Muscle preservation and cardiovascular health -
Sarcopenia is a multi-cause disease with risk factors including lifestyle, changes or imbalances of hormones and inflammatory factors, imbalances of protein synthesis and decomposition, motor unit reconstruction, development, and evolution. Sarcopenia often coexists with CVDs, tumors, chronic non-obstructive disease, chronic kidney disease, endocrine disease, and rheumatic immune disease Various causes of inhibition of skeletal muscle cell proliferation signaling pathways and excessive activation of apoptotic signaling pathways can disrupt the dynamic balance between muscle production and destruction, ultimately leading to diseases Malnutrition, physical inactivity, insulin resistance, inflammation, hormonal changes, autophagy, apoptosis, and oxidative stress are involved in the occurrence of CVDs and sarcopenia Sarcopenia and CVDs are closely related and interact to influence the course of the disease.
In addition, CVDs aggravate sarcopenia's adverse outcomes, including falls, fractures, frailty, cachexia, hospitalization, and mortality. At the same time, the prevalence of CVDs in sarcopenia patients is significantly increased, such as HF, hypertension, atherosclerosis, and CHD Figure 1.
HF leads to peripheral ischemia and hypoxia, induces skeletal muscle cell apoptosis, even necrosis, muscle atrophy, and decreases exercise ability; the reduced or lost exercise capacity caused by sarcopenia leads to obesity, dyslipidemia, inflammatory reaction, insulin resistance, and then promotes CVDs 3 , 30 , The pathophysiological mechanism underlying sarcopenia and CVDs is unclear and progressively focused on and explored by researchers.
It was suggested that mechanisms such as inflammation, oxidative stress, and insulin resistance might also be involved in the occurrence and development of CVDs and sarcopenia in the elderly.
The mechanism between sarcopenia and CVDs can be understood from the following aspects. Figure 1. The pathogenesis of sarcopenia and CVDs. Malnutrition, physical inactivity, insulin resistance, inflammation, hormonal changes, autophagy, apoptosis and oxidative stress are involved in the occurrence of CVDs and sarcopenia.
Sarcopenia is closely related to cardiovascular disease, which affects each other's course of disease. In addition, CVDs aggravates the adverse outcomes of sarcopenia, including falls, fracture, frailty, cachexia, hospitalization and mortality.
At the same time, the prevalence of CVDs in sarcopenia patients is significantly increased, such as HF, hypertension, atherosclerosis and CHD. Studies have shown that long-term systemic chronic inflammation seems to be involved in the whole process of CVDs, and sarcopenia in the elderly 63 — Senescence-associated secretory phenotype SASP is one of the key factors in chronic inflammation-induced atherosclerotic plaque instability, part of the pathogenesis of atherosclerosis 63 and an independent risk factor for myocardial infarction and cardiovascular death As an upstream factor in the inflammatory response, IL-6 reflects the level of systemic inflammation and can prompt the level of systemic catabolism and promote the downstream inflammatory response Studies have confirmed that the long-term activation of the IL-6 signaling pathway is significantly related to the degree of atherosclerosis in elderly patients Selective inhibition of the IL-6 signaling pathway and reduction of systemic inflammatory levels can substantially reduce the incidence of cardiovascular events As individuals age, the body's adipose tissue tends to increase, and levels of free cholesterol and fatty acids rise, which can induce a rise in chronic systemic inflammation by converting M2 macrophages into pro-inflammatory M1 macrophages that produce pro-inflammatory factors such as IL-6 In addition, it was found that the level of IL-6 in patients with sarcopenia is independently related to the occurrence of sarcopenia IL-6 can promote the catabolism of skeletal muscle and cause muscle atrophy.
The increase of IL-6 concentration in the blood circulation is related to the severity of HF and the activation of the sympathetic system Inflammation in heart failure patients may promote the development of sarcopenia.
The SICA-HF study observed that in patients with HF, IL-6 was significantly higher in the sarcopenia group than in the non-sarcopenia group, but IL-1β and tumor necrosis factor-α did not differ significantly between the two groups 25 , Studies have also shown that inflammation activates the body's catabolic pathways, promotes the hydrolysis of muscle protein, leads to an imbalance between protein synthesis and catabolism, and contributes to sarcopenia development During the aging process, the body produces large amounts of reactive oxygen species ROS due to changes in the function of the respiratory chain; and as the defense function of antioxidant cells is impaired, the ROS produced are not cleared in time and accumulate in the body This is when the body is in a state of oxidative stress.
