Corrigendum: Exosomes as a delivery tool of exercise-induced beneficial factors for the prevention and treatment of cardiovascular disease: a systematic review and meta-analysis.

[This corrects the article DOI: 10.3389/fphys.2023.1190095.].

Exercise Regulates Myokines in Aging-Related Diseases through Muscle-Brain Crosstalk.

BACKGROUND: The related functions of skeletal muscle and brain decrease significantly with age, and muscle-brain-related diseases are primarily associated with each other. Exercise can promote the secretion of myokines in skeletal muscle, showing a beneficial effect on the function of both, reflecting muscle-brain crosstalk. However, the key mechanism of action of exercise-regulated myokines in muscle-brain diseases remains unclear. SUMMARY: This review is intended to sort out and explore the key mechanism of the effect of exercise regulatory myokines on muscle-brain diseases through summarizing the relevant literature on the level of motor regulatory myokines in recent years and pay special attention to the impact of exercise type, intensity, and duration on myokine expression levels. KEY MESSAGES: The mechanism by which exercise regulates myokine levels in muscle-brain diseases is explained, and an effective exercise prescription for myokine expression that is more suitable for the elderly based on relevant literature is proposed. This work may hold certain value for subsequent exercise treatment of chronic diseases in the elderly and for further research on muscle-brain crosstalk.

Effects of Multi-Task Mode on Cognition and Lower Limb Function in Frail Older Adults: A Systematic Search and Review.

The application of multi-tasking (MT), especially dual-tasking (DT), in frail older adults is currently gaining attention. The aim was to review the application of the MT mode on cognition and lower limb function in frail older adults, including the MT test and MT training. By searching five electronic databases, Scopus, PubMed, PEDro, Web of Science and the Chinese electronic database, a total of 18 studies were finally included in this study, with 7 articles on MT testing and 11 articles on MT training. The results of the study showed that the current testing and training of MT is mainly based on the DT mode, with a wide variety of test types and protocols, as well as a variety of outcomes. The included studies suggested that DT can be used as a test to assess cognitive and lower limb function in the frail population and that an MT (DT) training program with an intervention period of ≥3 months or a duration of ≥60 min per session could improve cognitive and lower limb function in the frail population, thereby reducing the risk of falls. Further research is required to explore the effects of different types of MT and task prioritization in frail older adults.

Exosomes as a delivery tool of exercise-induced beneficial factors for the prevention and treatment of cardiovascular disease: a systematic review and meta-analysis.

Exercise-derived exosomes have been identified as novel players in mediating cell-to-cell communication in the beneficial effects of improving cardiovascular disease (CVD). This review aimed to systematically investigate exosomes as delivery tools for the benefits of exercise in the prevention and treatment of CVD and summarize these outcomes with an overview of their therapeutic implications. Among the 1417 articles obtained in nine database searches (PubMed, EBSCO, Embase, Web of Science, CENTRAL, Ovid, Science Direct, Scopus, and Wiley), 12 articles were included based on eligibility criteria. The results indicate that exercise increases the release of exosomes, increasing exosomal markers (TSG101, CD63, and CD81) and exosome-carried miRNAs (miR-125b-5p, miR-122-5p, miR-342-5p, miR-126, miR-130a, miR-138-5p, and miR-455). These miRNAs mainly regulate the expression of MAPK, NF-kB, VEGF, and Caspase to protect the cardiovascular system. Moreover, the outcome indicators of myocardial apoptosis and myocardial infarction volume are significantly reduced following exercise-induced exosome release, and angiogenesis, microvessel density and left ventricular ejection fraction are significantly increased, as well as alleviating myocardial fibrosis following exercise-induced exosome release. Collectively, these results further confirm that exercise-derived exosomes have a beneficial role in potentially preventing and treating CVD and support the use of exercise-derived exosomes in clinical settings.

Preparation of Hydrophobic Octadecylphosphonic Acid-Coated Magnetite Nanoparticles for the Demulsification of n-Hexane-in-Water Nanoemulsions.

