Protective Effect Of Exercise Research Articles

Protective Effect of Exercise Against Depression, Anxiety, and Stress Among University Students Based on Their Level of Academic Performance.

Background and Objectives: Certain lifestyle behaviors can act as either buffering or aggravating factors influencing the mental well-being of university students. The current investigation assessed the association between academic performance and the risk of anxiety, depression, and stress among university students and how physical activity might buffer the levels of these conditions. Materials and Methods: A cross-sectional design was utilized to reach a sample of university students from Saudi Arabia. Data about the demographics of the students, GPA, exercise regularity, and levels of anxiety, depression, and stress were collected. Logistic regression was performed to investigate the influence of exercise regularity on the presence of anxiety, depression, and stress, dividing the sample according to the GPA category. Result: A total of 506 students were recruited. The mean age of the students was 22 years, and 53% of the students were men. An assessment of the levels of depression, anxiety, and stress indicated that 60%, 57%, and 40% have abnormal levels of these conditions, respectively. Students with a GPA of "good" or lower exhibited higher levels of stress. Exercising regularly was associated with a protective effect against depression and stress (p < 0.05). However, the buffering effect of exercise was more apparent among students with a GPA of "very good" or above compared to students with lower academic achievement. Conclusions: The lack of a statistically significant association between physical activity regularity and mental well-being among students classified as low academic achievers may indicate the need for additional psychological support in addition to the promotion of a physically active lifestyle.

Exercise preconditioning mitigates brain injury after cerebral ischemia-reperfusion injury in rats by restraining TIMP1.

Cerebral ischemic disease is a common cerebrovascular disease, especially ischemic stroke. Exercise has protective functions on brain tissues following cerebral ischemia-reperfusion injury (CIRI), but its preventive effects and mechanisms in CIRI remain unclear. We aimed to investigate the effects and mechanisms of exercise preconditioning on CIRI. The middle cerebral artery occlusion (MCAO) operation was prepared to establish CIRI rats. All rats were randomized into the MCAO, exercise (exercise preconditioning plus MCAO operation), vector (exercise preconditioning, MCAO operation plus intraventricular injection of empty vector), and tissue inhibitor of metalloprotease 1 overexpression (OE-TIMP1, exercise preconditioning, MCAO operation plus intraventricular injection of OE-TIMP1) groups. The results indicated that exercise preconditioning suppressed approximately 66.67% of neurological deficit scores and 73.79% of TIMP1 mRNA expression in MCAO rats, which were partially offset by OE-TIMP1. The protective effects of exercise against neuron death status and cerebral infarction size in MCAO rats were reversed by OE-TIMP1. It also confirmed that exercise weakened apoptosis and oxidative stress damage, with notable increases of B-cell lymphoma-2, superoxide dismutase, and glutathione peroxidase production, and evident decreases of BCL2-associated X, caspase 3, and malondialdehyde in MCAO rats, while these effects were partially reversed by OE-TIMP1. Additionally, the inhibitory effects of exercise on the protein levels of TIMP1, hypoxia-inducible factor-alpha, vascular endothelial growth factor receptor 2, vascular endothelial growth factor, and neurogenic locus notch homolog protein 1 in MCAO rats were partially reversed by OE-TIMP1. Altogether, exercise preconditioning had protective effects on CIRI by restraining TIMP1, which provided new therapeutic strategies for preventing CIRI.

Exercise-Mediated Protection against Air Pollution-Induced Immune Damage: Mechanisms, Challenges, and Future Directions.