The increased level of oxidative stress in the body can lead to various CVDs such as hypertension, atherosclerosis, myocardial infarction, HF, and arrhythmia The main reasons are as follows: a the increase of ROS in the body causes vasoconstriction and promotes arterial hypertension; b ROS can negatively affect cardiac calcium processing, cause arrhythmia, and induce hypertrophic signaling and apoptosis to increase cardiac remodeling; c ROS has been shown to promote the formation of atherosclerotic plaques; d ROS can cause vascular endothelial dysfunction in patients with CVDs and cause adverse cardiovascular events 74 — Oxidative stress is a common mechanism in many age-related diseases.
As we age, the body's antioxidant capacity decreases significantly. The accumulation of ROS in the body will affect the nitrification, nitrosation, carbonylation, and glycation of proteins, thereby affecting muscle protein synthesis At the same time, ROS can also mediate and enhance the hydrolysis of muscle protein, leading to sarcopenia Furthermore, obese patients with sarcopenia have significantly increased levels of circulating oxidative stress and are significantly associated with CVDs risk in such patients In recent years, factors related to metabolism have been extensively studied.
Insulin resistance is the most representative pathway, and it seems to be related to sarcopenia and CVDs. Many studies have provided reliable clinical evidence, suggesting that insulin resistance is a major cardiovascular risk factor independent of other risk factors in CVDs in older adults in community populations and patients with type I and type II diabetes In patients with ischemic stroke, insulin resistance is independently associated with poor functional prognosis after acute ischemic stroke 80 , Skeletal muscle is the leading site of glucose uptake, deposition, and actin secretion, which protect insulin resistance.
A reduction in muscle mass can lead to insulin resistance. When the body becomes insulin resistant, on the one hand, insulin secretion in the body is reduced. Glucose homeostasis is disrupted, leading to glucose utilization disorders, while the muscle is an essential organ for the body to absorb and utilize glucose, making its energy supply to muscle significantly reduced; On the other hand, the metabolism of skeletal muscle in limbs of the body increases significantly, and the dysfunction of muscle microvascular function will substantially affect the function and state of skeletal muscles, which will lead to the decrease of skeletal muscle content and sarcopenia 82 — Currently, the central combined interventions for sarcopenia and CVDs come from physical exercise, proper nutrition, hormone therapy, and medication Figure 2.
Figure 2. The treatment of sarcopenia and CVDs. At present, the joint intervention of sarcopenia and CVDs is mainly from physical exercise, rational nutrition, hormone therapy and medication.
Physical exercise is an economical, safe, and effective intervention for both CVDs and sarcopenia. Physical exercise methods include active and passive exercise and aerobic and resistance exercise, increasing muscle mass and strength, improving exercise and balance ability, and reducing falls and fractures 52 , 85 — Aerobic exercise can be carried out with simple equipment such as swimming, jogging, and push-ups or with the aid of elastic bands.
These exercises effectively prevent CVDs that may be caused by an immediate increase in heart rate and blood pressure Resistance exercise can increase muscle volume and muscle contractility and improve submaximal exercise endurance in patients with heart failure.
Studies have shown that a combination of aerobic and resistance exercise can increase the effectiveness of exercise rehabilitation. Medium to long-term resistance training, aerobic exercise, and other forms of exercise or a mixture of exercise can significantly improve muscle strength, increase muscle mass, slow the progression of HF and inhibit skeletal muscle breakdown in some patients with sarcopenia In one study, patients with chronic heart failure were found to have significantly improved endurance and 6-min walking distance in all muscle groups after 10 weeks of high-intensity progressive resistance exercise Recent studies have further confirmed the importance of exercise training in suppressing inflammatory factors, reducing oxidative stress, reducing myostatin expression, and inhibiting the ubiquitin protease system in patients with HF Nutritional intervention is currently the primary prevention and treatment method for sarcopenia, including supplementation of protein and amino acids β-Hydroxy-β-Methyl butyrate HMB , antioxidants, long-chain fatty acids, vitamin D, and creatine 93 , Protein and vitamin D intake is crucial to the prevention and treatment of sarcopenia.
