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Biomolecules Oct 2019Sarcopenia is characterized by a loss of muscle mass, quality, and function, and negatively impacts health, functionality, and quality of life for numerous populations,... (Review)
Review
Sarcopenia is characterized by a loss of muscle mass, quality, and function, and negatively impacts health, functionality, and quality of life for numerous populations, particularly older adults. Creatine is an endogenously produced metabolite, which has the theoretical potential to counteract many of the morphological and metabolic parameters underpinning sarcopenia. This can occur through a range of direct and indirect mechanisms, including temporal and spatial functions that accelerate ATP regeneration during times of high energy demand, direct anabolic and anti-catabolic functions, and enhanced muscle regenerating capacity through positively impacting muscle stem cell availability. Studies conducted in older adults show little benefit of creatine supplementation alone on muscle function or mass. In contrast, creatine supplementation as an adjunct to exercise training seems to augment the muscle adaptive response to the training stimulus, potentially through increasing capacity for higher intensity exercise, and/or by enhancing post-exercise recovery and adaptation. As such, creatine may be an effective dietary strategy to combat age-related muscle atrophy and sarcopenia when used to complement the benefits of exercise training.
Topics: Aged; Aging; Animals; Creatine; Dietary Supplements; Exercise; Humans; Muscular Atrophy
PubMed: 31652853
DOI: 10.3390/biom9110642 -
Journal of Applied Physiology... Apr 2023Age-related skeletal muscle atrophy appears to be a muscle group-specific process, yet only a few specific muscles have been investigated and our understanding in this... (Review)
Review
Age-related skeletal muscle atrophy appears to be a muscle group-specific process, yet only a few specific muscles have been investigated and our understanding in this area is limited. This review provides a comprehensive summary of the available information on age-related skeletal muscle atrophy in a muscle-specific manner, nearly half of which comes from the quadriceps. Decline in muscle-specific size over ∼50 yr of aging was determined from 47 cross-sectional studies of 982 young (∼25 yr) and 1,003 old (∼75 yr) individuals and nine muscle groups: elbow extensors (-20%, -0.39%/yr), elbow flexors (-19%, -0.38%/yr), paraspinals (-24%, -0.47%/yr), psoas (-29%, -0.58%/yr), hip adductors (-13%, -0.27%/yr), hamstrings (-19%, -0.39%/yr), quadriceps (-27%, -0.53%/yr), dorsiflexors (-9%, -0.19%/yr), and triceps surae (-14%, -0.28%/yr). Muscle-specific atrophy rate was also determined for each of the subcomponent muscles in the hamstrings, quadriceps, and triceps surae. Of all the muscles included in this review, there was more than a fivefold difference between the least (-6%, -0.13%/yr, soleus) to the most (-33%, -0.66%/yr, rectus femoris) atrophying muscles. Muscle activity level, muscle fiber type, sex, and timeline of the aging process all appeared to have some influence on muscle-specific atrophy. Given the large range of muscle-specific atrophy and the large number of muscles that have not been investigated, more muscle-specific information could expand our understanding of functional deficits that develop with aging and help guide muscle-specific interventions to improve the quality of life of aging women and men.
Topics: Male; Humans; Female; Cross-Sectional Studies; Quality of Life; Muscle, Skeletal; Aging; Muscular Atrophy
PubMed: 36825643
DOI: 10.1152/japplphysiol.00768.2022 -
Nutrients Jan 2020Modifications of lean mass are a frequent critical determinant in the pathophysiology and progression of heart failure (HF). Sarcopenia may be considered one of the most... (Review)
Review
Modifications of lean mass are a frequent critical determinant in the pathophysiology and progression of heart failure (HF). Sarcopenia may be considered one of the most important causes of low physical performance and reduced cardiorespiratory fitness in older patients with HF. Sarcopenia is frequently misdiagnosed as cachexia. However, muscle wasting in HF has different pathogenetic features in sarcopenic and cachectic conditions. HF may induce sarcopenia through common pathogenetic pathways such as hormonal changes, malnutrition, and physical inactivity; mechanisms that influence each other. In the opposite way, sarcopenia may favor HF development by different mechanisms, including pathological ergoreflex. Paradoxically, sarcopenia is not associated with a sarcopenic cardiac muscle, but the cardiac muscle shows a hypertrophy which seems to be "not-functional." First-line agents for the treatment of HF, physical activity and nutritional interventions, may offer a therapeutic advantage in sarcopenic patients irrespective of HF. Thus, sarcopenia is highly prevalent in patients with HF, contributing to its poor prognosis, and both conditions could benefit from common treatment strategies based on pharmacological, physical activity, and nutritional approaches.
