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Endocrine relationships during human spaceflight

T P Stein¹, M D Schluter, L L Moldawer

¹Department of Surgery, University of Medicine and Dentistry of New Jersey, School of Osteopathic Medicine, Stratford, New Jersey 08084, USA.

The American Journal of Physiology

|January 14, 1999

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Human spaceflight causes muscle protein loss. This study found decreased urinary levels of thyroid hormone and prostaglandins during spaceflight, suggesting their role in muscle changes. Postflight, some hormone levels increased, indicating a complex hormonal response.

Area of Science:

Space medicine
Human physiology
Endocrinology

Background:

Human spaceflight is linked to chronic muscle protein loss.
Understanding the hormonal mechanisms behind this loss is crucial for astronaut health.
Previous research suggests prostaglandins may influence muscle protein content.

Purpose of the Study:

To investigate the role of urinary hormone excretion in muscle protein loss during human spaceflight.
To identify specific hormones that change during spaceflight and correlate with muscle changes.

Main Methods:

Urine samples were collected from astronauts before, during, and after space shuttle missions.
Urinary excretion of various hormones, including ACTH, growth hormone, IGF-I, C-peptide, thyroid hormones, cortisol, and prostaglandins (PGE2, PGE-M, PGF2alpha, PGF-M), was measured.

Keywords:

NASA Discipline Regulatory Physiology Non-NASA Center

Related Experiment Videos

Main Results:

Inflight, urinary free 3,5,3'-triiodothyronine, PGE2, and PGE-M significantly decreased.
Urinary ACTH, PGE2, PGF2alpha, and PGF-M were elevated postflight compared to preflight levels.
Hormones like growth hormone, IGF-I, and C-peptide showed no significant changes during spaceflight.

Conclusions:

Decreased thyroid hormone and prostaglandin excretion during spaceflight may contribute to muscle protein loss.
Elevated prostaglandin levels postflight suggest a role in recovery or adaptation.
These findings support the hypothesis that prostaglandins play a key role in modulating muscle protein content in response to mechanical loading or unloading.