Protein is essential for muscle metabolism in the body. Essential amino acids such as leucine and isoleucine are necessary to promote muscle protein synthesis 95 , There are still controversies regarding vitamin D supplementation for the prevention and treatment of sarcopenia.
The correlation between vitamin D level and muscle mass is poor, but it can slightly improve muscle strength 97 , In addition, HMB is the active metabolite of the essential amino acid leucine and has a critical interventional effect on sarcopenia.
It has been shown to inhibit muscle proteolysis, promote muscle protein synthesis, inhibit muscle protein decomposition, maintain cell membrane integrity, improve immunity and reduce inflammation.
A meta-analyses systematic study showed that nutritional supplementation with HMB can enhance lean muscle mass and preserve muscle strength and function in the elderly with sarcopenia or frailty A review of Clinical Trials showed that HMB supplementation is essential for the maintenance of muscle mass in the elderly over 65 years old, especially the elderly who are bedridden or sedentary, and contributes to the reduction of muscle metabolism.
Many studies have shown that HMB increased muscle mass and strength in older people with reduced lean body mass — In addition, studies have shown that HMB supplementation has a positive effect on lowering plasma cholesterol and blood pressure, thereby reducing the risk of cardiovascular disease — It was shown that HMB slows HF progression by maintaining lean body mass and limiting the effects of cachexia.
Therefore, HMB is likely to be crucial for the nutritional management of patients with HF-induced cachexia Therefore, nutritional support is essential for the recovery of sarcopenia patients. The Mediterranean diet is an ideal diet for patients with CHD, rich in nutrients and balanced.
The Mediterranean diet also helps delay muscle wasting in the elderly and reduces the risk of sarcopenia As with exercise, patients need to adhere to an appropriate diet for a long time to achieve good outcomes. Some studies have shown that supplementing testosterone is beneficial to muscle and skeletal tissues , , particularly in increasing muscle strength, improving mobility, and reducing the hospitalization rate of elderly patients with sarcopenia Decreased testosterone can cause fatigue and weakened exercise capacity, while testosterone supplementation can increase muscle strength and improve exercise capacity At lower doses, testosterone increases protein synthesis, thus increasing muscle mass In comparison, testosterone activates the recruitment of satellite cells at higher doses and reduces adipose-derived stem cells, thereby increasing myogenesis and reducing adipogenesis Testosterone replacement therapy can improve metabolism and exercise tolerance in patients with chronic heart failure.
Results showed an increase in peak oxygen uptake, 6-min walk distance, and body weight in the treatment group compared to the control group, directly related to the serum testosterone concentration However, testosterone therapy may increase the risk of benign prostatic hyperplasia and tumor in male patients and masculinize female patients, limiting its wide clinical application.
Ghrelin exerts protective effects in skeletal muscle by regulating autophagy, apoptosis, insulin resistance, and inflammation Ghrelin can also inhibit atherosclerosis, ischemia-reperfusion injury, ventricular remodeling, and improve cardiac function and endothelial function As ghrelin is highly expressed in tumor tissue, its clinical application needs careful evaluation.
However, attention should be paid to the side effects of testosterone therapy, such as benign prostatic hyperplasia, prostate cancer, polycythemia, and sleep apnea syndrome. Moreover, the intramuscular injection has higher safety than oral treatment. Growth hormone GH is an essential endogenous hormone that can promote the growth of organs and tissues, promote protein synthesis, and affect fat and mineral metabolism.
GH is involved in the regulation of skeletal muscle growth mainly through insulin growth factors. It can increase skeletal muscle mass but has no noticeable effect on muscle strength Notably, GH can increase the risk of fluid retention and insulin resistance and adversely affect the cardiovascular system.
Angiotensin-converting enzyme inhibitors ACEI and angiotensin receptor blockers ARB have multiple cardiovascular protective effects, and their anti-inflammatory and antioxidant effects also benefit muscle tissue Early studies have found that ACEI drugs can delay the decline of muscle mass.
Recent studies have negated its effect on muscle mass and muscle strength. However, ARB can effectively improve the muscle strength of hemodialysis patients In addition, recent studies have found that loop diuretics can increase the risk of sarcopenia in non-dialysis patients with chronic kidney disease.
