Identical responses of fast muscle to sustained activity  by low-frequency stimulation in young and aging rats

Škorjanc, Dejan; Traub, Irmtrud; Pette, Dirk

doi:10.1152/jappl.1998.85.2.437

Cited by 28 publications

(15 citation statements)

References 26 publications

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“…Previous studies have demonstrated that a relative decrease in the type IIb MHC isoform of rat fast muscle is induced by the increase in muscle activity that occurs in physical training or upon electric stimulation (Demirel et al 1999;Sullivan et al 1995;Sˇkorjanc et al 1998). Our data are in agreement with those previous results in that the percentage of the type IIb MHC isoform in PLA in each VE group was significantly lower than that in the corresponding SC group (Fig.…”

Section: Discussionsupporting

confidence: 93%

Effects of prolonged voluntary wheel-running on muscle structure and function in rat skeletal muscle

Kariya

Yamauchi

Kobayashi

et al. 2004

European Journal of Applied Physiology

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We examined the effects of prolonged voluntary wheel-running on skeletal muscle functional and/or structural characteristics in rats. Male Sprague-Dawley rats (5 weeks old) were divided into five groups: (1) 15W-SC, sedentary controls housed in normal plastic cages until age 15 weeks; (2) 15W-VE, housed in a voluntary-exercise (running-wheel) device equipped with housing space until age 15 weeks; (3) 35W-SC, housed in normal plastic cages until age 35 weeks; (4) 35W-VE, housed in the voluntary-exercise device until age 35 weeks, and (5) 35W-MVE, housed in normal plastic cages until age 15 weeks, then in the voluntary-exercise device from age 16 weeks to 35 weeks ("middle age"). At the end of each rat's experimental period, the plantaris muscle was dissected from each hindlimb for analysis of the muscle's functional and/or structural characteristics. Total running distance was similar in 15W-VE and 35W-VE, both being significantly greater than in 35-MVE. The percentage of type IIb myosin heavy chain isoform was significantly lower in each VE group than in the corresponding SC group. This shift from type IIb was significantly greater for 35W-VE than for the other VE groups, which were similar to each other. The cross-sectional area of type IIx fibers was significantly greater in 35W-VE than in 35W-SC, but this was not true for 15W-VE versus 15W-SC or for 35W-MVE versus 35W-SC. No significant difference in citrate synthase activity was detected between any VE group and the corresponding SC group. These results suggest that a prolongation of voluntary wheel-running leads to some advantageous enhancements of functional and/or structural characteristics in rat plantaris.

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Section: Discussionsupporting

confidence: 93%

Effects of prolonged voluntary wheel-running on muscle structure and function in rat skeletal muscle

Kariya

Yamauchi

Kobayashi

et al. 2004

European Journal of Applied Physiology

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“…Decreased aconitase levels agreed with a previous study which suggests that oxidative damage during aging targets mitochondrial aconitase (56). Interestingly, previous metabolic studies comparing chronic low-frequency stimulated young versus aged fibres suggest that both muscle types respond in a similar way to sustained neuromuscular activity (57,58). Therefore, the age-induced changes in glycolytic and mitochondrial enzymes might be a consequence of altered innervation patterns and not a primary pathological insult within the skeletal muscle fibres themselves.…”

Section: Discussionsupporting

confidence: 89%

Proteomic profiling reveals a severely perturbed protein expression pattern in aged skeletal muscle

O’Connell

Gannon²,

Doran³

et al. 2007

Int J Mol Med

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Abstract. Extended longevity is often accompanied by frailty and increased susceptibility to a variety of crippling disorders. One of the most striking features of human aging is sarcopenia, which is defined as the age-related decline in skeletal muscle mass and strength. Although various metabolic and functional defects in aging muscle fibres have been described over the last decade, it is not known whether a pathophysiological hierarchy exists within degenerative pathways leading to muscle wasting. Hence, in order to identify novel biomarkers of age-dependent skeletal muscle degeneration, we have here applied mass spectrometry-based proteomics for studying global muscle protein expression patterns. As a model system of sarcopenia, we have employed crude extracts from senescent rat gastrocnemius muscle, as compared to young adult tissue preparations. Using the highly sensitive protein dye Deep Purple for the analysis of the 2-D separated muscle proteome and peptide mass fingerprinting for the identification of individual protein spots, a differential expression pattern was observed for contractile proteins, metabolic factors, regulatory components and heat shock elements. A drastic increase was shown for αB-crystallin, myosin light chain MLC-1, phosphoglycerate kinase, adenylate kinase, triosephosphate isomerase, albumin, aconitase and nucleoside-diphosphate kinase in aged fibres. In contrast, the expression of pyruvate kinase, aldolase, creatine kinase, transferrin, α-tropomyosin and myosin light chain MLC-3 was decreased in old skeletal muscle. Comparative 2-D immunoblotting of selected candidate proteins has confirmed the effect of aging on the skeletal muscle proteome. These findings demonstrate a severely perturbed protein expression pattern in aged skeletal muscle, which reflects the underlying molecular alterations causing a drastic decline of muscle strength in the senescent organism. In the long-term, the systematic deduction of abnormal protein expression in aged muscle by proteomic profiling approaches may lead to the cataloguing of a cohort of novel therapeutic targets to treat muscular weakness in the aging population.

