Horm Metab Res 2005; 37(9): 577-584
DOI: 10.1055/s-2005-870426
Review
© Georg Thieme Verlag KG Stuttgart · New York

Exercise as a Stress Model and the Interplay Between the Hypothalamus-pituitary-adrenal and the Hypothalamus-pituitary-thyroid Axes

G.  Mastorakos1 , M.  Pavlatou1
  • 1Endocrine Unit, Second Department of Obstetrics and Gynecology, ARETAIEION Hospital, Athens Medical School, National Kapodistriakon University of Athens, Athens, Greece
Further Information

Publication History

Received 25 February 2005

Accepted after Revision 12 July 2005

Publication Date:
20 September 2005 (online)

Abstract

Exercise represents a physical stress that challenges homeostasis. In response to this stressor, the autonomic nervous system and hypothalamus-pituitary-adrenal axis are known to react and participate in the maintenance of homeostasis and the development of physical fitness. This includes elevation of cortisol and catecholamines in plasma. However, physical conditioning is associated with a reduction in pituitary-adrenal activation in response to exercise. On the other hand, highly trained athletes exhibit chronic mild hypercortisolism at baseline that may be an adaptive change to chronic exercise. In addition the proinflammatory cytokine, IL-6 is also activated, probably via catecholamines. On the other hand, the stress of chronic exercise induces certain changes to the thyroid axis. Peripheral thyroid hormone metabolism suppression is observed, and the result is a hormonal status similar to that of euthyroid sick syndrome (ESS), with suppression of T3 and elevation of rT3 plasma levels. One mechanism proposed involves exercise-activated pathways participating in the pathogenesis of ESS. This is realized through norepinephrine’s activation of NF-κB. Neuroendocrine response to exercise stress involves activation of NF-κB resulting in inactivation of T3-dependent 5’-deiodinase gene expression and enzyme activity. Thus, ESS is generated in the periphery. On the other hand, activation and nuclear translocation of NF-κB leads to increased transcription of proinflammatory genes responsible for the expression of proinflammatory cytokines such as TNF-α and IL-6. These cytokines could activate cortisol, which in turn inhibits NF-κB activation through IκB and finally shuts down this cycle.

References

G. Mastorakos

Endocrine Unit, Second Department of Obstetrics and Gynecology, ARETAIEION Hospital, Athens Medical School, National Kapodistriakon University of Athens

3, Neofytou Vamva · 10674 · Athens · Greece

Fax: +30 (210) 363 62 29

Email: mastorak@mail.kapatel.gr