In patients with HF, spironolactone can prevent skeletal muscle loss and improve muscle strength, possibly due to improved cardiac function Globally, t the incidence of sarcopenia is gradually increasing, and it has received full attention from European and American countries.
However, for the Asian region, the research on sarcopenia is still in its infancy. As for sarcopenia, from the initial focus on muscle mass to the latest EWGSOP2, muscle strength is the primary diagnostic element, indicating that the understanding of its essence is constantly deepening. However, many areas still need to be further explored, including the pathophysiological processes such as the occurrence, development, and outcome of sarcopenia, sarcopenia-related biomarkers, screening, and preventive measures for high-risk people.
In terms of the diagnosis of sarcopenia, there are some subjective diagnosis critical values at present. More objective and reasonable diagnosis critical value needs to be determined by standardized clinical research big data and gender and regional specificity.
In terms of treatment, it is considered that nutrition and exercise are two treatment methods that can be implemented clinically to delay sarcopenia. However, the specific application, usage, dosage, and effectiveness of related nutritional supplements in nutritional therapy still need more research data to support.
The exercise therapy method, frequency, and intensity also need clinical research to further confirm and refine. Although many studies have shown that nutritional s supplements combined with exercise are effective in treating sarcopenia, more research is also needed to standardize the treatment plan.
At present, in terms of drug treatment, there is still a lack of clinical first-line drugs, and a small number of drugs for the treatment of sarcopenia are expected to enter phase III clinical trials in the next few years.
However, the preliminary research of many drugs will face significant challenges. Sarcopenia needs more basic and clinical research to explore its risk factors, pathogenesis, and intervention measures. At present, there is no unified conclusion on the mechanism of the relationship between sarcopenia and CVDs.
However, according to the existing research, it can be determined that there are many similar pathophysiological mechanisms between sarcopenia and CVDs. Furthermore, sarcopenia has a specific correlation with the poor prognosis of CVDs. Therefore, it is necessary to pay attention to the common pathway of the two diseases, carry out systematic, basic, and large sample clinical research, and look for reliable biomarkers, so as to provide new ideas for the prediction and diagnosis of sarcopenia and cardiovascular diseases, as well as the early intervention of adverse prognosis.
In summary, sarcopenia and CVDs are highly prevalent in the elderly and share common pathogenesis and interactions. Understanding their relationship is still in its initial stages, and more clinical and experimental data are needed.
A large number of studies have shown that the progression of CVDs and the decline in muscle function will further worsen the patient's condition. By screening patients for sarcopenia at an early stage, establishing effective early detection methods and evaluation methods, and providing early and comprehensive interventions, the progression of the disease can be effectively delayed.
Nevertheless more importantly, patients with CVDs should be rehabilitated as soon as possible to break the vicious cycle of sarcopenia and CVDs through scientific nutritional programs and training guidance.
Effective treatment of either sarcopenia or CVDs can have a positive impact on another disease. However, some drugs have acted as a double-edged role in the treatment of the two diseases. A healthy lifestyle and proper drug treatment have become necessary means for preventing and treating CVDs and sarcopenia.
In the future, more high-quality research is still needed to provide a basis for optimal treatment options for people with specific diseases, such as CVDs co-morbid with sarcopenia.
NH drafted the manuscript of this review article. SZ and HY conceived and supervised the manuscript. YZ and LZ also collected and organized the information and prepared the table and figures for the manuscript.
All authors contributed to the article and approved the submitted version. This study was funded by the Ningbo Health Branding Subject Fund PPXK , Ningbo Medical Science and Technology project Z01 , Zhejiang Provincial Public Service and Application Research Foundation, China LGF20H , and Ningbo HwaMei Research Fund HMZD The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.
Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Bayraktar E, Tasar PT, Binici DN, Karasahin O, Timur O, Sahin S.
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Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis. Notably, these mitochondrial impairments were associated with measures of exercise intolerance, specifically peak VO 2 and 6-minute walk distance. However, these previous studies examining mitochondria in patients with HFpEF were limited due to the reliance on stored frozen tissues samples, which prevented analyses of mitochondrial function by respirometry, a direct and precise approach for assessing mitochondrial function.
In this study, we used high-resolution respirometric profiling of permeabilized skeletal muscle fiber bundles to provide, to our knowledge, the first direct analysis of mitochondrial function in patients with HFpEF.
