Journal of Applied Physiology AJP: Endocrinology and Metabolism
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J Appl Physiol 87: 1207-1212, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 3, 1207-1212, September 1999

Spaceflight suppresses exercise-induced release of bioassayable growth hormone

G. E. McCall1, C. Goulet1, R. R. Roy2, R. E. Grindeland3, G. I. Boorman1, A. J. Bigbee3, J. A. Hodgson1,2, M. C. Greenisen4, and V. R. Edgerton1,2

1 Department of Physiological Science and 2 Brain Research Institute, University of California, Los Angeles 90095; 3 National Aeronautics and Space Administration Ames Research Center, Moffett Field, California 94035; and 4 National Aeronautics and Space Administration Johnson Space Center, Houston, Texas 77058

We have reported that bed rest suppressed the release of bioassayable growth hormone (BGH) that normally occurs after an acute bout of unilateral plantar flexor exercise (G. E. McCall, C. Goulet, R. E. Grindeland, J. A. Hodgson, A. J. Bigbee, and V. R. Edgerton. J. Appl. Physiol. 83: 2086-2090, 1997). In the present study, the effects of spaceflight on the hormonal responses to this exercise protocol were examined. Four male astronauts on the National Aeronautics and Space Administration Shuttle Transport System (STS-78) mission completed the exercise protocol before, during, and after a 17-day spaceflight. The maximal voluntary contraction torque output at the onset of exercise was similar on all test days. Before spaceflight, plasma BGH increased 114-168% from pre- to postexercise. During spaceflight and after 2 days recovery at normal gravity (1 G), the BGH response to exercise was absent. After 4 days of recovery, this response was restored. Plasma concentrations of immunoassayable growth hormone were similar at all time points. The preexercise plasma immunoassayable insulin-like growth factor I (IGF-I) levels were elevated after 12 or 13 days of microgravity, and a approx 7% postexercise IGF-I increase was independent of this spaceflight effect. The suppression of the BGH response to exercise during spaceflight indicates that some minimum level of chronic neuromuscular activity and/or loading is necessary to maintain a normal exercise-induced BGH release. Moreover, these results suggest that there is a muscle afferent-pituitary axis that can modulate BGH release.

fatigue; human; maximum voluntary contraction; electromyography


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