Air pollution, a serious risk factor for human health, can lead to immune damage and various diseases. Long-term exposure to air pollutants can trigger oxidative stress and inflammatory responses (the main sources of immune impairment) in the body. Exercise has been shown to modulate anti-inflammatory and antioxidant statuses, enhance immune cell activity, as well as protect against immune damage caused by air pollution. However, the underlying mechanisms involved in the protective effects of exercise on pollutant-induced damage and the safe threshold for exercise in polluted environments remain elusive. In contrast to the extensive research on the pathogenesis of air pollution and the preventive role of exercise in enhancing fitness, investigations into exercise resistance to injury caused by air pollution are still in their infancy. In this review, we analyze evidence from humans, animals, and cell experiments on the combined effects of exercise and air pollution on immune health outcomes, with an emphasis on oxidative stress, inflammatory responses, and immune cells. We also propose possible mechanisms and directions for future research on exercise resistance to pollutant-induced damage in the body. Furthermore, we suggest strengthening epidemiological studies at different population levels and investigations on immune cells to guide how to determine the safety thresholds for exercise in polluted environments.

Exercise Inhibits Doxorubicin-Induced Cardiotoxicity via Regulating B Cells.

Doxorubicin is an effective chemotherapeutic agent, but its use is limited by acute and chronic cardiotoxicity. Exercise training has been shown to protect against doxorubicin-induced cardiotoxicity, but the involvement of immune cells remains unclear. This study aimed to investigate the role of exercise-derived B cells in protecting against doxorubicin-induced cardiotoxicity and to further determine whether B cell activation and antibody secretion play a role in this protection. Mice that were administered with doxorubicin (5 mg/kg per week, 20 mg/kg cumulative dose) received treadmill running exercise. The adoptive transfer of exercise-derived splenic B cells to μMT-/- (B cell-deficient) mice was performed to elucidate the mechanism of B cell regulation that mediated the effect of exercise. Doxorubicin-administered mice that had undergone exercise training showed improved cardiac function, and low levels of cardiac apoptosis, atrophy, and fibrosis, and had reduced cardiac antibody deposition and proinflammatory responses. Similarly, B cell pharmacological and genetic depletion alleviated doxorubicin-induced cardiotoxicity, which phenocopied the protection of exercise. In vitro performed coculture experiments confirmed that exercise-derived B cells reduced cardiomyocyte apoptosis and fibroblast activation compared with control B cells. Importantly, the protective effect of exercise on B cells was confirmed by the adoptive transfer of splenic B cells from exercised donor mice to μMT-/- recipient mice. However, blockage of Fc gamma receptor IIB function using B cell transplants from exercised Fc gamma receptor IIB-/- mice abolished the protection of exercise-derived B cells against doxorubicin-induced cardiotoxicity. Mechanistically, we found that Fc gamma receptor IIB, an important B cell inhibitory receptor, responded to exercise and increased B cell activation threshold, which participated in exercise-induced protection against doxorubicin-induced cardiotoxicity. Our results demonstrate that exercise training protects against doxorubicin-induced cardiotoxicity by upregulating Fc gamma receptor IIB expression in B cells, which plays an important anti-inflammatory role and participates in the protective effect of exercise against doxorubicin-induced cardiotoxicity.

PREVALENCE AND ASSOCIATED FACTORS OF MALNUTRITION AMONG ELDERLY PATIENTS AT AN OUTPATIENT CLINIC, COMMUNITY HOSPITAL IN THAILAND: A CROSS-SECTIONAL STUDY

Background: The number of Thais aged 60 and older has increased dramatically, and this trend will continue, making Thailand an increasingly aging society in the coming decades. The nutritional state of the elderly should be a major priority because it harms mortality and quality of life.&#x0D; Methods: From August to September 2022, the prevalence and associated determinants of malnutrition were determined based on a survey and hospital records using the Mini Nutritional Assessment (MNA®) as a screening tool for malnutrition among the elderly attending the outpatient department at Bangkhla Hospital. Multinomial regression analysis accounted for any confounding factors yielding an adjusted odds ratio (aOR) and 95% confidence intervals (95%CI).&#x0D; Results: This study enrolled a total of 91 individuals. Of these, 4.40% (95%CI= 0.01-0.11) of the participants were malnourished, while 18.70% (95%CI=0.11-0.28) were at risk of malnutrition. After controlling for potential confounding factors, a history of Covid-19 was associated with malnutrition (aOR=55.00, 95%CI= 2.70 to 1110.30), cancer (aOR= 25.80, 95%CI= 1.60-409.40) and gouty arthritis (aOR= 8.80, 95%CI= 1.20-59.60) was similarly associated with at risk of malnutrition. However, the protective effect of exercise was associated with malnutrition and risk of malnutrition, respectively (aOR= 0.04, 0.13, 95%CI= 0.00-0.80, 0.00-0.50).&#x0D; Conclusion: Overall, the study emphasized the significance of addressing malnutrition which was on the rise among the elderly in community hospitals in Thailand, especially in light of the aging population. Health professionals and policymakers should be aware of the various factors associated with malnutrition and strive to implement appropriate interventions to improve the nutritional status and quality of life of the elderly.