The major new finding is that compared with age-matched HCs, patients with HFpEF had lower mitochondrial respiration across measures of oxidative phosphorylation capacity of the nicotinamide adenine dinucleotide plus hydrogen NADH pathway through complex I respiration, convergent NADH and succinate NS pathways through complexes I and II respiration, and electron transfer capacity of the convergent NS pathway.
Multiple lines of evidence indicate that excess adipose tissue is associated with impaired mitochondrial function and reduced mitochondrial density. Adjusting for BMI did not affect the differences in mitochondrial respiration we observed between participants with HFpEF and HCs.
Thus, our results indicate that factors unrelated to obesity also contribute to skeletal muscle mitochondrial dysfunction in patients with HFpEF. This is consistent with findings from an animal model of HFpEF, which showed reduced skeletal muscle mitochondrial density compared with controls, despite no difference in body mass.
Among healthy persons, skeletal muscle mitochondrial function has been shown to be directly related to physical function and exercise capacity, supporting our observation that mitochondrial abnormalities in patients with HFpEF are associated with their severely impaired physical function. Notably, the average peak VO 2 in that study was Mitochondrial abnormalities are emerging as promising therapeutic targets for a number of common disorders, particularly those associated with aging, such as HFpEF.
The present data provide the foundation for future studies to examine interventions, such as exercise training, which has been shown to positively affect skeletal muscle mitochondria function.
Pharmacological interventions targeting mitochondrial abnormalities are also in development. For example, Szeto-Schiller peptides have been shown to target mitochondrial dysfunction in myocytes and are being tested in clinical trials.
The present data suggest that clinical trials targeting mitochondrial abnormalities in HFpEF may have beneficial effects on skeletal muscle metabolism and exercise performance. A primary strength of this article is the use of high-resolution respirometry to directly assess mitochondrial function in freshly isolated permeabilized skeletal muscle fiber bundles.
These precise ex vivo measurements have significantly advanced our understanding of human muscle metabolism. To our knowledge, the study presented here is the largest to use these assays in patients with HFpEF.
Other strengths include an age-matched HC group and the multiple measures of physical function and exercise capacity, including peak VO 2 , 6-minute walk distance, SPPB, and leg strength, to determine their association with the mitochondrial abnormalities.
This study has limitations. Patients with HFpEF compared with HC participants were well matched for age and sex distribution but had higher BMI.
However, we included models adjusting for BMI individually and in conjunction with age and sex in our analyses and found that differences between participants with HFpEF and HCs were largely unaffected.
Another potential difference that could affect our readouts of skeletal muscle mitochondrial function is the relative abundance of type 1 muscle fibers, which have a distinct metabolic phenotype. Our team has previously reported that the relative abundance of type 1 fibers is lower in the skeletal muscle of participants with HFpEF 18 ; however, comparative data reporting on the abundance of type 1 fibers are not available in this study.
Several studies in both animal models and humans have reported that physical activity and sedentary behavior are related to skeletal muscle mitochondrial function.
While we cannot definitely decipher whether skeletal muscle mitochondrial dysfunction is a cause or consequence of differences in physical activity in HFpEF compared with HCs, it should be noted that reduced physical function such as pVO 2 in HFpEF is not merely due to sedentary behavior.
This concept is supported by multiple lines of evidence for skeletal myopathy in HFpEF, as previously reviewed by our team. However, the causal relationship between mitochondrial dysfunction and exercise intolerance in patients with HFpEF remains to be determined.
In this study, older patients with HFpEF showed marked abnormalities in mitochondrial function that were significantly associated with their reduced exercise capacity and muscle strength. These results provide new insights into potential novel therapeutic targets. Published Online: May 10, Open Access: This is an open access article distributed under the terms of the CC-BY License.
JAMA Cardiology. Corresponding Author: Anthony J. Molina, PhD, Division of Geriatrics, Gerontology, and Palliative Care, UC San Diego School of Medicine, University of California, San Diego, Gilman Dr, Stein Clinical Research Building, La Jolla, CA ajmolina health. Author Contributions: Drs Kitzman and Molina had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Acquisition, analysis, or interpretation of data : Scandalis, Kitzman, Nicklas, Lyles, Brubaker, Nelson, Gordon, Stone, Bergstrom, Molina.
