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1,613 result(s) for "Exercise-training"
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Exercise intensity matters: A review on evaluating the effects of aerobic exercise intensity on muscle‐derived neuroprotective myokines
Exercise as a medical intervention is effective to help prevent and manage many chronic and complex diseases, including dementia. There is evidence to suggest that regular aerobic exercise protects against age‐related brain atrophy and reduces the risk of cognitive decline. The mechanisms by which exercise infers a neuroprotective effect remain to be established but may be related to a maintenance of brain volume and neuronal survival, improved cerebrovascular density and function, and/or increased synaptic plasticity. In addition, there is growing evidence to suggest the beneficial effects of exercise on brain health and cognitive function are, at least in part, mediated by factors released by skeletal muscle during contraction. The fact that the brain responds to exercise suggests that muscle‐derived peripheral factors, or “myokines,” may play a key role in muscle–brain crosstalk and exercise neuroprotection. However, the most effective “dose” of aerobic exercise to promote beneficial changes in these myokine pathways is currently unknown. Specifically, most of the evidence to date is from studies that have used moderate‐intensity exercise, and research investigating the merit of high‐intensity exercise is scarce. Considering the well‐established role of high‐intensity interval training in protecting against numerous medical conditions, more research is needed to identify the most effective “dose” of exercise to improve the beneficial effects of these myokines. Highlights Neuroprotection through exercise: Regular aerobic exercise mitigates age‐related brain atrophy and cognitive decline via multiple mechanisms, including brain volume maintenance, improved cerebrovascular function, and synaptic plasticity. Myokines as mediators: Muscle‐derived factors (myokines) play a crucial role in muscle–brain crosstalk, significantly contributing to the neuroprotective effects of exercise. Intensity matters: The review underscores the necessity to define and study exercise intensity, revealing high‐intensity exercise may be as effective, if not more, in promoting neuroprotective myokine levels compared to moderate‐intensity exercise. Future research directions: This review emphasizes the need for well‐controlled studies to explore the optimal exercise dose for enhancing myokine pathways and their implications for neurodegenerative disease prevention.
Exercise training and resting blood pressure: a large-scale pairwise and network meta-analysis of randomised controlled trials
ObjectiveTo perform a large-scale pairwise and network meta-analysis on the effects of all relevant exercise training modes on resting blood pressure to establish optimal antihypertensive exercise prescription practices.DesignSystematic review and network meta-analysis.Data sourcesPubMed (Medline), the Cochrane library and Web of Science were systematically searched.Eligibility criteriaRandomised controlled trials published between 1990 and February 2023. All relevant work reporting reductions in systolic blood pressure (SBP) and/or diastolic blood pressure (DBP) following an exercise intervention of ≥2 weeks, with an eligible non-intervention control group, were included.Results270 randomised controlled trials were ultimately included in the final analysis, with a pooled sample size of 15 827 participants. Pairwise analyses demonstrated significant reductions in resting SBP and DBP following aerobic exercise training (−4.49/–2.53 mm Hg, p<0.001), dynamic resistance training (–4.55/–3.04 mm Hg, p<0.001), combined training (–6.04/–2.54 mm Hg, p<0.001), high-intensity interval training (–4.08/–2.50 mm Hg, p<0.001) and isometric exercise training (–8.24/–4.00 mm Hg, p<0.001). As shown in the network meta-analysis, the rank order of effectiveness based on the surface under the cumulative ranking curve (SUCRA) values for SBP were isometric exercise training (SUCRA: 98.3%), combined training (75.7%), dynamic resistance training (46.1%), aerobic exercise training (40.5%) and high-intensity interval training (39.4%). Secondary network meta-analyses revealed isometric wall squat and running as the most effective submodes for reducing SBP (90.4%) and DBP (91.3%), respectively.ConclusionVarious exercise training modes improve resting blood pressure, particularly isometric exercise. The results of this analysis should inform future exercise guideline recommendations for the prevention and treatment of arterial hypertension.
Physical Activity, Cardiorespiratory Fitness, and the Metabolic Syndrome
Both observational and interventional studies suggest an important role for physical activity and higher fitness in mitigating the metabolic syndrome. Each component of the metabolic syndrome is, to a certain extent, favorably influenced by interventions that include physical activity. Given that the prevalence of the metabolic syndrome and its individual components (particularly obesity and insulin resistance) has increased significantly in recent decades, guidelines from various professional organizations have called for greater efforts to reduce the incidence of this condition and its components. While physical activity interventions that lead to improved fitness cannot be expected to normalize insulin resistance, lipid disorders, or obesity, the combined effect of increasing activity on these risk markers, an improvement in fitness, or both, has been shown to have a major impact on health outcomes related to the metabolic syndrome. Exercise therapy is a cost-effective intervention to both prevent and mitigate the impact of the metabolic syndrome, but it remains underutilized. In the current article, an overview of the effects of physical activity and higher fitness on the metabolic syndrome is provided, along with a discussion of the mechanisms underlying the benefits of being more fit or more physically active in the prevention and treatment of the metabolic syndrome.