Insights into the development of insulin resistance: Unraveling the interaction of physical inactivity, lipid metabolism and mitochondrial biology.

While impairments in peripheral tissue insulin signalling have a well-characterized role in the development of insulin resistance and type 2 diabetes (T2D), the specific mechanisms that contribute to these impairments remain debatable. Nonetheless, a prominent hypothesis implicates the presence of a high-lipid environment, resulting in both reactive lipid accumulation and increased mitochondrial reactive oxygen species (ROS) production in the induction of peripheral tissue insulin resistance. While the etiology of insulin resistance in a high lipid environment is rapid and well documented, physical inactivity promotes insulin resistance in the absence of redox stress/lipid-mediated mechanisms, suggesting alternative mechanisms-of-action. One possible mechanism is a reduction in protein synthesis and the resultant decrease in key metabolic proteins, including canonical insulin signaling and mitochondrial proteins. While reductions in mitochondrial content associated with physical inactivity are not required for the induction of insulin resistance, this could predispose individuals to the detrimental effects of a high-lipid environment. Conversely, exercise-training induced mitochondrial biogenesis has been implicated in the protective effects of exercise. Given mitochondrial biology may represent a point of convergence linking impaired insulin sensitivity in both scenarios of chronic overfeeding and physical inactivity, this review aims to describe the interaction between mitochondrial biology, physical (in)activity and lipid metabolism within the context of insulin signalling.

Role of muscle FOXO gene in exercise against the skeletal muscle and cardiac age-related defects and mortality caused by high-salt intake in Drosophila

FOXO has long been associated with aging, exercise, and tissue homeostasis, but it remains unclear what the role is of the muscle FOXO gene in E against high-salt intake(HSI)-induced age-related defects of the skeletal muscle, heart, and mortality. In this research, overexpression and RNAi of the FOXO gene in the skeletal and heart muscle of Drosophila were constructed by building Mhc-GAL4/FOXO-UAS-overexpression and Mhc-GAL4/FOXO-UAS-RNAi system. The skeletal muscle and heart function, the balance of oxidation and antioxidant, and mitochondrial homeostasis were measured. The results showed that exercise reversed the age-related decline in climbing ability and downregulation of muscle FOXO expression induced by HSI. Muscle-specific FOXO-RNAi (FOXO-RNAi) and -overexpression (FOXO-OE) promoted or slowed the age-related decline in climbing ability, heart function, and skeletal muscle and heart structure damage, which was accompanied by the inhibition or activation of FOXO/PGC-1α/SDH and FOXO/SOD pathway activity, and oxidative stress (ROS) increased or decreased in both skeletal muscle and heart. The protective effect of exercise on the skeletal muscle and heart was blocked by FOXO-RNAi in aged HSI flies. FOXO-OE prolonged its lifespan, but it did not resist the HSI-induced lifespan shortening. Exercise did not improve HSI-induced lifespan shortening in FOXO-RNAi flies. Therefore, current results confirmed that the muscle FOXO gene played a vital role in exercise against age-related defects of the skeletal muscle and heart induced by HSI because it determined the activity of muscle FOXO/SOD and FOXO/PGC-1α/SDH pathways. The muscle FOXO gene also played an important role in exercise against HSI-induced mortality in aging flies.