Critical revision of the manuscript for important intellectual content : All authors. Administrative, technical, or material support : Kitzman, Nicklas, Lyles, Nelson, Gordon, Stone, Neufer, Molina.
Conflict of Interest Disclosures: Dr Kitzman has received grants from the National Institutes of Health during the conduct of the study; grants from Novartis, Rivus, NovoNordisk, AstraZeneca, Pfizer, and Bayer; and personal fees from Bayer, Merck, Medtronic, Relypsa, Corvia Medical, Rivus, NovoNordisk, AstraZeneca, Pfizer, Novartis, and Boehringer Ingelheim outside the submitted work; and owns stock in Gilead Sciences.
Dr Nicklas has received grants from the National Institutes of Health during the conduct of the study. Dr Gnaiger is founder and CEO of Oroboros Instruments outside the submitted work.
No other disclosures were reported. This study was also supported in part by grant 15MCPRP from the American Heart Association and in part by the Kermit Glenn Phillips II Chair in Cardiovascular Medicine.
Data Sharing Statement: See Supplement 2. full text icon Full Text. Download PDF Comment. Top of Article Key Points Abstract Introduction Methods Results Discussion Conclusions Article Information References. Associations of Maximal Capacity With Exercise Capacity and Physical Ability.
View Large Download. Table 1. Characteristics of Patients With Heart Failure With Preserved Ejection Fraction HFpEF and Age-Matched Healthy Controls HCs. Table 2. Cardiopulmonary and Hemodynamic Responses During Peak Treadmill Exercise and Physical Function Measures.
Table 3. Skeletal Muscle Mitochondrial Respirometry. Supplement 1. Correlation Between Skeletal Muscle Respiration and Physical Function eTable 2. Correlation Between Skeletal Muscle Respiration and Peak VO 2 by HFpEF Status eFigure 1.
Representative High-Resolution Respirometry Trace eFigure 2. Supplement 2. Data Sharing Statement. Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM.
Trends in prevalence and outcome of heart failure with preserved ejection fraction. doi: Kitzman DW, Gardin JM, Gottdiener JS, et al; Cardiovascular Health Study Research Group.
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How to diagnose heart failure with preserved ejection fraction: the HFA-PEFF diagnostic algorithm: a consensus recommendation from the Heart Failure Association HFA of the European Society of Cardiology ESC.
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a systematic review. Seferović PM, Petrie MC, Filippatos GS, et al. Type 2 diabetes mellitus and heart failure: a position statement from the Heart Failure Association of the European Society of Cardiology. Kitzman DW, Little WC, Brubaker PH, et al. Pathophysiological characterization of isolated diastolic heart failure in comparison to systolic heart failure.
Borlaug BA, Melenovsky V, Russell SD, et al. Impaired chronotropic and vasodilator reserves limit exercise capacity in patients with heart failure and a preserved ejection fraction.
Haykowsky MJ, Brubaker PH, John JM, Stewart KP, Morgan TM, Kitzman DW. Determinants of exercise intolerance in elderly heart failure patients with preserved ejection fraction. Esposito F, Mathieu-Costello O, Shabetai R, Wagner PD, Richardson RS.
Limited maximal exercise capacity in patients with chronic heart failure: partitioning the contributors. Sullivan MJ, Knight JD, Higginbotham MB, Cobb FR.
Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure. muscle blood flow is reduced with maintenance of arterial perfusion pressure. Pandey A, Shah SJ, Butler J, et al. Exercise intolerance in older adults with heart failure with preserved ejection fraction: JACC State-of-the-Art Review.
Dhakal BP, Malhotra R, Murphy RM, et al. Mechanisms of exercise intolerance in heart failure with preserved ejection fraction: the role of abnormal peripheral oxygen extraction. Fleg JL, Cooper LS, Borlaug BA, et al; National Heart, Lung, and Blood Institute Working Group.
Exercise training as therapy for heart failure: current status and future directions. Haykowsky MJ, Brubaker PH, Stewart KP, Morgan TM, Eggebeen J, Kitzman DW. Effect of endurance training on the determinants of peak exercise oxygen consumption in elderly patients with stable compensated heart failure and preserved ejection fraction.
Haykowsky MJ, Brubaker PH, Morgan TM, Kritchevsky S, Eggebeen J, Kitzman DW. Impaired aerobic capacity and physical functional performance in older heart failure patients with preserved ejection fraction: role of lean body mass. Weiss K, Schär M, Panjrath GS, et al.