To design more environmentally friendly, economical, and efficient demulsifiers for oily wastewater treatment, hydrophobic octadecylphosphonic acid (ODPA)-modified Fe3O4 nanoparticles (referred to as Fe3O4@ODPA) were prepared by condensation of hydroxyl groups between ODPA and Fe3O4 nanoparticles using the co-precipitation method. The prepared magnetite nanoparticles were characterized by X-ray diffraction (XRD), transmission electron microscopy (TEM), scanning electron microscope (SEM), Fourier transform infrared (FTIR) spectroscopy, and thermogravimetric/differential thermogravimetric (TG/DTG) analysis. The water contact angles (θW) of Fe3O4@ODPA nanoparticles were more than 120°, indicating hydrophobic nature, and the diameter of the obtained spherical-shaped magnetite nanoparticles was 12-15 nm. The ODPA coating amount (AO) (coating weight per gram Fe3O4) and specific surface area (SO) of Fe3O4@ODPA were 0.124-0.144 g·g-1 and 78.65-91.01 m2·g-1, respectively. To evaluate the demulsification ability, stability, and reusability, the magnetite nanoparticles were used to demulsify an n-hexane-in-water nanoemulsion. The effects of the magnetite nanoparticle dosage (CS), pH value of nanoemulsion, and NaCl or CaCl2 electrolytes on the demulsification efficiency (RO) were investigated. The RO of Fe3O4@ODPA samples was found to be higher than that of bare Fe3O4 samples (S0, ST, and SN) under all CS values. With the increase in CS, the RO of Fe3O4@ODPA samples initially increased and then approached equilibrium value at Cs = 80.0 g·L-1. A maximum RO of ~93% was achieved at CS = 100.0 g·L-1 for the Fe3O4@ODPA sample S2. The pH and two electrolytes had a minor effect on RO. The Fe3O4@ODPA nanoparticles maintained high RO even after being reused for demulsification 11 times. This indicates that the hydrophobic Fe3O4@ODPA samples can be used as an effective magnetite demulsifer for oil-in-water nanoemulsions.

Exercise suppresses neuroinflammation for alleviating Alzheimer's disease.

Alzheimer's disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of toxic and side effects, and it is an urgent task to explore the underlying mechanisms for the benefits to prevent and treat AD. Herein, based on animal experiments and a few clinical trials, neuroinflammation in AD is characterized by long-term activation of pro-inflammatory microglia and the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. Damaged signals from the periphery and within the brain continuously activate microglia, thus resulting in a constant source of inflammatory responses. The long-term chronic inflammatory response also exacerbates endoplasmic reticulum oxidative stress in microglia, which triggers microglia-dependent immune responses, ultimately leading to the occurrence and deterioration of AD. In this review, we systematically summarized and sorted out that exercise ameliorates AD by directly and indirectly regulating immune response of the central nervous system and promoting hippocampal neurogenesis to provide a new direction for exploring the neuroinflammation activity in AD.

MicroRNA profiling of different exercise interventions for alleviating skeletal muscle atrophy in naturally aging rats.

BACKGROUND: Exercise is an affordable and practical strategy to alleviate several detrimental outcomes from the aging process, including sarcopenia. The elucidation of molecular mechanisms to alleviate sarcopenia is one of the most important steps towards understanding human aging. Although microRNAs (miRNAs) regulate muscle growth, regeneration and aging, the potential role of exercise-mediated miRNAs during the prevention and rehabilitation of skeletal muscle atrophy upon exercise interventions remains unclear. METHODS: A miRNA profile by miRNA sequencing for gastrocnemius muscle of a 24-month-old aged male rat model mimicking the naturally aging process was established through screening the differentially expressed miRNAs (DEMs) for alleviating aging-induced skeletal muscle atrophy upon optimal exercise intervention. The screened miRNAs and hub genes, as well as biomarkers with the most significantly enriched pathways, were validated by quantitative real-time polymerase chain reaction and western blotting. RESULTS: The sarcopenia index (SI) value and cross-sectional area (CSA) of rats from the old control (OC) group significantly decreased when compared with the youth control (YC) group (P < 0.001, P < 0.01), whereas an increased SI value and an enlarged CSA of rats from the old-aerobic exercise (OE), old-resistance exercise (OR) and old-mixed exercise (OM) groups were determined (P < 0.01, P < 0.001, P < 0.05; P < 0.01, P < 0.01, P < 0.05). Our results demonstrate that 764 known miRNAs, 201 novel miRNAs and 505 miRNA-mRNA interaction networks were identified to be related to aging-induced muscular atrophy. Among them, 13 miRNAs were differentially expressed (P < 0.05 and log2 |fold change| > 1) between the YC group and the OC group. Compared with the OC group, 7, 2 and 11 miRNAs were differentially expressed in the OE, OR and OM groups after exercise interventions, respectively. Meanwhile, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that the identified DEMs were primarily related to apoptosis, autophagy and the NF-κB/MuRF1 signalling pathways (P < 0.05). Meanwhile, four DEMs (miR-7a-1-3p, miR-135a-5p, miR-151-5p and miR-196b-5p), six hub genes (Ar, Igf1, Hif1a, Bdnf, Fak and Nras) and several biomarkers (LC3, Beclin1, p62, Bax, Bcl-2 and NF-κB/MuRF1) with the most significantly enriched pathways were confirmed, which may play a key role in muscular atrophy during the aging process. CONCLUSIONS: These findings are closely correlated with the progression of sarcopenia and could act as potential biomarkers for the diagnosis and interventional monitoring of aging-induced skeletal muscle atrophy.

