Ca2+ dependency of limb muscle fiber contractile mechanics in young and older adults.
Am J Physiol Cell Physiol
; 318(6): C1238-C1251, 2020 06 01.
Article
em En
| MEDLINE
| ID: mdl-32348175
ABSTRACT
Age-induced declines in skeletal muscle contractile function have been attributed to multiple cellular factors, including lower peak force (Po), decreased Ca2+ sensitivity, and reduced shortening velocity (Vo). However, changes in these cellular properties with aging remain unresolved, especially in older women, and the effect of submaximal Ca2+ on contractile function is unknown. Thus, we compared contractile properties of muscle fibers from 19 young (24 ± 3 yr; 8 women) and 21 older adults (77 ± 7 yr; 7 women) under maximal and submaximal Ca2+ and assessed the abundance of three proteins thought to influence Ca2+ sensitivity. Fast fiber cross-sectional area was ~44% larger in young (6,479 ± 2,487 µm2) compared with older adults (4,503 ± 2,071 µm2, P < 0.001), which corresponded with a greater absolute Po (young = 1.12 ± 0.43 mN; old = 0.79 ± 0.33 mN, P < 0.001). There were no differences in fast fiber size-specific Po, indicating the age-related decline in force was explained by differences in fiber size. Except for fast fiber size and absolute Po, no age or sex differences were observed in Ca2+ sensitivity, rate of force development (ktr), or Vo in either slow or fast fibers. Submaximal Ca2+ depressed ktr and Vo, but the effects were not altered by age in either sex. Contrary to rodent studies, regulatory light chain (RLC) and myosin binding protein-C abundance and RLC phosphorylation were unaltered by age or sex. These data suggest the age-associated reductions in contractile function are primarily due to the atrophy of fast fibers and that caution is warranted when extending results from rodent studies to humans.
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Base de dados:
MEDLINE
Assunto principal:
Envelhecimento
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Cálcio
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Fibras Musculares Esqueléticas
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Sinalização do Cálcio
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Músculo Quadríceps
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Força Muscular
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Contração Muscular
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article