Fatigability, exercise intolerance, and abnormal skeletal muscle energetics in heart failure. Kitzman DW, Nicklas B, Kraus WE, et al. Skeletal muscle abnormalities and exercise intolerance in older patients with heart failure and preserved ejection fraction.
Molina AJ, Bharadwaj MS, Van Horn C, et al. Skeletal muscle mitochondrial content, oxidative capacity, and Mfn2 expression are reduced in older patients with heart failure and preserved ejection fraction and are related to exercise intolerance.
Bowen TS, Rolim NP, Fischer T, et al; Optimex Study Group. Heart failure with preserved ejection fraction induces molecular, mitochondrial, histological, and functional alterations in rat respiratory and limb skeletal muscle. Kelley RC, Betancourt L, Noriega AM, et al. Skeletal myopathy in a rat model of postmenopausal heart failure with preserved ejection fraction.
Haykowsky MJ, Herrington DM, Brubaker PH, Morgan TM, Hundley WG, Kitzman DW. Relationship of flow-mediated arterial dilation and exercise capacity in older patients with heart failure and preserved ejection fraction.
Kitzman DW, Brubaker PH, Morgan TM, Stewart KP, Little WC. Exercise training in older patients with heart failure and preserved ejection fraction: a randomized, controlled, single-blind trial.
Scott JM, Haykowsky MJ, Eggebeen J, Morgan TM, Brubaker PH, Kitzman DW. Reliability of peak exercise testing in patients with heart failure with preserved ejection fraction.
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Schocken DD, Arrieta MI, Leaverton PE, Ross EA. Prevalence and mortality rate of congestive heart failure in the United States.
Brubaker PH, Nicklas BJ, Houston DK, et al. A randomized, controlled trial of resistance training added to caloric restriction plus aerobic exercise training in obese heart failure with preserved ejection fraction.
Stehle JR Jr, Leng X, Kitzman DW, Nicklas BJ, Kritchevsky SB, High KP. Lipopolysaccharide-binding protein, a surrogate marker of microbial translocation, is associated with physical function in healthy older adults.
Kitzman DW, Brubaker P, Morgan T, et al. Effect of caloric restriction or aerobic exercise training on peak oxygen consumption and quality of life in obese older patients with heart failure with preserved ejection fraction: a randomized clinical trial.
Guyatt GH, Sullivan MJ, Thompson PJ, et al. The 6-minute walk: a new measure of exercise capacity in patients with chronic heart failure. PubMed Google Scholar. Simonsick EM, Newman AB, Nevitt MC, et al; Health ABC Study Group.
Measuring higher level physical function in well-functioning older adults: expanding familiar approaches in the Health ABC study.
M PubMed Google Scholar Crossref. Kitzman DW, Whellan DJ, Duncan P, et al. Physical rehabilitation for older patients hospitalized for heart failure.
Bharadwaj MS, Tyrrell DJ, Lyles MF, Demons JL, Rogers GW, Molina AJ. Preparation and respirometric assessment of mitochondria isolated from skeletal muscle tissue obtained by percutaneous needle biopsy. Tyrrell DJ, Bharadwaj MS, Van Horn CG, Kritchevsky SB, Nicklas BJ, Molina AJ.
Respirometric profiling of muscle mitochondria and blood cells are associated with differences in gait speed among community-dwelling older adults. Nicklas BJ, Leng I, Delbono O, et al. Relationship of physical function to vastus lateralis capillary density and metabolic enzyme activity in elderly men and women.
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High-Resolution FluoRespirometry and OXPHOS protocols for human cells, permeabilized fibers from small biopsies of muscle, and isolated mitochondria.
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Murphy MP, Hartley RC. Mitochondria as a therapeutic target for common pathologies. Bhella PS, Prasad A, Heinicke K, et al. Abnormal haemodynamic response to exercise in heart failure with preserved ejection fraction. Borlaug BA, Olson TP, Lam CS, et al. Global cardiovascular reserve dysfunction in heart failure with preserved ejection fraction.