A Preclinical Systematic Review of the Effects of Chronic Exercise on Autophagy-Related Proteins in Aging Skeletal Muscle.

Background: Exercise is one of the most effective interventions for preventing and treating skeletal muscle aging. Exercise-induced autophagy is widely acknowledged to regulate skeletal muscle mass and delay skeletal muscle aging. However, the mechanisms underlying of the effect of different exercises on autophagy in aging skeletal muscle remain unclear. Methods: A systematic review was performed following an electronic search of SCOPUS, PubMed, Web of Science, ScienceDirect, and Google Scholar and two Chinese electronic databases, CNKI and Wan Fang. All articles published in English and Chinese between January 2010 and January 2022 that quantified autophagy-related proteins in aging skeletal muscle models. Results: The primary outcome was autophagy assessment, indicated by changes in the levels of any autophagy-associated proteins. A total of fifteen studies were included in the final review. Chronic exercise modes mainly comprise aerobic exercise and resistance exercise, and the intervention types include treadmill training, voluntary wheel running, and ladder training. LC3, Atg5-Atg7/9/12, mTOR, Beclin1, Bcl-2, p62, PGC-1α, and other protein levels were quantified, and the results showed that long-term aerobic exercise and resistance exercise could increase the expression of autophagy-related proteins in aging skeletal muscle (p < 0.05). However, there was no significant difference in short term or high-intensity chronic exercise, and different types and intensities of exercise yielded different levels of significance for autophagy-related protein expression. Conclusion: Existing evidence reveals that high-intensity exercise may induce excessive autophagy, while low-intensity exercise for a short period (Intervention duration <12 weeks, frequency <3 times/week) may not reach the threshold for exercise-induced autophagy. Precise control of the exercise dose is essential in the long term to maximize the benefits of exercise. Further investigation is warranted to explore the relationship between chronic exercise and different exercise duration and types to substantiate the delaying of skeletal muscle aging by exercise.

Ketogenic Diet Benefits to Weight Loss, Glycemic Control, and Lipid Profiles in Overweight Patients with Type 2 Diabetes Mellitus: A Meta-Analysis of Randomized Controlled Trails.

A ketogenic diet, characterized by low calories with high levels of fat, adequate levels of protein, and low levels of carbohydrates, has beneficial effects on body weight control in overweight patients. In the present study, a meta-analysis was conducted to investigate the role of a ketogenic diet in body weight control and glycemic management in overweight patients with type 2 diabetes mellitus (T2DM). In summary, we systematically reviewed articles from the Embase, PubMed, Web of Science and Cochrane Library databases and obtained eight randomized controlled trials for meta-analysis. The results show that a ketogenic diet had significantly beneficial effects on the loss of body weight (SMD, -5.63, p = 0.008), the reduction of waist circumference (SMD, -2.32, p = 0.04), lowering glycated hemoglobin (SMD, -0.38, p = 0.0008) and triglycerides (SMD, -0.36, p = 0.0001), and increasing high-density lipoproteins (SMD, 0.28, p = 0.003). Overall, these results suggest that a ketogenic diet may be an effective dietary intervention for body weight and glycemic control, as well as improved lipid profiles in overweight patients with T2DM. Hence, a ketogenic diet can be recommended for the therapeutic intervention of overweight patients with T2DM.

