Muscle preservation and cardiovascular health -
Scandalis L , Kitzman DW , Nicklas BJ, et al. Skeletal Muscle Mitochondrial Respiration and Exercise Intolerance in Patients With Heart Failure With Preserved Ejection Fraction. JAMA Cardiol. Question Does mitochondrial dysfunction underlie altered skeletal muscle metabolism and exercise intolerance in patients with heart failure with preserved ejection fraction HFpEF?
Findings In this cross-sectional study including 27 patients older than 60 years with HFpEF and 45 healthy age-matched controls, high-resolution respirometry of vastus lateralis muscles from patients with HFpEF revealed markedly reduced bioenergetic capacity associated with peak exercise oxygen consumption and exercise performance 6-minute walk distance, Short Physical Performance Battery, and leg strength.
Meaning In this study, detailed analysis of mitochondrial function provided evidence that skeletal muscle mitochondrial dysfunction can play a role in HFpEF exercise intolerance, which may impact the development of therapeutic strategies that target mitochondrial dysfunction in patients with HFpEF.
Importance The pathophysiology of exercise intolerance in patients with heart failure with preserved ejection fraction HFpEF remains incompletely understood. Multiple lines of evidence suggest that abnormal skeletal muscle metabolism is a key contributor, but the mechanisms underlying metabolic dysfunction remain unresolved.
Objective To evaluate the associations of skeletal muscle mitochondrial function using respirometric analysis of biopsied muscle fiber bundles from patients with HFpEF with exercise performance. Design, Setting, and Participants In this cross-sectional study, muscle fiber bundles prepared from fresh vastus lateralis biopsies were analyzed by high-resolution respirometry to provide detailed analyses of mitochondrial oxidative phosphorylation, including maximal capacity and the individual contributions of complex I—linked and complex II-linked respiration.
These bioenergetic data were compared between patients with stable chronic HFpEF older than 60 years and age-matched healthy control HC participants and analyzed for intergroup differences and associations with exercise performance. All participants were treated at a university referral center, were clinically stable, and were not undergoing regular exercise or diet programs.
Data were collected from March to December , and data were analyzed from November to May Main Outcomes and Measures Skeletal muscle mitochondrial function, including maximal capacity and respiration linked to complex I and complex II.
Exercise performance was assessed by peak exercise oxygen consumption, 6-minute walk distance, and the Short Physical Performance Battery. Skeletal muscle mitochondrial function measures were all markedly lower in skeletal muscle fibers obtained from patients with HFpEF compared with HCs, even when adjusting for age, sex, and body mass index.
Conclusions and Relevance In this study, patients with HFpEF had marked abnormalities in skeletal muscle mitochondrial function. Severely reduced maximal capacity and complex I—linked and complex II—linked respiration were associated with exercise intolerance and represent promising therapeutic targets.
Heart failure HF with preserved ejection fraction HFpEF is the most prevalent form of HF, particularly among older adults and women. The primary clinical manifestation of chronic stable HFpEF is severe exercise intolerance, which is associated with impaired quality of life, and can be measured objectively and reproducibly as reduced peak exercise oxygen uptake peak VO 2.
Multiple lines of evidence indicate that in addition to underlying cardiac dysfunction, noncardiac factors contribute to exercise intolerance in HFpEF. Endurance exercise training significantly improves peak VO 2 in clinically stable older patients with HFpEF, with most of the improvement mediated by noncardiac factors, such as skeletal muscle function.
Several lines of evidence indicate that skeletal muscle metabolism is impaired in patients with HFpEF. Further, Dhakal et al, 13 using hemodynamic monitoring during exercise, showed that oxygen extraction was significantly reduced in HFpEF and is a major contributor to reduced peak VO 2.
Examination of skeletal muscle biopsies has shown that patients with HFpEF have a decreased number of type I oxidative fibers. Additionally, we observed that the mitochondrial fusion regulator, mitofusin 2 Mfn2 , is significantly decreased in HFpEF skeletal muscle and may also contribute to exercise intolerance.
Importantly, these mitochondrial parameters were directly related to peak VO 2 and 6-minute walk distance. Despite evidence suggesting multifaceted skeletal muscle mitochondrial impairments, respirometric analyses of skeletal muscle tissue, the criterion-standard assessment of mitochondrial function, in the context of HFpEF are lacking.
