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运动后血清 T3 降低与糖皮质激素峰值无关。

Decreased serum T3 after an exercise session is independent of glucocorticoid peak.

机构信息

Laboratório de Biologia do Exercício, Escola de Educação Física e Desportos, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

出版信息

Horm Metab Res. 2013 Nov;45(12):893-9. doi: 10.1055/s-0033-1351279. Epub 2013 Aug 5.

DOI:10.1055/s-0033-1351279
PMID:23918684
Abstract

Physical exercise increases serum glucocorticoids, which is believed to be involved in the fall of T3 after high intensity exercise. The objective was to evaluate whether a physical exercise session alters the thyroid economy and adrenal axis in humans, and the possible role of corticosteroids in thyroid function disturbance. Active but not athlete subjects were enrolled in an open field competition and cortisol, TSH, T3, and T4 were measured before and after the race. To give new insights into the mechanisms underlying the changes in thyroid economy after exercise, we used a rat model to evaluate the impact of blocking corticosterone synthesis during treadmill exercise by metyrapone administration. Cortisol levels increased 1.5-fold (from 28.2±3.8 to 42.2±2.2 μg/dl; p<0.05), while serum T3 decreased by 13% (from 115±5 to 99±5 μg/dl; p<0.05) 6 h after the race in humans. Also, in rats, glucocorticoid increased by 2-fold while T3 decreased 15% after exercise session (p<0.05). However, the complete blockage of corticosterone peak did not impair serum T3 decrease observed in rats submitted to exercise. Interestingly, the lack of corticosterone peak led not only to lower serum T3, but also to decreased serum T4, indicating that corticosterone might be fundamental for the maintenance of serum thyroid hormone levels after high intensity exercise. Although cortisol increases and T3 decreases after high intensity exercise in both humans and rats, it does not seem to be a cause-effect response since pharmacological blockage of corticosterone peak does not modulate T3 response.

摘要

体育锻炼会增加血清糖皮质激素水平,这被认为与高强度运动后 T3 的下降有关。本研究旨在评估运动是否会改变人类的甲状腺代谢和肾上腺轴,以及皮质类固醇在甲状腺功能紊乱中的作用。我们招募了活跃但非运动员的受试者参加野外竞赛,并在比赛前后测量了皮质醇、TSH、T3 和 T4。为了深入了解运动后甲状腺代谢变化的机制,我们使用大鼠模型评估了在跑步机运动期间通过甲吡酮给药阻断皮质酮合成对其的影响。人类在比赛后 6 小时,皮质醇水平升高了 1.5 倍(从 28.2±3.8 至 42.2±2.2μg/dl;p<0.05),而血清 T3 降低了 13%(从 115±5 至 99±5μg/dl;p<0.05)。同样,在大鼠中,运动后糖皮质激素增加了 2 倍,而 T3 降低了 15%(p<0.05)。然而,完全阻断皮质酮峰值并不能阻止运动后大鼠血清 T3 的下降。有趣的是,缺乏皮质酮峰值不仅导致血清 T3 降低,还导致血清 T4 降低,这表明皮质酮可能是维持高强度运动后血清甲状腺激素水平的关键因素。尽管人类和大鼠在高强度运动后皮质醇增加,T3 降低,但这似乎不是一种因果关系,因为皮质醇峰值的药理学阻断并不能调节 T3 的反应。

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