4.5 Article

Rate of force development is Ca2+-dependent and influenced by Ca2+-sensitivity in human single muscle fibres from older adults

Journal

EXPERIMENTAL GERONTOLOGY
Volume 150, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2021.111348

Keywords

Aging; Muscle contractility; Calcium sensitivity; Rate of force development; Cross-bridge; Myosin

Funding

  1. Natural Sciences and Engineering Research Council of Canada (NSERC)
  2. University of Guelph

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This study investigated the relationship between impaired Ca2+ sensitivity and rapid force production in single muscle fibers of young and older adults. The findings showed impaired Ca2+ sensitivity in older adults, but no difference in rapid force production between young and old muscle fibers.
Natural adult aging is associated with declines in skeletal muscle performance, including impaired Ca2+ sensitivity and a slowing of rapid force production (rate of force redevelopment; ktr). The purpose of this study was to investigate the relationship between impaired Ca2+ sensitivity and ktr of single muscle fibres from young and older adults. Participants included 8 young (22-35 yrs) and 8 older (60-81 yrs) males who were living independently. A percutaneous muscle biopsy of the vastus lateralis of each participant was performed. Single muscle fibre mechanical tests included maximal Ca2+-activated force (Po), force-pCa curves, and ktr. We showed a decrease in pCa50 in old type II fibres compared to young, indicating impaired Ca2+ sensitivity in older adults. The ktr behaved in a Ca2+-dependent manner such that with increasing [Ca2+], ktr increases, to a plateau. Interestingly, ktr was not different between young and old muscle fibres. Furthermore, we found strong associations between pCa50 and ktr in both old type I and type II fibres, such that those fibres with lower Ca2+ sensitivity had a slowed ktr. This Ca2+ association, combined with impaired Ca2+ handling in older adults suggests a potential Ca2+-dependent mechanism affecting the transition from weakly- to strongly-bound crossbridge states, leading to a decline in skeletal muscle performance. Future research is needed to explore the role alterations to Ca2+ sensitivity/handling could be playing in age-related whole muscle performance declines.

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