Using a rat model of HFpEF, Bowen et al 20 reported impaired mitochondrial respiration that was ameliorated with exercise training. To elucidate the role of mitochondria in impaired skeletal muscle metabolism in patients with HFpEF, the study presented here used high-resolution respirometry of freshly obtained skeletal muscle specimens to provide detailed analyses of mitochondrial function, including precise assessments of the maximal capacity of the electron transfer system and the individual contributions of complex I—linked and complex II—linked respiration.
These bioenergetic data were then associated with key measures of exercise performance across HFpEF and age-matched HC participants. HF signs and symptoms were confirmed by a board-certified cardiologist and met the criteria of the National Health and Nutrition Examination Survey HF clinical score of 3 or higher and the criteria of Rich et al.
Participants in this study were drawn from a parent clinical trial of patients with HFpEF. The results of that trial, including a detailed description of the study participants, have been published.
Age-matched, healthy, sedentary persons were recruited to serve as HCs. Cardiopulmonary exercise testing was performed on a treadmill using the modified Naughton protocol for patients with HFpEF and using the modified Bruce protocol for HCs, as previously described.
Breath-by-breath gas exchange data were measured continuously during exercise and averaged every 15 seconds, and peak values were averaged from the last two second intervals during peak exercise. A 6-minute walk test was performed using the method of Guyatt et al.
Peak upper leg strength in newton meters was measured on a dynamometer Biodex Medical Systems at 60° per second, with the participant seated and the hips and knees flexed at 90°.
To stabilize the hip joint and the trunk, participants were secured with straps at the chest, hip, and thigh. Seat height and depth, and the position of the lever arm ankle pad were adjusted to accommodate each participant.
Participants were asked to extend the knee and push as hard as possible against the ankle pad. Strength of the right and left legs recorded as peak torque was used for analyses.
Vastus lateralis biopsies were performed in the morning after an overnight fast, as previously described. Mitochondrial oxidative phosphorylation can be evaluated by measuring the rate of oxygen consumption in cells and tissues.
Together, these primary outcomes complex I respiration, complexes I and II respiration, and maximal capacity report on the maximal bioenergetic capacity of the electron transport system and the contributions of the 2 major electron transport chain entry points to this capacity.
Following previously published protocols, 40 approximately 2. Each sample was run in duplicate, and all data were normalized to measured muscle fiber bundle wet weight.
All assays were performed under a high initial oxygen concentration uM to uM in the O2K chamber Oroboros Instruments. Shapiro-Wilk tests were performed to check for normal distribution of all variables.
Log transformations were performed for parameters with nonnormal distribution. Intergroup HFpEF vs HC comparisons of participant characteristics were made by independent-samples t tests and χ 2 tests. Intergroup differences in bioenergetics parameters were compared using independent-samples t tests; additionally, to account for the differences in sex, BMI, and age, adjustments for these variables were made using analysis of covariance.
Intergroup in-exercise and physical function measures were assessed using independent-samples t tests as well as adjustment for sex using analysis of covariance. Pearson correlation coefficients were assessed between all variables, both raw and normalized values, and partial correlations adjusted for age, sex, and BMI were also assessed.
Analyses were performed using SPSS software version 26 IBM. A total of 27 patients with HFpEF and 45 age-matched HCs were included. Patients with HFpEF and HCs were well matched for age; however, there were more women in the HFpEF group.
Body mass, fat mass, percentage body fat, and BMI were higher in those with HFpEF compared with HCs, in accord with observations in multiple population-based studies and trials that have reported significantly higher BMI in patients with HFpEF compared with the general population.
Patients with HFpEF had severely reduced peak VO 2 compared with HCs Table 2. There was nonsignificantly lower peak heart rate in patients with HFpEF vs HC. Six-minute walk distance was also significantly reduced in HFpEF compared with HC. Both SPPB chair stand and walk 4 m times were higher in patients with HFpEF compared with HC, resulting in overall lower SPPB scores in patients with HFpEF.
Left leg strength was significantly reduced in patients with HFpEF compared with HCs. A representative trace depicting the high-resolution respirometry protocol used for this project is shown in eFigure 1 in Supplement 1. Comparisons of bioenergetic measures between patients with HFpEF and HCs are shown in Table 3.
Across complex I respiration, complexes I and II respiration, and maximal capacity, the mean oxygen consumption rates per mg muscle were significantly reduced in patients with HFpEF compared with HCs.
When the data were adjusted for sex, age, and BMI, individually and together, differences remained statistically significant.
Pearson correlation coefficients were used to examine correlations between skeletal muscle mitochondrial function and measures of physical function across participants with HFpEF and HCs.
