Chronic low-grade inflammation and age-related sarcopenia

Curr Opin Clin Nutr Metab Care. 2012 Jan;15(1):12-22. doi: 10.1097/MCO.0b013e32834dd297.

Abstract

Purpose of review: Age-related chronic low-grade inflammatory profile (CLIP) has been recognized as an important causative factor for sarcopenia. Here, we report the recent evidence concerning CLIP and sarcopenia.

Recent findings: Twenty-one studies were included (12 observational, five interventional studies and four randomized controlled trials). Observational studies strengthen the association between CLIP and sarcopenia in cross-sectional and longitudinal designs. Interleukin (IL)-6 and tumour necrosis factor-α are the most reported inflammatory parameters. Biopsy studies confirm the role of oxidative mechanisms, protein kinase B and nuclear factor kappa-light-chain-enhancer of activated B cells pathways and implicate stress response mechanisms and heat shock protein. Adipose tissue as source of inflammatory cytokines remains unclear and correction for fat mass is advisable in new research. Exercise interventions (both aerobic and resistance training) demonstrate beneficial effects on CLIP even in the absence of decreases in weight, BMI or fat mass. IL-6 is also released during exercise, in hormone-like fashion unrelated to inflammation, and exercise-induced IL-6 changes require careful interpretation. Soy supplementation in one study showed no influence on CLIP and no recent pharmacological trials were retrieved.

Summary: Associations between CLIP and sarcopenia are observed quite consistently and underlying mechanisms become apparent. Exercise remains the mainstay intervention to lower CLIP and counter sarcopenia. More research is warranted to unravel the exact dose-response relationship.

Publication types

  • Review

MeSH terms

  • Adipose Tissue / metabolism
  • Age Factors
  • Chronic Disease
  • Exercise Therapy
  • Humans
  • Inflammation / complications*
  • Inflammation / metabolism
  • Inflammation Mediators / metabolism*
  • Sarcopenia / etiology*
  • Sarcopenia / metabolism
  • Stress, Physiological

Substances

  • Inflammation Mediators