Age-associated decrease in contraction-induced activation of downstream targets of Akt/mTor signaling in skeletal muscle

Funai, Katsuhiko; Parkington, Jascha; Carambula, Silvia; Fielding, Roger A.

doi:10.1152/ajpregu.00277.2005

Cited by 66 publications

(56 citation statements)

References 54 publications

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“…Another possible explanation for these findings are age-related defects in the signaling mechanisms per se. Similar age-related declines in the responsiveness of the Akt/mTOR/p70 S6K pathway in compensatory overload (65), high-frequency electrical stimulation (27), and amino acid supplementation (23) models support the notion of signaling defects with age. Additionally, Li et al (47) demonstrated intraperitoneally injected des IGF-I phosphorylates Akt-1 equally in nonspecified muscles of young and old mice, while p-p70 S6K (Thr421/Ser424) abundance increases significantly in young but not in old.…”

Section: Discussionmentioning

confidence: 69%

Functional deficits and insulin-like growth factor-I gene expression following tourniquet-induced injury of skeletal muscle in young and old rats

Hammers

Merritt

Matheny

et al. 2008

Journal of Applied Physiology

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Section: Discussionmentioning

confidence: 69%

Functional deficits and insulin-like growth factor-I gene expression following tourniquet-induced injury of skeletal muscle in young and old rats

Hammers

Merritt

Matheny

et al. 2008

Journal of Applied Physiology

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“…Our studies, and those of others, have revealed that, after acute exercise, aged muscle is less capable of activating these upstream kinases (FIGURE 3) (52, 100, 135). Interestingly, this attenuated signaling, leading to a reduced mRNA response, has also been repeatedly demonstrated in response to resistance exercise protocols in old compared with young subjects (41,42,86,134,136). Thus the reduced activation of important kinases regulating mitochondrial biogenesis may be partly responsible for the delayed and diminished adaptation of mitochondria to exercise in senescent muscle.…”

Section: Mitochondrial Adaptations With Exercise In Aging Musclementioning

confidence: 80%

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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“…Studies utilising surgical ablation and high-frequency electrical stimulation consistently show an increase in 4E-BP1 phosphorylation in skeletal muscle in rodents (Bodine et al 2001b;Atherton et al 2005;Funai et al 2006;Thomson and Gordon 2006). Furthermore, as translation initiation cap binding is prevented when dephosphorylated 4E-BP1 is bound to eukaryotic initiation factor (eIF) 4E, skeletal muscle overload has also been shown to produce a decrease in 4E-BP1-eIF4E binding and subsequent increases in eIF4E-eIF4G association (Bodine et al 2001b;Kubica et al 2005).…”

Section: S6kmentioning

confidence: 99%