Effects of Resistance Training on Insulin-Like Growth Factor and its Binding Proteins in Men and Women Aged 60 to 85
Version of Record online: 28 MAY 2002
Journal of the American Geriatrics Society
Volume 50, Issue 5, pages 884–888, May 2002
How to Cite
Borst, S. E., Vincent, K. R., Lowenthal, D. T. and Braith, R. W. (2002), Effects of Resistance Training on Insulin-Like Growth Factor and its Binding Proteins in Men and Women Aged 60 to 85. Journal of the American Geriatrics Society, 50: 884–888. doi: 10.1046/j.1532-5415.2002.50215.x
- Issue online: 28 MAY 2002
- Version of Record online: 28 MAY 2002
- Training volume;
- strength training;
- weight training
OBJECTIVES: We have reported that resistance training (RT) elevates insulin-like growth factor (IGF-I) in healthy young adults. Our goals were to determine whether RT produces a similar effect in the healthy older persons and to determine the effects of low- versus high-intensity RT on hormonal status.
SETTING: Center for Exercise Science, University of Florida, Gainesville.
PARTICIPANTS: Sixty-two men and women (mean age = 68.1).
INTERVENTION: A 6-month, 3-day/week program of low-intensity RT (LEX), high-intensity RT (HEX), or no exercise (CON).
MEASUREMENTS: Before and after training, blood was drawn for hormone analysis. IGF-I, IGF binding protein-1 (IGFBP-1), and IGFBP-3 were measured at rest. Testosterone and cortisol were measured at rest and immediately after exercise.
RESULTS: RT caused significant increases in 1-repetition maximum (1RM) strength and peak oxygen consumption (V02peak), which we have reported separately. Currently, we report that RT had no effect on the resting serum concentrations of IGF-I, IGFBP-1, IGFBP-3, testosterone, or cortisol. Acute resistance exercise caused no change in circulating testosterone in men or women but did cause a significant elevation of cortisol in the HEX group. This increase in cortisol was blunted as a result of training.
CONCLUSIONS: We conclude that the increases in strength and endurance caused by RT were not mediated by increases in circulating IGF-I, IGFBPs, or testosterone.