Analysis and Research on the Impact of Physical Exercise on Residents' Health Based on the Improved BP Neural Network Model.

With the rapid improvement of social economy and the enhancement of people's health awareness, it is necessary to make an in-depth analysis of the rationality of physical exercise and the physical quality of residents. Hence, this study aims to explore the algorithm optimization of the improved BP model to analyze the effect of exercise intervention on improving public sports effect. K-clustering and Levenberg-Marquardt algorithm were used to construct an improved BP neural network model to determine the sample clustering center, as well as the weight and threshold of the indicators, so as to optimize the analysis algorithm of improving public sports effect. MATLAB simulation shows that under the target error conditions of 0.01, 0.005, 0.001, and 0.0001, the target error rate and iteration times of the improved BP model are better than the standard BP model, and the time consumption is shorter, which can be conducive to more accurately analyzing the changes of improving public sports effect under exercise intervention. Therefore, the improved BP model can effectively solve the problems of data clustering and result error rate adjustment in the process of improving public sports effect analysis and improve the analysis speed and accuracy.

Irisin, an exercise-induced bioactive peptide beneficial for health promotion during aging process.

Irisin is an exercise-induced myokine expressed as a bioactive peptide in multiple tissues and organs, and exercise and cold exposure are the major inducers for its secretion. Irisin presents a decreasing trend with the extension of age and is also closely associated with a wide range of aging-related diseases. Currently, many studies on irisin are being conducted with respect to physiological functions for health promotion, and the prevention, treatment and rehabilitation of chronic diseases, as well as mechanisms associated with improving energy metabolic balance, enhancing cellular homeostasis by optimizing autophagy, promoting mitochondrial quality control, reducing reactive oxygen species (ROS) production, and mitigating inflammatory responses. These diseases include: metabolic diseases (obesity, type 2 diabetes, and bone metabolism); cardiovascular diseases (hypertension, coronary heart disease, cardiomyopathy and stroke); nervous system diseases (Alzheimer's disease, Parkinson's disease, and stroke); and others (cancer and sarcopenia). Although the current studies on irisin are relatively extensive, some studies have produced unexplained experimental results. This article introduces an overview of the generation, secretion, and tissue distribution, of irisin, and its targeting of tissues or organs for the prevention and treatment of above-mentioned chronic diseases is systematically summarized, with discussion of the underlying molecular mechanisms. This study is expected to improve the understanding of irisin, which may be beneficial to identify novel and effective targets for the screening, diagnosis, or therapy of these chronic diseases, or develop promising interventional strategies, effective drug candidates, functional foods, or exercise mimetics.

The Potential Role of miRNA-Regulated Autophagy in Alzheimer's Disease.

As a neurodegenerative disease, Alzheimer's disease (AD) shows a higher incidence during the aging process, mainly revealing the characteristics of a significant decrease in cognition, uncontrolled emotion, and reduced learning and memory capacity, even leading to death. In the prevention and treatment of AD, some pharmacological therapy has been applied in clinical practice. Unfortunately, there are still limited effective treatments for AD due to the absence of clear and defined targets. Currently, it is recognized that the leading causes of AD include amyloid-ß peptide (Aß) deposition, hyperphosphorylation of tau protein, neurofibrillary tangles, mitochondrial dysfunction, and inflammation. With in-depth mechanistic exploration, it has been found that these causes are highly correlated with the dysfunctional status of autophagy. Numerous experimental results have also confirmed that the development and progression of AD is accompanied by an abnormal functional status of autophagy; therefore, regulating the functional status of autophagy has become one of the important strategies for alleviating or arresting the progression of AD. With the increasing attention given to microRNAs (miRNAs), more and more studies have found that a series of miRNAs are involved in the development and progression of AD through the indirect regulation of autophagy. Therefore, regulating autophagy through targeting these miRNAs may be an essential breakthrough for the prevention and treatment of AD. This article summarizes the regulation of miRNAs in autophagy, with the aim of providing a new theoretical reference point for the prevention and treatment of AD through the indirect regulation of miRNA-mediated autophagy.