Topics: Aged; Aged, 80 and over; Female; Heart; Heart Failure; Humans; Hypertrophy; Male; Muscle, Skeletal; Muscular Atrophy; Nutritional Status; Prognosis; Sarcopenia
PubMed: 31947528
DOI: 10.3390/nu12010211 -
Medicina (Kaunas, Lithuania) Jun 2022Vulvovaginal atrophy (VVA) is a chronic progressive disease involving the female genital apparatus and lower urinary tract. This condition is related to hypoestrogenism... (Review)
Review
Vulvovaginal atrophy (VVA) is a chronic progressive disease involving the female genital apparatus and lower urinary tract. This condition is related to hypoestrogenism consequent to menopause onset but is also due to the hormonal decrease after adjuvant therapy for patients affected by breast cancer. Considering the high prevalence of VVA and the expected growth of this condition due to the increase in the average age of the female population, it is easy to understand its significant social impact. VVA causes uncomfortable disorders, such as vaginal dryness, itching, burning, and dyspareunia, and requires constant treatment, on cessation of which symptoms tend to reappear. The currently available therapies include vaginal lubricants and moisturizers, vaginal estrogens and dehydroepiandrosterone (DHEA), systemic hormone therapy, and Ospemifene. Considering, however, that such therapies have some problems that include contraindications, ineffectiveness, and low compliance, finding an innovative, effective, and safe treatment is crucial. The present data suggest great efficacy and safety of a vaginal laser in the treatment of genital symptoms and improvement in sexual function in patients affected by VVA. The beneficial effect tends to be sustained over the long-term, and no serious adverse events have been identified. The aim of this review is to report up-to-date efficacy and safety data of laser energy devices, in particular the microablative fractional carbon dioxide laser and the non-ablative photothermal Erbium-YAG laser.
Topics: Atrophy; Female; Humans; Lasers, Gas; Menopause; Treatment Outcome; Vagina; Vaginal Diseases
PubMed: 35744033
DOI: 10.3390/medicina58060770 -
Biomedicine & Pharmacotherapy =... Jul 2021Muscle atrophy and weakness are the adverse effects of long-term or high dose usage of glucocorticoids. In the present study, we explored the effects of fucoxanthin...
Muscle atrophy and weakness are the adverse effects of long-term or high dose usage of glucocorticoids. In the present study, we explored the effects of fucoxanthin (10 μM) on dexamethasone (10 μM)-induced atrophy in C2C12 myotubes and investigated its underlying mechanisms. The diameter of myotubes was observed under a light microscope, and the expression of myosin heavy chain (MyHC), proteolysis-related, autophagy-related, apoptosis-related, and mitochondria-related proteins was analyzed by western blots or immunoprecipitation. Fucoxanthin alleviates dexamethasone-induced muscle atrophy in C2C12 myotubes, indicated by increased myotubes diameter and expression of MyHC, decreased expression of muscle atrophy F-box (Atrogin-1) and muscle ring finger 1 (MuRF1). Through activating SIRT1, fucoxanthin inhibits forkhead box O (FoxO) transcriptional activity to reduce protein degradation, induces autophagy to enhance degraded protein clearance, promotes mitochondrial function and diminishes apoptosis. In conclusion, we identified fucoxanthin ameliorates dexamethasone induced C2C12 myotubes atrophy through SIRT1 activation.
