained unchanged. Total plasma protein (TPP) concentrations increased in line with antioxidant capacity. As predicted, both the plasma ascorbate concentration and PAOC increased immediately after ascorbate administration, but was not modified after the race, such as TBAR. However, in both groups plasma creatine kinase activity increased after the race. These results would suggest that the administration of ascorbate could nullify the oxidative stress produced by exercise in thoroughbred racehorses, but could not prevent muscular damage.