scholarly journals Exercise as a Peripheral Circadian Clock Resynchronizer in Vascular and Skeletal Muscle Aging

2021 ◽  
Vol 18 (24) ◽  
pp. 12949
Author(s):  
Bruna Spolador de Alencar Silva ◽  
Juliana Souza Uzeloto ◽  
Fábio Santos Lira ◽  
Telmo Pereira ◽  
Manuel J. Coelho-E-Silva ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Circadian Rhythm ◽  
Vascular Health ◽  
Physiological Changes ◽  
Skeletal Muscle Function ◽  
Muscle Aging ◽  
Muscle Changes ◽  
Skeletal Muscle Aging ◽  
Influence Behavior

Aging is characterized by several progressive physiological changes, including changes in the circadian rhythm. Circadian rhythms influence behavior, physiology, and metabolic processes in order to maintain homeostasis; they also influence the function of endothelial cells, smooth muscle cells, and immune cells in the vessel wall. A clock misalignment could favor vascular damage and indirectly also affect skeletal muscle function. In this review, we focus on the dysregulation of circadian rhythm due to aging and its relationship with skeletal muscle changes and vascular health as possible risk factors for the development of sarcopenia, as well as the role of physical exercise as a potential modulator of these processes.

scholarly journals Role of miRNAs in skeletal muscle aging

2018 ◽  
Vol Volume 13 ◽  
pp. 2407-2419 ◽  
Author(s):  
Yan Zheng ◽  
Jian Kong ◽  
Qun Li ◽  
Yan Wang ◽  
Jie Li
Keyword(s):  
Skeletal Muscle ◽  
Muscle Aging ◽  
Skeletal Muscle Aging

scholarly journals Role of Age-Related Mitochondrial Dysfunction in Sarcopenia

2020 ◽  
Vol 21 (15) ◽  
pp. 5236 ◽  
Author(s):  
Evelyn Ferri ◽  
Emanuele Marzetti ◽  
Riccardo Calvani ◽  
Anna Picca ◽  
Matteo Cesari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cellular Senescence ◽  
Significant Loss ◽  
Muscle Aging ◽  
Age Related ◽  
Mitochondrial Functions ◽  
Health Quality ◽  
Skeletal Muscle Aging ◽  
And Function

Skeletal muscle aging is associated with a significant loss of skeletal muscle strength and power (i.e., dynapenia), muscle mass and quality of life, a phenomenon known as sarcopenia. This condition affects nearly one-third of the older population and is one of the main factors leading to negative health outcomes in geriatric patients. Notwithstanding the exact mechanisms responsible for sarcopenia are not fully understood, mitochondria have emerged as one of the central regulators of sarcopenia. In fact, there is a wide consensus on the assumption that the loss of mitochondrial integrity in myocytes is the main factor leading to muscle degeneration. Mitochondria are also key players in senescence. It has been largely proven that the modulation of mitochondrial functions can induce the death of senescent cells and that removal of senescent cells improves musculoskeletal health, quality, and function. In this review, the crosstalk among mitochondria, cellular senescence, and sarcopenia will be discussed with the aim to elucidate the role that the musculoskeletal cellular senescence may play in the onset of sarcopenia through the mediation of mitochondria.

scholarly journals THE ROLE OF MITOCHONDRIAL ENERGETICS IN CARDIAC AND SKELETAL MUSCLE AGING

2018 ◽  
Vol 2 (suppl_1) ◽  
pp. 348-348
Author(s):  
P Rabinovitch ◽  
D J Marcinek
Keyword(s):  
Skeletal Muscle ◽  
Muscle Aging ◽  
Skeletal Muscle Aging

Healthy skeletal muscle aging: The role of satellite cells, somatic mutations and exercise

2019 ◽  
pp. 157-200 ◽  
Author(s):  
Irene Franco ◽  
Rodrigo Fernandez-Gonzalo ◽  
Peter Vrtačnik ◽  
Tommy R. Lundberg ◽  
Maria Eriksson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Somatic Mutations ◽  
Muscle Aging ◽  
Skeletal Muscle Aging

scholarly journals Aging Triggers H3K27 Trimethylation Hoarding in the Chromatin of Nothobranchius Furzeri Skeletal Muscle

2019 ◽  
Author(s):  
Chiara Cencioni ◽  
Johanna Heid ◽  
Anna Keprelova ◽  
Seyed Mohammad Mahdi Rasa ◽  
Carsten Kuenne ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Skeletal Muscle Function ◽  
Muscle Aging ◽  
Aging Studies ◽  
Nothobranchius Furzeri ◽  
Landscape Alteration ◽  
Epigenetic Analysis ◽  
Skeletal Muscle Aging ◽  
Polycomb Complex