Swimming Suppresses Cognitive Decline of HFD-Induced Obese Mice through Reversing Hippocampal Inflammation, Insulin Resistance, and BDNF Level.

Obesity is an important public health problem nowadays. Long-term obesity can trigger a series of chronic diseases and impair the learning and memory function of the brain. Current studies show that scientific exercise can effectively improve learning and memory capacity, which also can provide benefits for obese people. However, the underlying mechanisms for the improvement of cognitive capacity under the status of obesity still need to be further explored. In the present study, the obesity-induced cognition-declined model was established using 4-week-old mice continuously fed with a high-fat diet (HFD) for 12 weeks, and then the model mice were subjected to an 8-week swimming intervention and corresponding evaluation of relevant indicators, including cognitive capacity, inflammation, insulin signal pathway, brain-derived neurotrophic factor (BNDF), and apoptosis, for exploring potential regulatory mechanisms. Compared with the mice fed with regular diets, the obese mice revealed the impairment of cognitive capacity; in contrast, swimming intervention ameliorated the decline in cognitive capacity of obese mice by reducing inflammatory factors, inhibiting the JNK/IRS-1/PI3K/Akt signal pathway, and activating the PGC-1α/BDNF signal pathway, thereby suppressing the apoptosis of neurons. Therefore, swimming may be an important interventional strategy to compensate for obesity-induced cognitive impairment.

The effectiveness of traditional Chinese medicine-based exercise on physical performance, balance and muscle strength among older adults: a systematic review with meta-analysis.

BACKGROUND: Traditional Chinese medicine (TCM) based exercises have been widely used in the prevention and treatment of balance, cardiopulmonary, and other related diseases in older adults. However, there seems to be no consensus on the improvement and comparison of physical performance, balance, and muscle strength in the elderly population. OBJECTIVES: To systematically examine the impact of different TCM-based exercises on physical performance, balance, and muscle strength outcomes in the elderly. METHODS: We searched PubMed, EMBASE, Scopus, and Cochrane Center, CNKI and Wan Fang between their date of inception and March 2021. This meta-analysis was performed using RevMan5.3 software. Only randomized controlled trials (RCT) or controlled clinical trials (CCT) were considered in TCM-based exercises (Tai Chi, Ba Duan Jin, Qigong). The overall mean difference (MD) or standardized mean difference (SMD), and its 95% confidence interval (CI) were calculated. MAIN RESULTS: A total of 27 studies with 2580 older adults met the inclusion criteria. The pooled analysis indicated that Tai Chi could be more effective in Times up and go (TUG) (MD = - 2.62, 95% CI - 4.00 to - 1.24, P = 0.0002), 5 times sit-stand (MD = - 1.89; 95%CI - 3.38 to - 0.40; P = 0.01), and handgrip strength outcomes (SMD = 0.69; 95%CI 0.52-0.86; P < 0.0001) compared to Ba Duan Jin and Qigong. The older adults performing Qigong could have a better benefit in Single-bed balance (SLB) with eyes closed compared to Tai Chi and Ba Duan Jin (MD = 3.42; 95%CI 1.55 to 5.29; P = 0.0003). Tai Chi also had benefits in terms of balance outcomes compared to those in the control group: Berg Balance scale (BBS) (MD = 1.41; 95% CI 0.03-2.85; P = 0.05), Functional reach test (FRT) (MD = 1.57; 95%CI 1.22-1.93; P < 0.0001). The Tai Chi study meta-analysis demonstrated significant effects on lower limb strength: knee extension (SMD = 0.56; 95%CI 0.26-0.86; P = 0.0003), ankle dorsiflexion (SMD = 0.67; 95%CI 0.02-1.31; P = 0.04) compared to the controls. CONCLUSION: This systematic review reveals that TCM-based exercises can effectively improve physical performance outcomes, balance outcomes, and muscle strength in the elderly population. While there is limited evidence on the efficacy of other TCM-based lifestyle interventions, more high-quality clinical trials on this topic are warranted.

Exercise-Induced Benefits for Alzheimer's Disease by Stimulating Mitophagy and Improving Mitochondrial Function.

