High-affinity growth hormone binding protein and acute heavy resistance exercise

Document Type

Journal Article

Publisher

American College of Sports Medicine

Faculty

Faculty of Computing, Health and Science

School

School of Exercise, Biomedical and Health Science / Centre for Alzheimer's Disease

RAS ID

9228

Comments

RUBIN, M. R., KRAEMER, W. J., MARESH, C. M., VOLEK, J. S., RATAMESS, N. A., VANHEEST, J. L., ... & GÓMEZ, A. L. (2005). High-affinity growth hormone binding protein and acute heavy resistance exercise. Medicine & Science in Sports & Exercise, 37(3), 395-403.

Abstract

Purpose: The purpose of this investigation was to examine the influence of resistance training on circulating concentrations of growth hormone binding protein (GHBP) in response to acute heavy resistance exercise. Methods: Using a cross-sectional experimental design, a group of resistance-trained men (RT, N 9, 7.9 + 1.3 yr resistance training experience) and a group of untrained men (UT, N 10) performed an acute heavy resistance exercise protocol (AHREP) consisting of 6 sets of 10 repetition maximum parallel squats. Blood samples were obtained 72 h before exercise, immediately before exercise, and 0, 15, 30, 45, and 60 min after exercise. Results: Significant increases (P < 0.05) in GHBP, immunoreactive growth hormone (iGH), and IGF-1 were observed in both subject groups after AHREP. There were no differences (P > 0.05) between groups in GHBP at rest or after AHREP. However, RT exhibited a significantly greater iGH response to AHREP than UT subjects, and significantly higher IGF-1 values at rest and after exercise. Significant positive correlations were found between GHBP and BMI, body fat, and leptin in both groups. A significant positive correlation also was observed between resting leptin and GHBP values in UT but not RT subjects. Conclusions: In summary, these data indicate that resistance training does not increase blood GHBP. Nevertheless, the increases observed with IGF-1 concentrations in the resistance-trained subjects do suggest an apparent adaptation with the regulation of this hormone. If there was in fact an increase in GH sensitivity and GH receptor expression at the liver that was not detected by blood GHBP in this study, it may be possible that factors contributing to the circulating concentration of GHBP other than hepatocytes (e.g., leptin and adipocytes) may serve to mask training-induced increases in circulating GHBP of a hepatic origin, thus masking any detectable increase in GH receptor expression.

DOI

10.1249/01.MSS.0000155402.93987.C0

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free_to_read

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Link to publisher version (DOI)

10.1249/01.MSS.0000155402.93987.C0