Aging associates with progressive loss of skeletal muscle function leading up to sarcopenia, a process characterized by impaired mobility and weakening of muscle strength. Molecular mechanisms underpinning sarcopenia are still poorly characterized. Since aging associates with profound epigenetic changes, epigenetic landscape alteration analysis in the skeletal muscle promises to highlight molecular mechanisms of age-associated sarcopenia. The study was conducted exploiting the short-lived turquoise killifish Nothobranchius furzeri (Nfu), a relatively new model for aging studies. The epigenetic analysis suggested for a less accessible and more condensed chromatin in old Nfu skeletal muscle. Specifically, an accumulation of heterochromatin regions was observed as consequence of increased levels of H3K27me3, HP1alpha, polycomb complex subunits and senescence associated heterochromatic foci (SAHFs). Consistently, euchromatin histone marks, including H3K9ac, decreased. The integrative bioinformatics analysis of RNASeq and ChIPSeq, related to skeletal muscle of Nfu at different ages, revealed a down-modulation of genes involved in cell cycle, differentiation and DNA repair and an up-regulation of inflammation and senescence genes. Undoubtedly, more studies are needed to disclose the detailed mechanisms, but this approach revealed an unprecedented specific features of Nfu skeletal muscle aging, potentially associated with sarcopenia onset and consequent impairment of swimming and mobility typical of old Nfu.

scholarly journals Exercise rescues mitochondrial coupling in aged skeletal muscle: a comparison of different modalities in preventing sarcopenia

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Colin Harper ◽  
Venkatesh Gopalan ◽  
Jorming Goh
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Fiber Type ◽  
Skeletal Muscle Function ◽  
Atp Production ◽  
Muscle Aging ◽  
Age Related ◽  
Key Factor ◽  
Underlying Mechanisms ◽  
Skeletal Muscle Aging

AbstractSkeletal muscle aging is associated with a decline in motor function and loss of muscle mass- a condition known as sarcopenia. The underlying mechanisms that drive this pathology are associated with a failure in energy generation in skeletal muscle, either from age-related decline in mitochondrial function, or from disuse. To an extent, lifelong exercise is efficacious in preserving the energetic properties of skeletal muscle and thus may delay the onset of sarcopenia. This review discusses the cellular and molecular changes in skeletal muscle mitochondria during the aging process and how different exercise modalities work to reverse these changes. A key factor that will be described is the efficiency of mitochondrial coupling—ATP production relative to O2 uptake in myocytes and how that efficiency is a main driver for age-associated decline in skeletal muscle function. With that, we postulate the most effective exercise modality and protocol for reversing the molecular hallmarks of skeletal muscle aging and staving off sarcopenia. Two other concepts pertinent to mitochondrial efficiency in exercise-trained skeletal muscle will be integrated in this review, including- mitophagy, the removal of dysfunctional mitochondrial via autophagy, as well as the implications of muscle fiber type changes with sarcopenia on mitochondrial function.

scholarly journals Biological Aspects of Selected Myokines in Skeletal Muscle: Focus on Aging

2021 ◽  
Vol 22 (16) ◽  
pp. 8520
Author(s):  
Rosa Mancinelli ◽  
Franco Checcaglini ◽  
Francesco Coscia ◽  
Paola Gigliotti ◽  
Stefania Fulle ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Potential Role ◽  
Immunological Response ◽  
Active Lifestyle ◽  
Muscle Aging ◽  
Biological Aspects ◽  
Skeletal Muscle Aging ◽  
Cellular Components ◽  
Proteins And Peptides

In the last decade, clear evidence has emerged that the cellular components of skeletal muscle are important sites for the release of proteins and peptides called “myokines”, suggesting that skeletal muscle plays the role of a secretory organ. After their secretion by muscles, these factors serve many biological functions, including the exertion of complex autocrine, paracrine and/or endocrine effects. In sum, myokines affect complex multi-organ processes, such as skeletal muscle trophism, metabolism, angiogenesis and immunological response to different physiological (physical activity, aging, etc.) or pathological states (cachexia, dysmetabolic conditions, chronic inflammation, etc.). The aim of this review is to describe in detail a number of myokines that are, to varying degrees, involved in skeletal muscle aging processes and belong to the group of proteins present in the functional environment surrounding the muscle cell known as the “Niche”. The particular myokines described are those that, acting both from within the cell and in an autocrine manner, have a defined relationship with the modulation of oxidative stress in muscle cells (mature or stem) involved in the regulatory (metabolic or regenerative) processes of muscle aging. Myostatin, IGF-1, NGF, S100 and irisin are examples of specific myokines that have peculiar features in their mechanisms of action. In particular, the potential role of one of the most recently characterized myokines—irisin, directly linked to an active lifestyle—in reducing if not reversing senescence-induced oxidative damage is discussed in terms of its possible application as an agent able to counteract the deleterious effects of muscle aging.

scholarly journals Lifelong Ulk1-mediated autophagy deficiency in muscle induces mitochondrial dysfunction and contractile weakness

2020 ◽  
Author(s):  
Anna S. Nichenko ◽  
Jacob R. Sorensen ◽  
W. Michael Southern ◽  
Anita E. Qualls ◽  
Albino G. Schifino ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Tibialis Anterior Muscle ◽  
Metabolic Function ◽  
Metabolic Dysfunction ◽  
Cross Sectional ◽  
Mouse Muscle ◽  
Muscle Aging ◽  
Age Related ◽  
Skeletal Muscle Aging