Loss of cardiorespiratory fitness and its recovery following two weeks of head-down bed rest and the protective effects of exercise in 55- to 65-yr-old adults.

Cardiorespiratory fitness declines with age and this decline can be accelerated by inactivity and bed rest. Recovery of fitness is possible, but the timeline in 55- to 65-yr-old adults is unknown. Furthermore, the effectiveness of exercise to prevent deconditioning during bed rest is unexplored in this age group. Twenty-two adults (11 women, 59 ± 3 yr) completed 2 wk of strict 6° head-down bed rest (HDBR). Half of the participants performed approximately 1 h of daily exercises, including high-intensity interval cycling, aerobic cycling, and upper- and lower-body resistance training, whereas control participants were inactive. Step-incremental cycling tests to exhaustion were conducted pre-HDBR and at three times during the recovery phase (day 1 or 2, day 6, and 4 wk) to assess peak oxygen uptake (V̇o2). Peak V̇o2 was reduced in the control group throughout the first 6 days of recovery, but did return to pre-HDBR levels by the 4-wk recovery time point (interaction: P = 0.002). In the exercise group, peak V̇o2 was not different at any time point during recovery from pre-HDBR. Ventilatory threshold V̇o2 (interaction: P = 0.002) and heart rate at 15 W (interaction: P = 0.055) mirrored the changes in peak V̇o2 in each respective group. Overall, this study showed that approximately 1 h of daily exercise effectively protected 55- to 65-yr-old adults' cardiorespiratory fitness during 2 wk of HDBR. HDBR without exercise countermeasures caused substantial reductions in cardiorespiratory fitness, but fitness recovered within 4 wk of resuming daily activities. These findings highlight the importance of physical activity in late middle-age adults.NEW & NOTEWORTHY We report the complete time-course of cardiorespiratory fitness recovery back to baseline levels following 2 wk of head-down bed rest in 55- to 65-yr-old adults and found that multimodal training, consisting of high-intensity interval, aerobic and resistive exercises, performed throughout the 2 wk of head-down bed rest prevented reductions in cardiorespiratory fitness.

Transcriptional Profile of Exercise-Induced Protection Against Relapse to Cocaine Seeking in a Rat Model

BackgroundExercise has shown promise as a treatment for cocaine use disorder; however, the mechanism underlying its efficacy has remained elusive. MethodsWe used a rat model of relapse (cue-induced reinstatement) and exercise (wheel running, 2 hours/day) coupled with RNA sequencing to establish transcriptional profiles associated with the protective effects of exercise (during early withdrawal [days 1–7] or throughout withdrawal [days 1–14]) versus noneffective exercise (during late withdrawal [days 8–14]) against cocaine-seeking and sedentary conditions. ResultsAs expected, cue-induced cocaine seeking was highest in the sedentary and late-withdrawal exercise groups; both groups also showed upregulation of a Grin1-associated transcript and enrichment of Drd1-Nmdar1 complex and glutamate receptor complex terms. Surprisingly, these glutamate markers were also enriched in the early- and throughout-withdrawal exercise groups, despite lower levels of cocaine seeking. However, a closer examination of the Grin1-associated transcript revealed a robust loss of transcripts spanning exons 9 and 10 in the sedentary condition relative to saline controls that was normalized by early- and throughout-withdrawal exercise, but not late-withdrawal exercise, indicating that these exercise conditions may normalize RNA mis-splicing induced by cocaine seeking. Our findings also revealed novel mechanisms by which exercise initiated during early withdrawal may modulate glutamatergic signaling in dorsomedial prefrontal cortex (e.g., via transcripts associated with non-NMDA glutamate receptors or those affecting signaling downstream of NMDA receptors), along with mechanisms outside of glutamatergic signaling such as circadian rhythm regulation and neuronal survival. ConclusionsThese findings provide a rich resource for future studies aimed at manipulating these molecular networks to better understand how exercise decreases cocaine seeking.

Relationship between physical exercise and COVID-19 (SARS-CoV-2): systematic review.