Topics: Animals; Apoptosis; Atrophy; Autophagy; Cell Line; Cell Survival; Dexamethasone; Forkhead Box Protein O3; Mice; Muscle Fibers, Skeletal; Proto-Oncogene Proteins c-akt; Sirtuin 1; Xanthophylls
PubMed: 33865017
DOI: 10.1016/j.biopha.2021.111590 -
Journal of Gastroenterology Oct 2019Sarcopenia (severe muscle depletion) is a prevalent muscle abnormality in patients with cirrhosis that confers poor prognosis both pre- and post-liver transplantation.... (Review)
Review
Sarcopenia (severe muscle depletion) is a prevalent muscle abnormality in patients with cirrhosis that confers poor prognosis both pre- and post-liver transplantation. The pathogenesis of sarcopenia is multifactorial and results from an imbalance between protein synthesis and breakdown. Nutritional, metabolic, and biochemical abnormalities seen in chronic liver disease alter whole body protein homeostasis. Hyperammonemia, increased autophagy, proteasomal activity, lower protein synthesis, and impaired mitochondrial function play an important role in muscle depletion in cirrhosis. Factors including cellular energy status, availability of metabolic substrates (e.g., branched-chain amino acids), alterations in the endocrine system (insulin resistance, circulating levels of insulin, insulin-like growth factor-1, corticosteroids, and testosterone), cytokines, myostatin, and exercise are involved in regulating muscle mass. A favored atrophy of type II fast-twitch glycolytic fibers seems to occur in patients with cirrhosis and sarcopenia. Identification of muscle biological abnormalities and underlying mechanisms is required to plan clinical trials to reverse sarcopenia through modulation of specific mechanisms. Accordingly, a combination of nutritional, physical, and pharmacological interventions might be necessary to reverse sarcopenia in cirrhosis. Moderate exercise should be combined with appropriate energy and protein intake, in accordance with clinical guidelines. Interventions with branched chain amino acids, testosterone, carnitine, or ammonia-lowering therapies should be considered individually. Various factors such as dose, type, duration of supplementations, etiology of cirrhosis, amount of dietary protein intake, and compliance with supplementation and exercise should be the focus of future large randomized controlled trials investigating both prevention and treatment of sarcopenia in this patient population.
Topics: Animals; Disease Models, Animal; Humans; Hyperammonemia; Liver Cirrhosis; Malnutrition; Muscle Proteins; Muscle, Skeletal; Muscular Atrophy; Risk Factors; Sarcopenia
PubMed: 31392488
DOI: 10.1007/s00535-019-01605-6 -
Cellular Signalling Aug 2022Muscle atrophy and sarcopenia (the term given to the age-related decline in muscle mass and function), influence an individuals risk of falls, frailty, functional... (Review)
Review
Muscle atrophy and sarcopenia (the term given to the age-related decline in muscle mass and function), influence an individuals risk of falls, frailty, functional decline, and, ultimately, impaired quality of life. Vitamin D deficiency (low serum levels of 25-hydroxyvitamin D (25(OH)D)) has been reported to impair muscle strength and increase risk of sarcopenia. The mechanisms that underpin the link between low 25(OH)D and sarcopenia are yet to be fully understood but several lines of evidence have highlighted the importance of both genomic and non-genomic effects of active vitamin D (1,25-dihydroxyvitamin D (1,25(OH)D)) and its nuclear vitamin D receptor (VDR), in skeletal muscle functioning. Studies in vitro have demonstrated a key role for the vitamin D/VDR axis in regulating biological processes central to sarcopenic muscle atrophy, such as proteolysis, mitochondrial function, cellular senescence, and adiposity. The aim of this review is to provide a mechanistic overview of the proposed mechanisms for the vitamin D/VDR axis in sarcopenic muscle atrophy.
Topics: Humans; Muscle, Skeletal; Muscular Atrophy; Quality of Life; Receptors, Calcitriol; Sarcopenia; Vitamin D
PubMed: 35595176
DOI: 10.1016/j.cellsig.2022.110355 -
Cell Death & Disease May 2023Astrocyte atrophy is the main histopathological hallmark of major depressive disorder (MDD) in humans and in animal models of depression. Here we show that...