Neurons are highly specialized post-mitotic cells that are inherently dependent on mitochondria due to their higher bioenergetic demand. Mitochondrial dysfunction is closely associated with a variety of aging-related neurological disorders, such as Alzheimer's disease (AD), and the accumulation of dysfunctional and superfluous mitochondria has been reported as an early stage that significantly facilitates the progression of AD. Mitochondrial damage causes bioenergetic deficiency, intracellular calcium imbalance and oxidative stress, thereby aggravating ß-amyloid (Aß) accumulation and Tau hyperphosphorylation, and further leading to cognitive decline and memory loss. Although there is an intricate parallel relationship between mitochondrial dysfunction and AD, their triggering factors, such as Aß aggregation and hyperphosphorylated Tau protein and action time, are still unclear. Moreover, many studies have confirmed abnormal mitochondrial biosynthesis, dynamics and functions will present once the mitochondrial quality control is impaired, thus leading to aggravated AD pathological changes. Accumulating evidence shows beneficial effects of appropriate exercise on improved mitophagy and mitochondrial function to promote mitochondrial plasticity, reduce oxidative stress, enhance cognitive capacity and reduce the risks of cognitive impairment and dementia in later life. Therefore, stimulating mitophagy and optimizing mitochondrial function through exercise may forestall the neurodegenerative process of AD.

Lifelong Aerobic Exercise Alleviates Sarcopenia by Activating Autophagy and Inhibiting Protein Degradation via the AMPK/PGC-1α Signaling Pathway.

Sarcopenia is an aging-induced syndrome characterized by a progressive reduction of skeletal muscle mass and strength. Increasing evidence has attested that appropriate and scientific exercise could induce autophagy or optimize the functional status of autophagy, which plays a critical role in senescent muscular dystrophy. As a publicly recognized strategy for extending lifespan and improving the health of the elderly, the underlying mechanisms of lifelong regular aerobic exercise for the prevention of sarcopenia have not been fully elucidated. To explore the role of lifelong aerobic exercise in the beneficial regulation of autophagic signaling pathways in senescent skeletal muscle, the natural aging mice were used as the sarcopenia model and subjected to lifelong treadmill running to evaluate corresponding parameters related to skeletal muscle atrophy and autophagic signaling pathways. Compared with the young control mice, the aged mice showed a significant reduction in skeletal muscle mass, gastrocnemius muscle weight/body weight (GMW/BW) ratio, and cross-sectional areas (CSA) of skeletal muscle fibers (p < 0.01). In contrast, lifelong aerobic exercise effectively rescued these reduced biomarkers associated with muscle atrophy. Moreover, as shown in the activated AMPK/PGC-1α signaling pathway, lifelong aerobic exercise successfully prevented the aging-induced impairment of the ubiquitin-proteasome system (UPS), excessive apoptosis, defective autophagy, and mitochondrial dysfunction. The exercise-induced autophagy suppressed the key regulatory components of the UPS, inhibited excessive apoptosis, and optimized mitochondrial quality control, thereby preventing and delaying aging-induced skeletal muscle atrophy.

Exercise-Induced Autophagy Suppresses Sarcopenia Through Akt/mTOR and Akt/FoxO3a Signal Pathways and AMPK-Mediated Mitochondrial Quality Control.

Exercise training is one of the most effective interventional strategies for sarcopenia in aged people. Nevertheless, the underlying mechanisms are not well recognized. Increasing studies have reported abnormal regulation of autophagy in aged skeletal muscle. Our current study aims to explore the efficiency of exercise interventions, including treadmill exercise, resistance exercise, alternating exercise with treadmill running and resistance exercise, and voluntary wheel running, on 21-month-old rats with sarcopenia and to detect the underlying mechanisms. Results showed the declined mass of gastrocnemius muscle with deficient autophagy and excessive apoptosis as a result of up-regulated Atrogin-1 and MuRF1, declined Beclin1 level and LC3-II/LC3-I ratio, accumulated p62, increased Bax, and reduced Bcl-2 levels, and also exhibited a defective mitochondrial quality control due to declined PGC-1α, Mfn2, Drp1, and PINK1 levels. However, 12-week exercise interventions suppressed the decline in mass loss of skeletal muscle, accompanied by down-regulated Atrogin-1 and MuRF1, increased Beclin1 level, improved LC3-II/LC3-I ratio, declined p62 level, and reduced Bax and increased Bcl-2 level, as well as enhanced mitochondrial function due to the increased PGC-1α, Mfn2, Drp1, and PINK1 levels. Moreover, exercise interventions also down-regulated the phosphorylation of Akt, mTOR, and FoxO3a, and up-regulated phosphorylated AMPK to regulate the functional status of autophagy and mitochondrial quality control. Therefore, exercise-induced autophagy is beneficial for remedying sarcopenia by modulating Akt/mTOR and Akt/FoxO3a signal pathways and AMPK-mediated mitochondrial quality control, and resistance exercise exhibits the best interventional efficiency.