The SARS-CoV virus is a precursor to the SARS-CoV-2 virus (COVID-19) and has caused millions of deaths worldwide. Although exercise can be a non-pharmacological means for the prevention and treatment of various diseases, the effects on COVID-19 patients are not yet completely clear. The aim of this study was to investigate the relationship between physical exercise and symptoms caused by COVID-19. The present systematic review was sent for evaluation and received the PROSPERO registration protocol-CRD42021257475. The search for studies related to health and physical exercise was carried out in the following databases; the "National Library in Medicine MEDLINE-Ovid", "Embase", "Web of Science", "SportDiscus-Ebsco", and "Scopus". Ten articles were included in the systematic review and the findings demonstrated the protective effects of physical exercise in patients with COVID-19. These effects were observed both in symptoms and in the period of hospitalization. In addition, the results show that the benefits of physical exercise seem to collaborate both in an individual manner and as an alternative to drug therapy. Finally, it was possible to verify the effect of physical exercise on variables, such as quality of life, cardiorespiratory capacity, and immunological biomarkers, and on the symptoms of the new Coronavirus. It is possible to conclude that physical exercise can be a component for the treatment of COVID-19. In addition, it could help to reduce the symptoms and severity of COVID-19, and may be considered as an adjunct to drug therapy in patients contaminated with SARS-CoV-2.

Impact of handgrip exercise and ischemic preconditioning on local and remote protection against endothelial reperfusion injury in young men.

Ischemic preconditioning (IPC), cyclical bouts of nonlethal ischemia, provides immediate protection against ischemic injury, which is evident both locally and remotely. Given the similarities in protective effects of exercise with ischemic preconditioning, we examined whether handgrip exercise also offers protection against endothelial ischemia-reperfusion (IR) injury and whether this protection is equally present in the local (exercised) and remote (contralateral, nonexercised) arm. Fifteen healthy males (age, 24 ± 3 yr; body mass index, 25 ± 2 kg/m2) attended the laboratory on three occasions. Bilateral brachial artery flow-mediated dilation (FMD) was examined at rest and after a temporary IR injury in the upper arm. Before the IR injury, in the dominant (local) arm, participants performed (randomized, counterbalanced): 1) 4 × 5 min unilateral handgrip exercise (50% maximal voluntary contraction), 2) 4 × 5 min unilateral IPC (220 mmHg), or 3) 4 × 5 min rest (control). Data were analyzed using repeated-measures general linear models. Allometrically scaled FMD declined after IR in the control condition (4.6 ± 1.3% to 2.2 ± 1.7%, P < 0.001), as well as following handgrip exercise (4.6 ± 1.6% to 3.4 ± 1.9%, P = 0.01), however, was significantly attenuated with IPC (4.5 ± 1.4% to 3.8 ± 3.5%, P = 0.14). There were no differences between the local and remote arm. Our findings reinforce the established protective effects of IPC in young, healthy males and also highlight a novel strategy to protect against IR injury with handgrip exercise, which warrants further study.

Investigation of the effects of swimming exercises in rats given acrylamide

Acrylamide is a toxic substance used in industrial and laboratory processes. Acrylamide exposure has a toxic effect on many systems. Protective mechanisms should be developed against the effects caused by acrylamide. In our study, we investigated whether exercise has a protective effect against the changes that acrylamide will cause in pancreas. 32 adult Sprague-Dawley male rats were used. Control group was given only saline. Exercise group was applied swimming exercise for 1hour daily for 4 weeks. Acrylamide group was given 50mg/kg acrylamide by gavage for 4 weeks. Acrylamide+exercise group was applied 50mg/kg acrylamide for 4 weeks and swimming exercise for 1hour daily. After the experiment, fasting blood glucose and oral glucose tolerance test measurements were performed. Then, blood and pancreas samples were taken. Acrylamide exposure caused an increase in fasting blood glucose and oral glucose tolerance, a decrease in insulin levels and oxidative stress in acrylamide group. In exercise group, these values were similar to control group and no significant change was observed in acrylamide+exercise group. While there was an increase in the number of alpha cells in acrylamide group compared to the other groups, here was a decrease in the number of beta cells compared to control group. We can say that acrylamide causes changes in the islets of Langerhans by affecting alpha and beta cell numbers. The protective effect of exercise on beta and alpha cell mass was not statistically significant in the acrylamide+exercise group. When the results were examined, the decrease in oxidative stress and the higher number of beta and alpha cells in the acrylamide+exercise group compared to the acrylamide group suggested that 4 weeks of swimming exercise may have an effect on acrylamide exposure.