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“…Yet, by 90 days, young and aged animals had equivalent levels of this mitochondrial enzyme marker. In another study, CCA over 50 days effectively increased mitochondrial content and reduced the number of COX-deficient fibers in aged muscle (125,150). These data illustrate the potential corrective nature of chronic exercise in ameliorating ETC dysfunction but also suggest that the kinetics of mitochondrial adaptations in old muscle are delayed in response to an exercise regimen.…”

Section: Mitochondrial Adaptations With Exercise In Aging Musclementioning

confidence: 76%

Mitochondria, Muscle Health, and Exercise with Advancing Age

2015

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Skeletal muscle health is dependent on the optimal function of its mitochondria. With advancing age, decrements in numerous mitochondrial variables are evident in muscle. Part of this decline is due to reduced physical activity, whereas the remainder appears to be attributed to age-related alterations in mitochondrial synthesis and degradation. Exercise is an important strategy to stimulate mitochondrial adaptations in older individuals to foster improvements in muscle function and quality of life.Heather N. Carter, Chris C. W. The process of aging exploits the malleable nature of skeletal muscle. The age-related loss of muscle mass was termed sarcopenia, based on the Greek (sarx, flesh) and (penia, poverty) in 1988 (139). Accompanying this loss are profound architectural and molecular changes that alter muscle quality and are manifested in functional limitations. Decreases in muscle fiber number as well as fiber cross-sectional area are both contributing factors to sarcopenia (92) and consequently adversely affect force production (strength) (46, 63) and endurance of the older individual (12). Muscle mass typically peaks in the mid-20s (12, 34,92), and thereafter several distinct phases of muscle loss have been identified. In the third to fifth decade of life, a slow rate of muscle mass loss is noted, amounting to ϳ10% in total (34,92). In later adulthood (Ͼ45 yr), the rate of muscle loss increases, with appraisals ranging between 0.5 and 1.4% per year (12, 34,69). Even more dramatic changes are noted beyond the sixth decade of life. Along with the functional impairments imposed by sarcopenia, are the associated escalations in health care costs, along with coincident rises in metabolic diseases (e.g., Type 2 diabetes, obesity) and a greater risk of falls (67). In the U.S., it is expected that those 65 years of age and over will comprise ϳ20% of the population, or ϳ72 million people, by the year 2030 (20). Since the proportion of older adults is increasing, continued research into the mechanisms of muscle loss is warranted, along with the investigation of therapeutic strategies that can mitigate muscle atrophy during aging. Mitochondria have been implicated as potential mediators of sarcopenia. Recently, it has been suggested that dysfunction of these organelles can be considered a feature of aging (105). However, considerable controversy exists regarding the extent to which muscle mitochondria may be dysfunctional with aging, and thereby contribute to the loss of this tissue. Thus the purpose of this review is to examine the literature with respect to mitochondrial content and function in muscle with advancing age, and provide a perspective on the effectiveness of endurance/aerobic exercise as an intervention for mitochondrial biogenesis and muscle homeostasis in older individuals. Structural Features of Muscle Relevant to SarcopeniaIn young, healthy individuals, skeletal muscle comprises ϳ40% of total body mass and is important for locomotion and whole body metabolism. Myosin ATPase histochemistry and electrop...

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Identical responses of fast muscle to sustained activity by low-frequency stimulation in young and aging rats

Cited by 28 publications

References 26 publications

Effects of prolonged voluntary wheel-running on muscle structure and function in rat skeletal muscle

Effects of prolonged voluntary wheel-running on muscle structure and function in rat skeletal muscle

Proteomic profiling reveals a severely perturbed protein expression pattern in aged skeletal muscle

Mitochondria, Muscle Health, and Exercise with Advancing Age

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