[Regulatory roles of microRNAs in sarcopenia and exercise intervention].

Sarcopenia is an age-related degenerative disease, in which skeletal muscle mass and function are reduced during aging process. Physical intervention is one of the most effective strategies available for the treatment of sarcopenia. Studies have shown that microRNAs (miRNAs), as important regulators of gene expression, play an important role in maintaining the homeostasis of senescent skeletal muscle cells by regulating skeletal muscle cell development (proliferation and differentiation), mitochondrial biogenesis, protein synthesis and degradation, inflammatory response and metabolic pathways. Furthermore, exercise can combat age-related changes in muscle mass, composition and function, which is associated with the changes in the expression and biological functions of miRNAs in skeletal muscle cells. In this article, we systematically review the regulatory mechanisms of miRNAs in skeletal muscle aging, and discuss the regulatory roles and molecular targets of exercise-mediated miRNAs in muscular atrophy during aging process, which may provide novel insights into the prevention and treatment of sarcopenia.

Do not neglect the role of circadian rhythm in muscle atrophy.

In addition to its role in movement, human skeletal muscle also plays important roles in physiological activities related to metabolism and the endocrine system. Aging and disease onset and progression can induce the reduction of skeletal muscle mass and function, thereby exacerbating skeletal muscle atrophy. Recent studies have confirmed that skeletal muscle atrophy is mainly controlled by the balance between protein synthesis and degradation, the activation of satellite cells, and mitochondrial quality in skeletal muscle. Circadian rhythm is an internal rhythm related to an organism's adaptation to light-dark or day-night cycles of the planet, and consists of a core biological clock and a peripheral biological clock. Skeletal muscle, as the most abundant tissue in the human body, is an essential part of the peripheral biological clock in humans. Increasing evidence has confirmed that maintaining a normal circadian rhythm can be beneficial for increasing protein content, improving mitochondrial quality, and stimulating regeneration and repairing of cells in skeletal muscle to prevent or alleviate skeletal muscle atrophy. In this review, we summarize the roles and underlying mechanisms of circadian rhythm in delaying skeletal muscle atrophy, which will provide a theoretical reference for incorporating aspects of circadian rhythm to the prevention and treatment of skeletal muscle atrophy.

Kinetic, thermodynamic and isotherm investigations of Cu2+ and Zn2+ adsorption on LiAl hydrotalcite-like compound.

LiAl hydrotalcite-like compound (LiAl HTlc) was synthesized via a hydrothermal method and used to adsorb Cu2+ and Zn2+ for investigating the adsorption characteristics of heavy metal cations. The X-Raydiffraction (XRD), fourier transform infrared spectroscopy (FTIR), scanning electron microscope (SEM) and transmission electron microscopy (TEM) characterizations revealed the interconnecting flower-like layered structure of LiAl HTlc. The adsorption kinetics and isotherms of Cu2+ and Zn2+ on LiAl HTlc agreed with the pseudo-second-order model and the Langmuir model at a given sorbent concentration (Cs), respectively. The Cs-effect on the adsorption kinetics and isotherms was observed, and the Langmuir-surface component activity (SCA) equation could be utilized to characterize the effect of Cs in the adsorption isotherms. The adsorption process was spontaneous and endothermic. The adsorption mechanism denoted that the adsorption process was controlled using two main mechanisms, i.e., surface complexation and isomorphic substitution. This is the first report, to the best of our knowledge, on the usage of LiAl HTlc for the removal of heavy metal cations Cu2+ and Zn2+ from a solution. LiAl HTlc is a promising sorbent for treating water containing heavy metal cations.