An Exercise-Induced Metabolic Shield in Distant Organs Blocks Cancer Progression and Metastatic Dissemination.

Exercise protects against cancer progression and metastasis by inducing a high nutrient demand in internal organs, indicating that reducing nutrient availability to tumor cells represents a potential strategy to prevent metastasis. See related commentary by Zerhouni and Piskounova, p. 4124.

Roles and Molecular Mechanisms of Physical Exercise in Sepsis Treatment.

Physical exercise is a planned, purposeful action to keep a healthy lifestyle and improve physical fitness. Physical exercise has been widely used as a non-pharmacological approach to preventing and improving a wide range of diseases, including cardiovascular disease, cancer, metabolic disease, and neurodegenerative disease. However, the effects of physical exercise on sepsis have not been summarized until now. In this review, we discuss the effects of physical exercise on multiple organ functions and the short- and long-time outcomes of sepsis. Furthermore, the molecular mechanisms underlying the protective effects of physical exercise on sepsis are discussed. In conclusion, we consider that physical exercise may be a beneficial and non-pharmacological alternative for the treatment of sepsis.

Exercise Preconditioning Alters Markers of Cellular Senescence and Prevents DOX‐Induced Cardiorespiratory Dysfunction

Doxorubicin (DOX) is a highly effective chemotherapeutic agent; however its clinical use is limited due to cardiorespiratory complications, including the development of dyspnea, exercise intolerance, and cardiomyopathy. While the mechanisms responsible for DOX‐induced cardiorespiratory dysfunction remain unclear, evidence indicates that DOX administration causes DNA damage and promotes oxidative stress‐induced cellular senescence. Factors shown to contribute to DOX‐induced cellular senescence include cell cycle arrest, driven by signaling through the p16INK4a/Rb and p21/p53 pathways, impaired mitochondrial function, upregulation of pro‐survival pathways, increased lysosomal mass, and expression of the proinflammatory senescence‐associated secretory phenotype (SASP). In contrast, exercise has been shown to prevent cellular senescence in several tissues, leading to the hypothesis that endurance exercise preconditioning is sufficient to prevent senescence induced in the heart and diaphragm muscle following DOX chemotherapy treatment. To determine the relationship between DOX‐induced cardiorespiratory impairment, exercise preconditioning and the impact of accelerated cellular senescence, female Sprague‐Dawley rats underwent two weeks of endurance exercise training (treadmill running, 5 days/week, 60 min/day, 30m/min, 0% grade) before receiving a bolus dose of DOX (20mg/kg IP) or saline treatment. Functional measures were evaluated 48 hours after DOX or saline administration, followed by tissue collection for subsequent analysis of cellular senescence markers. Our results revealed that exercise preconditioning prior to DOX administration prevented diastolic and systolic dysfunction in the heart, with marked improvements in fractional shortening, myocardial performance index, and posterior wall shortening velocity compared to sedentary DOX‐treated animals. DOX‐induced weight loss, reduction in grip strength, and diaphragm weakness were partially rescued with exercise as well, with diaphragm specific force production preserved at frequencies of 60‐160Hz. Finally, both exercise and DOX appear to alter expression of proteins associated with the senescent phenotype in the heart and diaphragm. Therefore, the protective effects of exercise against DOX cardiorespiratory dysfunction may be related to changes in muscle cellular senescence.

