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Effect of exercise on erythrocyte β‐adrenergic receptors and plasma concentrations of catecholamines and thyroid hormones in Thoroughbred horses
Author(s) -
GONZÁLEZ O.,
GONZÁLEZ EMA,
SÁNCHEZ C.,
PINTO J.,
GONZÁLEZ I.,
ENRÍQUEZ O.,
MARTÍNEZ R.,
FILGUEIRA G.,
WHITE A.
Publication year - 1998
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/j.2042-3306.1998.tb04091.x
Subject(s) - thyroid hormones , hormone , endocrinology , medicine , adrenergic , receptor , thyroid , horse , adrenergic receptor , biology , paleontology
Summary The effects of exercise stress on erythrocyte β‐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/1 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 (T 3 ), but not thyroxine (T 4 ) 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 pg/dl respectively). No differences were observed in basal values of thyroid hormones or in the percentage of T 3 increment, when comparing HP vs. LP horses. Erythrocyte membranes obtained 5 min after racing showed decreased concentrations of β‐adrenergic receptors (β‐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 β‐AR characteristics could be mediated by catecholamines, but not by thyroid hormones, in this model. This down regulation of β‐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 T 3 and a parallel decrease in β‐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.