Astrocyte atrophy is the main histopathological hallmark of major depressive disorder (MDD) in humans and in animal models of depression. Here we show that electroacupuncture prevents astrocyte atrophy in the prefrontal cortex and alleviates depressive-like behaviour in mice subjected to chronic unpredictable mild stress (CUMS). Treatment of mice with CUMS induced depressive-like phenotypes as confirmed by sucrose preference test, tail suspension test, and forced swimming test. These behavioural changes were paralleled with morphological atrophy of astrocytes in the prefrontal cortex, revealed by analysis of 3D reconstructions of confocal Z-stack images of mCherry expressing astrocytes. This morphological atrophy was accompanied by a decrease in the expression of cytoskeletal linker Ezrin, associated with formation of astrocytic leaflets, which form astroglial synaptic cradle. Electroacupuncture at the acupoint ST36, as well as treatment with anti-depressant fluoxetine, prevented depressive-like behaviours, astrocytic atrophy, and down-regulation of astrocytic ezrin. In conclusion, our data further strengthen the notion of a primary role of astrocytic atrophy in depression and reveal astrocytes as cellular target for electroacupuncture in treatment of depressive disorders.
Topics: Humans; Mice; Animals; Depression; Antidepressive Agents; Astrocytes; Depressive Disorder, Major; Electroacupuncture; Hippocampus; Atrophy; Disease Models, Animal
PubMed: 37248211
DOI: 10.1038/s41419-023-05839-4 -
International Journal of Molecular... Nov 2021Skin aging is a complex process influenced by intrinsic and extrinsic factors. Together, these factors affect the structure and function of the epidermis and dermis.... (Review)
Review
Skin aging is a complex process influenced by intrinsic and extrinsic factors. Together, these factors affect the structure and function of the epidermis and dermis. Histologically, aging skin typically shows epidermal atrophy due to decreased cell numbers. The dermis of aged skin shows decreased numbers of mast cells and fibroblasts. Fibroblast senescence contributes to skin aging by secreting a senescence-associated secretory phenotype, which decreases proliferation by impairing the release of essential growth factors and enhancing degradation of the extracellular matrix through activation of matrix metalloproteinases (MMPs). Several molecular mechanisms affect skin aging including telomere shortening, oxidative stress and MMP, cytokines, autophagic control, microRNAs, and the microbiome. Accumulating evidence on the molecular mechanisms of skin aging has provided clinicians with a wide range of therapeutic targets for treating aging skin.
Topics: Atrophy; Cell Proliferation; Cellular Senescence; Epidermal Cells; Fibroblasts; Humans; Mast Cells; Matrix Metalloproteinases; Skin Aging; Telomere Shortening
PubMed: 34830368
DOI: 10.3390/ijms222212489 -
International Journal of Molecular... Sep 2020Sarcopenia is primarily characterized by skeletal muscle disturbances such as loss of muscle mass, quality, strength, and physical performance. It is commonly seen in... (Review)
Review
Sarcopenia is primarily characterized by skeletal muscle disturbances such as loss of muscle mass, quality, strength, and physical performance. It is commonly seen in elderly patients with chronic diseases. The prevalence of sarcopenia in chronic heart failure (HF) patients amounts to up to 20% and may progress into cardiac cachexia. Muscle wasting is a strong predictor of frailty and reduced survival in HF patients. Despite many different techniques and clinical tests, there is still no broadly available gold standard for the diagnosis of sarcopenia. Resistance exercise and nutritional supplementation represent the currently most used strategies against wasting disorders. Ongoing research is investigating skeletal muscle mitochondrial dysfunction as a new possible target for pharmacological compounds. Novel agents such as synthetic ghrelin and selective androgen receptor modulators (SARMs) seem promising in counteracting muscle abnormalities but their effectiveness in HF patients has not been assessed yet. In the last decades, many advances have been accomplished but sarcopenia remains an underdiagnosed pathology and more efforts are needed to find an efficacious therapeutic plan. The purpose of this review is to illustrate the current knowledge in terms of pathogenesis, diagnosis, and treatment of sarcopenia in order to provide a better understanding of wasting disorders occurring in chronic heart failure.
Topics: Aged; Aged, 80 and over; Cachexia; Chronic Disease; Exercise; Heart Failure; Humans; Middle Aged; Muscle Strength; Muscle, Skeletal; Muscular Atrophy; Sarcopenia
PubMed: 32911600
DOI: 10.3390/ijms21186549