Exercise training improves cardiac function and regulates myocardial mitophagy differently in ischaemic and pressure‐overload heart failure mice

What is the central question of this study? What are the cardioprotective effects of different aerobic exercises on chronic heart failure with different aetiologies, and is mitophagy involved? What is the main finding and its importance? Moderate-intensity continuous training may be the 'optimum' modality for improving cardiac structure and function in ischaemic heart failure, while both moderate-intensity continuous training and high-intensity interval training were suitable for pressure-overload heart failure. Various mitophagy pathways, especially parkin-dependent pathways, participated in the protective effects of exercise on heart failure. The cardioprotective effects of different aerobic exercises on chronic heart failure with different aetiologies and whether mitophagy is involved remain elusive. In the current research, left anterior descending ligation and transverse aortic constriction surgeries were used to establish mouse models of heart failure, followed by 8weeks of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT). The results showed that for ischaemic heart failure MICT significantly improved ejection fraction (P<0.05) and fractional shortening (P<0.05), mitigated left ventricular end-systolic dimension (P<0.01), decreased brain natriuretic peptide (P<0.0001) and mitigated fibrosis (P<0.0001), while HIIT only decreased brain natriuretic peptide (P<0.0001) and fibrosis (P<0.0001). For pressure-overload heart failure, both MICT and HIIT significantly increased ejection fraction (P<0.0001) and fractional shortening (MICT: P<0.001, HIIT: P<0.0001), and reduced left ventricular end-diastolic and end-systolic dimensions, brain natriuretic peptide (P<0.0001), and fibrosis (MICT: P<0.01, HIIT: P<0.0001); HIIT was even better in reducing brain natriuretic peptide. Myocardial autophagy and mitophagy were compromised in heart failure, and the exercises improved myocardial autophagic flux and mitophagy inconsistently in heart failure with different aetiologies. Significant correlations were found between multiple mitophagy pathways and the cardioprotection of the exercises. Collectively, MICT may be the 'optimum' modality for ischaemic heart failure, while both MICT and HIIT (especially HIIT) were suitable for pressure-overload heart failure. Exercises differently improved myocardial autophagy/mitophagy, and multiple mitophagy-related pathways were closely implicated in cardioprotection of exercises for chronic heart failure.

Aerobic Exercise Training-Induced Changes on DNA Methylation in Mild Cognitively Impaired Elderly African Americans: Gene, Exercise, and Memory Study - GEMS-I.

BackgroundDNA methylation at CpG sites is a vital epigenetic modification of the human genome affecting gene expression, and potentially, health outcomes. However, evidence is just budding on the effects of aerobic exercise-induced adaptation on DNA methylation in older mild cognitively impaired (MCI) elderly African American (AAs). Therefore, we examined the effects of a 6-month aerobic exercise-intervention on genome-wide DNA methylation in elderly AA MCI volunteers.DesignElderly AA volunteers confirmed MCI assigned into a 6-month program of aerobic exercise (eleven participants) underwent a 40-min supervised-training 3-times/week and controls (eight participants) performed stretch training. Participants had maximal oxygen consumption (VO2max) test and Genome-wide methylation levels at CpG sites using the Infinium HumanMethylation450 BeadChip assay at baseline and after a 6-month exercise program. We computed false discovery rates (FDR) using Sidak to account for multiplicity of tests and performed quantitative real-time polymerase chain-reaction (qRT-PCR) to confirm the effects of DNA methylations on expression levels of the top 5 genes among the aerobic participants. CpG sites identified from aerobic-exercise participants were similarly analyzed by the stretch group to quantify the effects of exercise-induced methylation changes among the group of stretch participants.ResultsEleven MCI participants (aerobic: 73% females; mean age 72.3 ± 6.6 years) and eight MCI participants (stretch: 75% female; mean age 70.6 ± 6.7 years) completed the training. Aerobic exercise-training was associated with increases in VO2max and with global hypo- and hypermethylation changes. The most notable finding was CpG hypomethylation within the body of the VPS52 gene (P = 5.4 × 10–26), a Golgi-associated protein, involved in intracellular protein trafficking including amyloid precursor protein. qRT-PCR confirmed a nearly twofold increased expression of VPS52. Other top findings with FDR q-value < 10–5, include hypomethylations of SCARB1 (8.8 × 10–25), ARTN (6.1 × 10–25), NR1H2 (2.1 × 10–18) and PPP2R5D (9.8 × 10–18).ConclusionWe conclude that genome-wide DNA methylation patterns is associated with exercise training-induced methylation changes. Identification of methylation changes around genes previously shown to interact with amyloid biology, intracellular protein trafficking, and lipoprotein regulations provide further support to the likely protective effect of exercise in MCI. Future studies in larger samples are needed to confirm our findings.