Outpatient Pulmonary Rehabilitation in Patients with Long COVID Improves Exercise Capacity, Functional Status, Dyspnea, Fatigue, and Quality of Life
Background: COVID-19 survivors face the risk of long-term sequelae including fatigue, breathlessness, and functional limitations. Pulmonary rehabilitation has been recommended, although formal studies quantifying the effect of rehabilitation in COVID-19 patients are lacking. Methods: We conducted a prospective observational cohort study including consecutive patients admitted to an outpatient pulmonary rehabilitation center due to persistent symptoms after COVID-19. The primary endpoint was change in 6-min walk distance (6MWD) after undergoing a 6-week interdisciplinary individualized pulmonary rehabilitation program. Secondary endpoints included change in the post-COVID-19 functional status (PCFS) scale, Borg dyspnea scale, Fatigue Assessment Scale, and quality of life. Further, changes in pulmonary function tests were explored. Results: Of 64 patients undergoing rehabilitation, 58 patients (mean age 47 years, 43% women, 38% severe/critical COVID-19) were included in the per-protocol-analysis. At baseline (i.e., in mean 4.4 months after infection onset), mean 6MWD was 584.1 m (±95.0), and functional impairment was graded in median at 2 (IQR, 2–3) on the PCFS. On average, patients improved their 6MWD by 62.9 m (±48.2, p < 0.001) and reported an improvement of 1 grade on the PCFS scale. Accordingly, we observed significant improvements across secondary endpoints including presence of dyspnea (p < 0.001), fatigue (p < 0.001), and quality of life (p < 0.001). Also, pulmonary function parameters (forced expiratory volume in 1 s, lung diffusion capacity, inspiratory muscle pressure) significantly increased during rehabilitation. Conclusion: In patients with long COVID, exercise capacity, functional status, dyspnea, fatigue, and quality of life improved after 6 weeks of personalized interdisciplinary pulmonary rehabilitation. Future studies are needed to establish the optimal protocol, duration, and long-term benefits as well as cost-effectiveness of rehabilitation.
Freeweight training anatomy : an illustrated guide to the muscles used while exercising with dumbbells, barbells, kettlebells and more
\"Picturing hundreds of step-by-step exercises and clearly colored muscle illustrations, Freeweight Training Anatomy reveals precisely which muscle groups are being built, stretched and sculpted in every workout. This extensive anatomy and fitness guide is the ultimate resource for creating smart, balanced fitness routines that employ barbells, dumbbells, kettlebells, sandbags and even your own bodyweight.\"--Provided by publisher.
Exercise‐induced effects on atherogenesis and tryptophan catabolism via the kynurenine pathway in an HIV‐associated atherosclerosis mouse model
A mouse model of HIV‐associated atherosclerosis ( Tg26 +/− ApoE −/− ) exhibited increased plaque area compared with the ApoE −/− mouse, linked to elevated indoleamine 2,3‐dioxygenase (IDO) activity. IDO catalyses the conversion of tryptophan (TRP) into kynurenine (KYN), measured by the KYN‐to‐TRP ratio. As a biomarker of inflammation, IDO has been implicated as a risk factor for cardiovascular disease. To investigate the effect of exercise training on atherogenesis and IDO activity in Tg26 +/− ApoE −/− mice, nine Tg26 +/− ApoE −/− and 18 ApoE −/− male mice were fed an atherogenic diet and randomized into exercised or control groups. The exercised groups underwent an 8‐week treadmill protocol at moderate intensity (five times per week at 60% maximum velocity). Concentrations of KYN, TRP and cytokines were measured using ELISA, immune expression by flow cytometry, and lipid profile by a biochemistry analyser. Aortas were harvested post mortem for en face analysis. Tg26 +/− ApoE −/− mice showed ∼40% larger plaques than ApoE −/− mice ( P  = 0.01), with slightly higher neutrophil ( P  = 0.05) and monocyte expression ( P  = 0.06). Plaque area was reduced by 40% in exercised ApoE −/− mice ( P  = 0.04), but by only 12% in exercised Tg26 +/− ApoE −/− animals ( P  = 0.85). Exercised Tg26 +/− ApoE −/− mice showed higher IDO activity than exercised ApoE −/− mice (58.57% ± 6.88% vs. −4.62% ± 17.20%, P  = 0.01), which was positively correlated with plaque area ( R  = 0.99, P  = 0.02). Exercised ApoE − / − mice showed significantly lower triglyceride levels compared with exercised Tg26 +/− ApoE −/− mice (75.8 ± 14.8 vs. 165.2 ± 43.6 mg/dL; P  = 0.02). Unlike ApoE −/− mice, moderate‐intensity aerobic training did not reduce plaque area in mice with HIV‐associated atherosclerosis. Moreover, exercise training appeared to increase inflammation in Tg26 +/− ApoE −/− mice, as indicated by elevated IDO activity. What is the central question of this study? Does moderate‐intensity aerobic exercise training influence the development of human immunodeficiency virus (HIV)‐associated atherosclerosis and tryptophan metabolism via the kynurenine pathway in an HIV‐associated atherosclerosis mouse model? What is the main finding and its importance? Moderate‐intensity aerobic exercise reduced atherosclerotic plaque size in ApoE −/− mice, but not in HIV‐transgenic mice, in which it was associated with elevated indoleamine 2,3‐dioxygenase activity. It is possible that HIV‐associated inflammation might attenuate the usual benefits of exercise on atherosclerosis, highlighting the need for further investigation and tailored exercise recommendations for people living with HIV.