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Reaction time in healthy elderly is associated with chronic low-grade inflammation and advanced glycation end product

Tijdschriftbijdrage - Tijdschriftartikel

Chronic inflammation and Advanced Glycation End products (AGE) are associated with sarcopenia. Decreased voluntary muscle activation and increased antagonist coactivation can contribute to age-related muscle weakness. The influence of chronic inflammation and AGE in these neuromuscular mechanisms is not clear. We studied whether a relation exists between circulating levels of inflammatory cytokines and AGEs as well as the interplay between agonist and antagonist muscle activation. We studied 64 community-dwelling old subjects, during a maximal isometric voluntary contraction (MVC) and a reaction-time (RT) test of the upper limb. Twenty-five circulating inflammatory biomarkers were determined. Linear regression showed significant relationships between chronic inflammation and six muscle activation parameters. MIP-1β showed a significant negative relation with antagonist coactivation (during MVC) and antagonist muscle activity during pre-movement time (PMT) and movement time (MT) (during RT). A higher level of pentosidine (AGE) was predictive for a longer PMT. We conclude that in older relatively healthy persons antagonist muscle activation is influenced by chronic inflammation, contributing to age-related muscle weakness. Our results also suggest a mechanical and inflammatory influence of pentosidine in upper limb slowing of movement. These findings show novel insight in underlying mechanisms of age-related muscle weakness.

Tijdschrift: Experimental Gerontology
ISSN: 0531-5565
Volume: 108
Pagina's: 118-124
Aantal pagina's: 7
Jaar van publicatie:2018
Trefwoorden:Advanced glycation end product, Aging, Antagonist coactivation, Chronic inflammation, Cytokines
  • DOI: https://doi.org/10.1016/j.exger.2018.04.002
  • Scopus Id: 85045556730
  • WoS Id: 000434472500017
  • ORCID: /0000-0002-8853-6031/work/58609311
  • ORCID: /0000-0003-0054-1520/work/61309731
  • ORCID: /0000-0002-6598-9505/work/61772827
  • ORCID: /0000-0002-6820-9586/work/75885392