Resistance exercise increases NF-κB activity in human skeletal muscle

Am J Physiol Regul Integr Comp Physiol. 2012 Mar 15;302(6):R667-73. doi: 10.1152/ajpregu.00336.2011. Epub 2011 Dec 21.

Abstract

Intense resistance exercise causes a significant inflammatory response. NF-κB has been identified as a prospective key transcription factor mediating the postexercise inflammatory response. The purpose of this study was to determine whether a single bout of intense resistance exercise regulates NF-κB signaling in human skeletal muscle. Muscle biopsy samples were obtained from the vastus lateralis of five recreationally active, but not strength-trained, males (21.9 ± 1.3 yr) prior to, and at 2 and 4 h following, a single bout of intense resistance exercise. A further five subjects (4 males, 1 female) (23 ± 0.89 yr) were recruited as a nonexercise control group to examine the effect of the muscle biopsy protocol on key markers of skeletal muscle inflammation. Protein levels of IκBα and phosphorylated NF-κB (p65), as well as the mRNA expression of inflammatory myokines monocyte chemoattractant protein 1 (MCP-1), IL-6, and IL-8 were measured. Additionally, NF-κB (p65) DNA binding to the promoter regions of MCP-1, IL-6, and IL-8 was investigated. IκBα protein levels decreased, while p-NF-κB (p65) protein levels increased 2 h postexercise and returned to near-baseline levels by 4-h postexercise. Immunohistochemical data verified these findings, illustrating an increase in p-NF-κB (p65) protein levels, and nuclear localization at 2 h postexercise. Furthermore, NF-κB DNA binding to MCP-1, IL-6, and IL-8 promoter regions increased significantly 2 h postexercise as did mRNA levels of these myokines. No significant change was observed in the nonexercise control group. These novel data provide evidence that intense resistance exercise transiently activates NF-κB signaling in human skeletal muscle during the first few hours postexercise. These findings implicate NF-κB in the transcriptional control of myokines known to be central to the postexercise inflammatory response.

Publication types

  • Controlled Clinical Trial

MeSH terms

  • Biopsy
  • Chemokine CCL2 / metabolism
  • DNA / metabolism
  • Exercise / physiology*
  • Female
  • Humans
  • I-kappa B Proteins / metabolism
  • Interleukin-6 / metabolism
  • Interleukin-8 / metabolism
  • Male
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / pathology
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / metabolism*
  • Signal Transduction / physiology*
  • Young Adult

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • I-kappa B Proteins
  • Interleukin-6
  • Interleukin-8
  • NF-kappa B
  • NFKBIA protein, human
  • NF-KappaB Inhibitor alpha
  • DNA