Sarcopenia Related to Human Immunodeficiency Virus: Protective Effects of Exercise.

We discuss recent evidence supporting the hypothesis that sarcopenia is an emerging health concern among people with human immunodeficiency virus (HIV) because of increasing life expectancy and HIV- and treatment-related comorbidities. We also hypothesize that combined exercise at higher intensity has a key role in managing sarcopenia in this population because it directly (increases muscle strength and stimulates hypertrophy) and indirectly (prevents mitochondrial dysfunction, oxidative stress, and persistent inflammation) counteracts sarcopenia hallmarks.

Protective Effects of Exercise Become Especially Important for the Aging Immune System in The Covid-19 Era.

Aging is a complex, multietiological process and a major risk factor for most non-genetic, chronic diseases including geriatric syndromes that negatively affect healthspan and longevity. In the scenario of “healthy or good aging”, especially during the COVID-19 era, the proper implementation of exercise as “adjuvant” or “polypill” to improve disease-related symptoms and comorbidities in the general population is a top priority. However, there is still a gap concerning studies analyzing influence of exercise training to immune system in older people. Therefore, the aim of this review is to provide a brief summary of well-established findings in exercise immunology and immunogerontology, but with a focus on the main exercise-induced mechanisms associated with aging of the immune system (immunosenescence). The scientific data strongly supports the notion that regular exercise as a low-cost and non-pharmacological treatment approach, when adjusted on an individual basis in elderly, induce multiple rejuvenating mechanisms: (1) affects the telomere-length dynamics (a “telo-protective” effect), (2) promote short- and long-term anti-inflammatory effects (via e.g., triggering the anti-inflammatory phenotype), 3) stimulates the adaptive immune system (e.g., helps to offset diminished adaptive responses) and in parallel inhibits the accelerated immunosenescence process, (4) increases post-vaccination immune responses, and (5) possibly extends both healthspan and lifespan.

Advanced Glycation End Products Increase Salivary Gland Hypofunction in d-Galactose-Induced Aging Rats and Its Prevention by Physical Exercise.

A declined salivary gland function is commonly observed in elderly people. Advanced glycation end products (AGEs) are believed to contribute to the pathogenesis of aging. Although physical exercise is shown to increase various organ functions in human and experimental models, it is not known whether it has a similar effect in the salivary glands. In the present study, we evaluated the AGEs burden in the salivary gland in the aging process and the protective effect of physical exercise on age-related salivary hypofunction. To accelerate the aging process, rats were peritoneally injected with D-galactose for 6 weeks. Young control rats and d-galactose-induced aging rats in the old group were not exercised. The rats in the physical exercise group ran on a treadmill (12 m/min, 60 min/day, 3 days/week for 6 weeks). The results showed that the salivary flow rate and total protein levels in the saliva of the d-galactose-induced aging rats were reduced compared to those of the young control rats. Circulating AGEs in serum and secreted AGEs in saliva increased with d-galactose-induced aging. AGEs also accumulated in the salivary glands of these aging rats. The salivary gland of aging rats showed increased reactive oxygen species (ROS) generation, loss of acinar cells, and apoptosis compared to young control mice. However, physical exercise suppressed all of these age-related salivary changes. Overall, physical exercise could provide a beneficial option for age-related salivary hypofunction.