The exercise-induced biochemical milieu enhances collagen content and tensile strength of engineered ligaments

J Physiol. 2015 Oct 15;593(20):4665-75. doi: 10.1113/JP270737. Epub 2015 Sep 14.

Abstract

Exercise stimulates a dramatic change in the concentration of circulating hormones, such as growth hormone (GH), but the biological functions of this response are unclear. Pharmacological GH administration stimulates collagen synthesis; however, whether the post-exercise systemic milieu has a similar action is unknown. We aimed to determine whether the collagen content and tensile strength of tissue-engineered ligaments is enhanced by serum obtained post-exercise. Primary cells from a human anterior cruciate ligament (ACL) were used to engineer ligament constructs in vitro. Blood obtained from 12 healthy young men 15 min after resistance exercise contained GH concentrations that were ∼7-fold greater than resting serum (P < 0.001), whereas IGF-1 was not elevated at this time point (P = 0.21 vs. rest). Ligament constructs were treated for 7 days with medium supplemented with serum obtained at rest (RestTx) or 15 min post-exercise (ExTx), before tensile testing and collagen content analysis. Compared with RestTx, ExTx enhanced collagen content (+19%; 181 ± 33 vs. 215 ± 40 μg per construct P = 0.001) and ligament mechanical properties - maximal tensile load (+17%, P = 0.03 vs. RestTx) and ultimate tensile strength (+10%, P = 0.15 vs. RestTx). In a separate set of engineered ligaments, recombinant IGF-1, but not GH, enhanced collagen content and mechanics. Bioassays in 2D culture revealed that acute treatment with post-exercise serum activated mTORC1 and ERK1/2. In conclusion, the post-exercise biochemical milieu, but not recombinant GH, enhances collagen content and tensile strength of engineered ligaments, in association with mTORC1 and ERK1/2 activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Collagen / metabolism*
  • Exercise / physiology*
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Human Growth Hormone / blood
  • Humans
  • Insulin-Like Growth Factor I / metabolism
  • Ligaments / metabolism*
  • Ligaments / physiology*
  • MAP Kinase Signaling System
  • Male
  • Mechanistic Target of Rapamycin Complex 1
  • Multiprotein Complexes / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Smad2 Protein / metabolism
  • Smad3 Protein / metabolism
  • TOR Serine-Threonine Kinases / metabolism
  • Tensile Strength
  • Tissue Engineering

Substances

  • Multiprotein Complexes
  • SMAD2 protein, human
  • SMAD3 protein, human
  • Smad2 Protein
  • Smad3 Protein
  • Human Growth Hormone
  • Insulin-Like Growth Factor I
  • Collagen
  • Mechanistic Target of Rapamycin Complex 1
  • TOR Serine-Threonine Kinases