The results are summarized in eTable 1 in Supplement 1. Sensitivity analyses were conducted to assess whether the correlation between skeletal muscle mitochondrial function and peak VO 2 differed between the patients with HFpEF and HCs using both stratified correlation analysis eTable 2 and eFigure 2 in Supplement 1 and regression analysis with an interaction term.
This study using respirometry of skeletal muscle fiber bundles obtained from biopsy in patients with HFpEF compared with age-matched HCs, to our knowledge, provides the first direct evidence indicating that cellular-level mitochondrial dysfunction underlies skeletal muscle metabolic abnormalities in those with HFpEF and is associated with multiple objective measures of severe exercise intolerance, including reduced peak VO 2 , 6-minute walk distance, SPPB, and leg strength.
These mitochondrial abnormalities represent potential therapeutic targets, as the function of these organelles is linked to many common disease processes and potentially modifiable by both pharmacological interventions as well as behavioral interventions, such as diet and exercise.
Patients with chronic HFpEF have severe exercise intolerance that is associated with impaired quality of life. Multiple lines of evidence indicate that in addition to cardiac factors, noncardiac peripheral factors, including abnormal skeletal muscle metabolism, contribute to the severe exercise intolerance in patients with HFpEF.
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. Get helpful tips and guidance for everything from fighting inflammation to finding the best diets for weight loss from exercises to build a stronger core to advice on treating cataracts.
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The EWGSOP definition of sarcopenia is now widely used internationally. Sarcopenia is associated with various adverse outcomes, including falls, dysfunction, weakness, and death. Sarcopenia is now officially recognized as a muscle disorder with the diagnosis code ICDMC, suggesting that it will receive widespread attention from the medical community as a disorder with unique characteristics and a more accurate understanding of screening, diagnosis, intervention, and treatment of the condition Due to the lack of specific clinical manifestations of sarcopenia and the fact that human muscle mass is affected by various factors such as race, region, age, and gender, there is currently no unified standard for diagnosing sarcopenia at home and abroad.
EWGSOP 9AWGs 10IWGS 7FNIH 12 all state that the diagnosis of sarcopenia should take into account a combination of muscle mass and muscle function, with the leading indicators including muscle mass, muscle strength, and muscle function. Specific updated diagnostic criteria for sarcopenia are shown in Table 1.
The prevalence of sarcopenia varies with different diagnostic criteria and different measures of muscle mass. The prevalence of sarcopenia in the elderly in the community ranges from 8.
Epidemiological studies have found that skeletal muscle begins to degenerate after the 40 and accelerates with age. Due to differences in study populations, research methods and diagnostic criteria, the prevalence of sarcopenia varies greatly between different studies.
There are also significant differences in the incidence of sarcopenia in different regions. The prevalence of sarcopenia is In the UK, the prevalence of sarcopenia in men and women is 4. Research on sarcopenia in the Asian population is still in its infancy.
In Asia, the incidence of sarcopenia in Thailand was The study included elderly inpatients with an average age of Among them, the in-hospital mortality rate of patients with sarcopenia was There is an increased length of stay and mortality in older inpatients with sarcopenia 1.
Differences in the prevalence of sarcopenia may be related to ethnicity, lifestyle, exercise habits, and the use of quantitative diagnostic criteria adopted by different research institutes.
It is estimated that bythere will be more than million elderly patients with sarcopenia in the world 6. Sarcopenia can increase the risk of weakness, falls and fractures, decrease the quality of life, even the ability to live independently, and increase the infection rate, and mortality rate in patients.
Sarcopenia is associated with CVDs, diabetes, renal insufficiency, cancer, cognitive impairment, and even with the prognosis of some diseases 19 — The main feature of sarcopenia is skeletal muscle disorders such as loss of muscle mass, quality, strength, and physical performance.
Sarcopenia may be considered one of the most important causes of poor physical performance and reduced cardiorespiratory fitness in older patients with CVDs. CVDs may induce sarcopenia through common pathogenetic pathways such as hormonal changes, malnutrition, and physical inactivity, mechanisms that influence each other.
Sarcopenia is also an age-related disease closely related to CVDs, and there are similarities between the two in terms of risk factors and pathogenesis. The prevalence of sarcopenia is high in older HF patients, with sarcopenia also predictor of HF prognosis. Patients with HF are often associated with decreased muscle and strength.
The ubiquitin protease system, myogenic protein signaling pathways, apoptosis, malnutrition due to gastrointestinal edema, and inflammatory factors may all contribute to sarcopenia 23 The impaired exercise tolerance of HF patients is related to the changes of failed cardiomyocytes and skeletal muscle cells.
