Skeletal muscle fiber quality in older men and women

Abstract

Whole muscle strength and cross-sectional area (WMCSA), and contractile properties of chemically skinned segments from single fibers of the quadriceps were studied in 7 young men (YM, 36.5 +/- 3. 0 yr), 12 older men (OM, 74.4 +/- 5.9 yr), and 12 older women (OW, 72.1 +/- 4.3 yr). WMCSA was smaller in OM compared with YM (56.1 +/- 10.1 vs. 79.7 +/- 13.1 cm(2); P = 0.031) and in OW (44.9 +/- 7.5; P < 0.003) compared with OM. Age-related, but not sex-related, differences in strength were eliminated after adjusting for WMCSA. Maximal force was measured in 552 type I and 230 type IIA fibers. Fibers from YM (type I = 725 +/- 221; type IIA = 792 +/- 271 microN) were stronger (P < 0.001) than fibers from OM (I = 505 +/- 179; IIA = 577 +/- 262 microN) even after correcting for size. Type IIA fibers were stronger (P < 0.005) than type I fibers in YM and OM but not in OW (I = 472 +/- 154; IIA = 422 +/- 97 microN). Sex-related differences in type I and IIA fibers were dependent on fiber size. In conclusion, differences in WMCSA explain age-related differences in strength. An intrinsic defect in contractile proteins could explain weakness in single fibers from OM. Sex-related differences exist at the whole muscle and single fiber levels.

Eccentric contraction-induced injury to type I, IIa, and IIa/IIx muscle fibers of elderly adults

“…The heightened susceptibility to damage observed here, coupled with an impaired ability to recover from injury or adapt to repeated exercise reported by others (Dedrick and Clarkson 1990;McBride et al 1995;Brooks and Faulkner 1990;Rader and Faulkner 2006;Lavender and Nosaka 2006b;Cutlip et al 2006) could be a contributor to the reduced lower limb muscle strength of elderly adults. Because contraction-induced damage impairs excitation-contraction coupling and cross-bridge function (Balnave and Allen 1995;Warren et al 1994), a heightened susceptibility to injury could initiate the age-related deterioration in muscle fiber activation and contractility (Delbono et al 1995;Wang et al 2002;Larsson et al 1997;Thompson and Brown 1999;Lowe et al 2001;Frontera et al 2000;Hook et al 2001;Krivickas et al 2001). Consistent with our results, studies conducted on skinned fibers from EDL muscles of young and old laboratory rodents have identified age-related deficits at the level of the force-producing or force-transmitting components of the cell (Lynch et al 2008;Brooks and Faulkner 1996).…”

“…Cross-bridge kinetics are altered with aging (Larsson et al 1997;Thompson and Brown 1999;Lowe et al 2001;Frontera et al 2000;Hook et al 2001;Krivickas et al 2001) but whether these changes are directly responsible for an age-related increase in damage is unknown. Alternatively, desmin, titin, myosin light chain 2, tropomyosin, and α-actinin covary (either in concentration or isoform expression) with fiber MHC isoform content (Prado et al 2005;Chopard et al 2001;Schiaffino and Reggiani 1996) and have all been implicated in contraction-induced muscle injury (Meyer et al 2010;Lieber et al 1996;Koh and Escobedo 2004;Zhang et al 2008;Lehti et al 2007;Belcastro 1993;Childers and McDonald 2004).…”

“…The latter includes fiber loss and atrophy (Larsson et al 1979;Sato et al 1984;Lexell et al 1988), impairments in the excitation-contraction process (Delbono et al 1995;Wang et al 2002), and perturbations to actomyosin cross-bridge function (Larsson et al 1997; Thompson and Brown 1999;Lowe et al 2001;Frontera et al 2000;Hook et al 2001;Krivickas et al 2001). These factors are specific to the mode of muscle contraction, impacting force during isometric and shortening contractions but having much less effect on force during lengthening or eccentric, muscular activity (Porter et al 1997;Poulin et al 1992;Phillips et al 1991;Ochala et al 2006;Hortobagyi et al 1995).…”

Correlation of knee‐joint cartilage morphology with muscle cross‐sectional areas vs. anthropometric variables

“…Nevertheless, we refute the hypothesis that the age-dependent decrease in cartilage thickness is generally caused by (or associated with) a decrease in MCSAs. Despite the nonsignificant changes in MCSAs, we cannot rule out the possibility that there is a significant decrease in muscle force in elderly subjects, as it is still a matter of controversy whether changes in muscle fiber type and alterations in recruitment (specific muscle force) occur with aging (Frontera et al, 2000;Cannon et al, 2001;Goodpaster et al, 2001;Urbancheck et al, 2001). Moreover, correlations between MCSAs and muscle strength have been shown to be only moderate (Dowling and Cardone, 1994;Bruce et al, 1997;Overend et al, 1992).…”

How pleiotropic genetics of the musculoskeletal system can inform genomics and phenomics of aging

“…Sex hormones Special relations exist between the phenotypes of musculoskeletal aging and the sex hormones, such as levels of androgen (testosterone) in men and endogenous estrogen in women, as is evident in the sexual dimorphism in bones, joints dimensions, muscle size, and strength (Frontera et al 2000). Estrogen is essential in growth plate closure and therefore is important in defining the adult body size.…”