Effects of resistance exercise and growth hormone administration at low doses on lipid metabolism in middle-aged female rats

Eur J Pharmacol. 2006 Jun 6;539(1-2):99-107. doi: 10.1016/j.ejphar.2006.03.079. Epub 2006 May 9.


hGH (human growth hormone) is a key factor for metabolism as well as for growth. Lack of hGH usually increases LDL (low-density lipoprotein) while impairing exercise capacity and cardiac function [Amato G., Carella C., Fazio S., La Montagna G., Cittadini A., Sabatini D., Marciano-Mone C., Sacca L., and Bellastella A., 1993. Body composition, bone metabolism, and heart structure and function in growth hormone (GH)-deficient adults before and after GH replacement therapy at low doses. J. Clin. Endocrinol. Metab. 77, 1671-1676.]. It is still unclear, however, whether the administration of hGH to humans or animals has a synergic effects on body composition and the desired metabolic parameters with endurance resistance exercise. Therefore, the present study seeks to establish whether or not lipid metabolism is altered by both recombinant GH (growth hormone) and X (resistance exercise) in middle-aged female rats. GH administration resulted in greater weight gain compared with control and exercised animals, but the effect was reduced when combined with exercise. The increased body weight was largely due to increased muscle mass. Exercise did not result in any additional effect of GH on muscle mass. In the exercise group, hepatic HDL (high density lipoprotein) increased compared to the C (control group). The GX (growth hormone+exercise) group's serum and X group's kidney IGF-I (Insulin-like growth factor-I) concentration increased compared to the C group. In G and GX groups, serum insulin and leptin concentrations were higher than in the control, suggesting that GH may induce an insulin resistant state. Any gains in muscle mass were minimal and were not synergistic with exercise. These results suggest that hGH may not be useful for increasing performance in athletes and may induce and acquired insulin resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism*
  • Animals
  • Body Composition / drug effects
  • Carbon-Carbon Ligases / biosynthesis
  • Carbon-Carbon Ligases / genetics
  • Carnitine / blood
  • Carnitine O-Palmitoyltransferase / biosynthesis
  • Carnitine O-Palmitoyltransferase / genetics
  • Coenzyme A Ligases / biosynthesis
  • Coenzyme A Ligases / genetics
  • Female
  • Gene Expression Regulation, Enzymologic
  • Human Growth Hormone / pharmacology*
  • Insulin / blood
  • Insulin-Like Growth Factor I / metabolism
  • Leptin / blood
  • Lipid Metabolism / drug effects*
  • Liver / enzymology
  • Liver / metabolism
  • Organ Specificity
  • Physical Conditioning, Animal*
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Sprague-Dawley
  • Recombinant Proteins / pharmacology


  • Insulin
  • Leptin
  • RNA, Messenger
  • Recombinant Proteins
  • Human Growth Hormone
  • Insulin-Like Growth Factor I
  • Carnitine O-Palmitoyltransferase
  • Coenzyme A Ligases
  • Carbon-Carbon Ligases
  • acyl-CoA carboxylase
  • Carnitine