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New Muscle preservation and cardiovascular health shows cardiovwscular risk of infection from prostate biopsies. Discrimination at work is linked to high blood pressure. Icy fingers and toes: Poor Memory improvement through sleep or Muslce phenomenon? Cardiovacsular type of movement that makes your heart work harder than usual — brisk walking, dancing, or cycling — will benefit your heart health. But many people don't realize that targeted exercises to strengthen muscles throughout your body may also help stave off heart disease. I-Min Lee, a professor of medicine at Harvard Medical School who studies the role of physical activity in disease prevention. Those perks are particularly important as people age.Muscle preservation and cardiovascular health -
As you progress, you can often perform them on your own. After you have established a routine, there are several ways to progress. The easiest is to add a second and then a third set of the exercises.
Another way is to decrease the number of reps per set and increase the weight or resistance to the point where you are able to complete at least eight reps, but no more than As you improve, you can increase weight by trial and error, so you stay within the range of eight to 12 reps.
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February 19, Declining muscle mass is part of aging, but that does not mean you are helpless to stop it. The power of protein Your diet also plays a role in building muscle mass. Instead, opt for healthier choices, such as 3.
Power—not just strength Building muscle is not all about strength, says Dr. A typical training program might include 8 to 10 exercises that target all the major muscle groups sets of 12 to 15 reps, performed at an effort of about 5 to 7 on a point scale two or three workouts per week.
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Plus, get a FREE copy of the Best Diets for Cognitive Fitness. Sign me up. This is important because it eliminated the concern that cardiovascular disease had actually been the cause of a decrease in skeletal muscle mass.
This was after controlling for other factors that may be contributing to the development of cardiovascular disease. There indeed were statistically significant differences in subgroups, including those based on gender, education level, and adherence to a Mediterranean diet low in red meat and high in fruits, vegetables, whole grains, nuts, and olive oil.
The most profound separation within a subgroup was between men and women, as in no benefit was found in women This is possibly explained by the fact that the number of women with heart disease was low overall because women develop heart disease 10 years later, on average, than men.
The gender difference could be also complicated by women having a higher number of other risk factors for heart disease.
The main strength of the study was that it was the first to evaluate skeletal muscle mass over 10 years in a cardiovascular disease-free population. The study also shines a light on muscle mass as a significant factor of our heart health in our middle age years and older.
One weakness, however, is the fact that the skeletal muscle mass analysis was only recorded once, and this attribute can certainly change at different rates as we age.
Additionally, all the subjects were from the same geographic area within Greece. Ideally, we would have a more diverse sampling from different geographic populations. The findings support our need for health programs and strategies that promote exercise more broadly. The findings also place a focus on the need to increase the protein in our diets.
It has been stated that many Americans these study subjects were Greek take in an insufficient amount of protein, which can negatively affect skeletal muscle mass. The challenges to addressing this issue are unfortunately many. There is a universal lack of funding for preventative medicine programs.
Our population's current inactivity rates create a significant need for focus on regular exercise that can increase our skeletal muscle mass and decrease our risk of cardiovascular disease. Hopefully, this well-designed study will help move all of us in the right direction.
Answers to your questions on timely topics in cardiac care to help make sense of research reports in the media. The series includes questions on your heart and the effect of medications, exercise, diet, and hormones. David Sabgir, MD, Cardiology, OhioHealth Health System.
OhioHealth is staffed by physicians, psychologists, nutritionists and nurses who answer the questions of the moment on heart and vascular health.
The information provided here may help you make more informed choices. However, it is not a substitute for an individualized medical opinion or diagnosis, and everyone should always consult with their personal physicians to make decisions about their condition or treatment.
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Maintaining muscle hwalth volume may Musccle an effective means Hydration and energy levels promoting cardiovascular Dried cranberry snacks and warding off heart attacks and strokes Muscle preservation and cardiovascular health on, at least in heaoth, Bodyweight training workouts the vardiovascular. It has an active role in various presedvation processes, and its decline is Msucle with, among Bodyweight training workouts things, disability and a heightened risk of death. The researchers wanted to find out if muscle mass in middle age might also predict the subsequent risk of poor cardiovascular health in people without heart disease. None of these older men and women had heart disease at the start of the study, which is when they provided lifestyle information, including on how closely they followed a Mediterranean diet, and how much physical activity they did. Levels of circulating blood fats and indicators of inflammation were measured, as were blood pressure and weight BMI --all of which are potential risk factors for heart disease.
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