Format

Send to:

Choose Destination
See comment in PubMed Commons below
Horm Metab Res. 2005 Sep;37(9):577-84.

Exercise as a stress model and the interplay between the hypothalamus-pituitary-adrenal and the hypothalamus-pituitary-thyroid axes.

Author information

  • 1Endocrine Unit, Second Department of Obstetrics and Gynecology, ARETAIEION Hospital, Athens Medical School, National Kapodistriakon University of Athens, Athens, Greece. mastorak@mail.kapatel.gr

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-kappaB. Neuroendocrine response to exercise stress involves activation of NF-kappaB 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-kappaB leads to increased transcription of proinflammatory genes responsible for the expression of proinflammatory cytokines such as TNF-alpha and IL-6. These cytokines could activate cortisol, which in turn inhibits NF-kappaB activation through IkappaB and finally shuts down this cycle.

PMID:
16175498
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Georg Thieme Verlag Stuttgart, New York
    Loading ...
    Write to the Help Desk