AbstractThe accumulation of damaged mitochondria due to insufficient autophagy has been implicated in the pathophysiology of sarcopenia resulting in reduced contractile and metabolic function. Ulk1 is an autophagy-related kinase that initiates autophagosome assembly and may also play a role in autophagosome degradation (i.e., autophagy flux), but the contribution of Ulk1 to healthy muscle aging is unclear. We found that Ulk1 phosphorylation declines in both human and mouse muscle tissue with age, therefore the purpose of this study was to investigate the role of Ulk1-mediated autophagy in skeletal muscle aging. At age 22 months (80% survival rate), muscle contractile and metabolic function were assessed using electrophysiology in muscle specific Ulk1 knockout mice (MKO) and their littermate controls (LM). Specific peak-isometric torque of the ankle dorsiflexors (normalized by tibialis anterior muscle cross-sectional area) and specific force of the fast-twitch extensor digitorum longus muscles were reduced in MKO mice compared to LM mice (p<0.03). Permeabilized muscle fibers from MKO mice had greater mitochondrial content, yet lower mitochondrial oxygen consumption and greater reactive oxygen species production compared to fibers from LM mice (p≤ 0.04). Altered neuromuscular junction innervation patterns and changes in autophagosome numbers and/or flux in muscles from MKO may have contributed to decrements in contractile and metabolic function. Results from this study support an important role of Ulk1-mediated autophagy in skeletal muscle with age, reflecting Ulk1’s dual role in maintaining mitochondrial integrity through autophagosome assembly and degradation. A lifetime of insufficient Ulk-1-mediated autophagy in skeletal muscle exacerbates age-related contractile and metabolic dysfunction.

scholarly journals Advanced Glycation End-Products in Skeletal Muscle Aging

2021 ◽  
Vol 8 (11) ◽  
pp. 168
Author(s):  
Lucas C. Olson ◽  
James T. Redden ◽  
Zvi Schwartz ◽  
David J. Cohen ◽  
Michael J. McClure
Keyword(s):  
Skeletal Muscle ◽  
Advanced Glycation End Products ◽  
Future Research ◽  
Cross Linking ◽  
Advanced Glycation ◽  
Muscle Aging ◽  
Glycation End Products ◽  
End Products ◽  
Skeletal Muscle Aging

Advanced age causes skeletal muscle to undergo deleterious changes including muscle atrophy, fast-to-slow muscle fiber transition, and an increase in collagenous material that culminates in the age-dependent muscle wasting disease known as sarcopenia. Advanced glycation end-products (AGEs) non-enzymatically accumulate on the muscular collagens in old age via the Maillard reaction, potentiating the accumulation of intramuscular collagen and stiffening the microenvironment through collagen cross-linking. This review contextualizes known aspects of skeletal muscle extracellular matrix (ECM) aging, especially the role of collagens and AGE cross-linking, and underpins the motor nerve’s role in this aging process. Specific directions for future research are also discussed, with the understudied role of AGEs in skeletal muscle aging highlighted. Despite more than a half century of research, the role that intramuscular collagen aggregation and cross-linking plays in sarcopenia is well accepted yet not well integrated with current knowledge of AGE’s effects on muscle physiology. Furthermore, the possible impact that motor nerve aging has on intramuscular cross-linking and muscular AGE levels is posited.

scholarly journals Aging Triggers H3K27 Trimethylation Hoarding in the Chromatin of Nothobranchius furzeri Skeletal Muscle

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1169 ◽  
Author(s):  
Chiara Cencioni ◽  
Johanna Heid ◽  
Anna Krepelova ◽  
Seyed Mohammad Mahdi Rasa ◽  
Carsten Kuenne ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Skeletal Muscle Function ◽  
Muscle Aging ◽  
Aging Studies ◽  
Nothobranchius Furzeri ◽  
Landscape Alteration ◽  
Epigenetic Analysis ◽  
Skeletal Muscle Aging ◽  
Reduced Mobility

Aging associates with progressive loss of skeletal muscle function, sometimes leading to sarcopenia, a process characterized by impaired mobility and weakening of muscle strength. Since aging associates with profound epigenetic changes, epigenetic landscape alteration analysis in the skeletal muscle promises to highlight molecular mechanisms of age-associated alteration in skeletal muscle. This study was conducted exploiting the short-lived turquoise killifish Nothobranchius furzeri (Nfu), a relatively new model for aging studies. The epigenetic analysis suggested a less accessible and more condensed chromatin in old Nfu skeletal muscle. Specifically, an accumulation of heterochromatin regions was observed as a consequence of increased levels of H3K27me3, HP1α, polycomb complex subunits, and senescence-associated heterochromatic foci (SAHFs). Consistently, euchromatin histone marks, including H3K9ac, were significantly reduced. In this context, integrated bioinformatics analysis of RNASeq and ChIPSeq, related to skeletal muscle of Nfu at different ages, revealed a down-modulation of genes involved in cell cycle, differentiation, and DNA repair and an up-regulation of inflammation and senescence genes. Undoubtedly, more studies are needed to disclose the detailed mechanisms; however, our approach enlightened unprecedented features of Nfu skeletal muscle aging, potentially associated with swimming impairment and reduced mobility typical of old Nfu.

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