The onset, development, and progression of sarcopenia follow the same clinical course as HF, with the two interacting. One SICA-HF study covered HF patients, with the average age of the patients was It was showed a prevalence of sarcopenia of Another study reported that The coexistence of sarcopenia and HF may be the result of their common pathophysiological pathways.
The imbalance of muscle protein synthesis and decomposition is a major factor in the development of sarcopenia Oxidative stress can accelerate skeletal muscle degeneration and increase muscle protein decomposition.
Levels of inflammatory markers tend to be elevated in patients with HF. Studies have shown that high levels of inflammatory cytokines are negatively associated with muscle strength and mass In patients with heart failure and sarcopenia, the level of growth hormone GH is increased, while the level of insulin-like growth factor-1 IGF-1 is significantly reduced, suggesting that there may be GH resistance, leading to an inhibition of skeletal muscle formation.
In addition, patients with HF may suffer from poor appetite and malabsorption due to urinary difficulties, nausea, adverse drug reactions, which leads to inadequate or excessive nutrient loss and gastrointestinal symptoms and is associated with the pathogenesis of sarcopenia.
Reduced peripheral perfusion due to left ventricular insufficiency from HF and reduced physical activity, which limits daily activities, can also cause a reduction in skeletal muscle, leading to the development of sarcopenia In a FLEAR study of elderly hospitalized patients, it was found that Through an echocardiographic study, it was discovered a correlation between sarcopenia and cardiac hypertrophy Previous studies have shown a negative correlation between grip strength and heart mass in patients at risk of sarcopenia.
Heart failure with preserved ejection fraction HFpEF represents an important cardiovascular entity with increasing prevalence and relatively high mortality.
Therefore, the earliest description of HFpEF is mainly conceptualized as a diastolic filling disorder. Only later inflammation and multimorbidity, which play a key role in the development of sarcopenia, are considered the main factors in developing HFpEF 36 Thus it can be seen that the interaction and mechanism between sarcopenia and HF are very complicated.
At present, there are few studies on the relationship between sarcopenia and hypertension. The results showed that the high prevalence of sarcopenia in the Chinese elderly population is related to CVRF. In addition, diabetes and hypertension, rather than dyslipidemia, were significantly associated with sarcopenia.
It indicated that CVRF, especially diabetes and hypertension, may help predict the risk of sarcopenia in the elderly 4. A follow-up study of 3, people in Korea found that the year risk of CVDs in obese patients with sarcopenia was higher than those with non-obesity and non-sarcopenia.
In contrast, the year risk of CVDs in patients with simple obesity or sarcopenia was not significantly increased. A British study followed up 4, older men and found that patients with sarcopenia obesity highly correlated with CVD mortality.
Patients with sarcopenia obesity have a higher mortality rate, but the study did not observe an increase in CVD incidence. Studies have also shown that patients with sarcopenia obesity are at high risk of developing type 2 diabetes mellitus, hypertension, and hyperlipidemia 38 — In the early stage, it was considered that sarcopenia caused by aging is related to an increased incidence of hypertensive retinopathy and hypertensive kidney damage.
More recently, it has been found that hypertension is related to the decrease in the number of capillaries around muscle cells Therefore, it has been hypothesized that blood pressure-induced changes in the capillary network of muscle tissue are one of the risk factors for the occurrence of sarcopenia in elderly patients.
Atherosclerotic cardiovascular diseases ACVDssuch as coronary atherosclerotic heart disease, atherogenic stroke or transient ischemic attack, transient ischemic attack, and peripheral artery disease, are acute diseases that affect the health of older people.
They are also a direct cause of death, disability, and high medical costs. Exploring the related comorbidities and risk factors, looking for reliable prognostic markers has become a current research hotspot.
A study of Japanese subjects mean age A large-scale cohort study showed that early atherosclerosis index carotid-femoral pulse wave velocity PWV independently and negatively correlated with skeletal muscle mass in Americans aged 70 to 79 The decline in muscle mass and muscle strength was associated with endothelial dysfunction in another study of Brazilian people over 80 years of age, with a 3.
: Muscle preservation and cardiovascular health| globals_asset_name | Statistical Analysis. Prevalence of Muscle preservation and cardiovascular health interventions for Glutamine powder Effective antifungal therapy ageing adults: Gut-friendly recipes systematic ;reservation. Sarcopenia Muecle age-related loss of muscle mass associated with low muscle strength and or low physical performance. Campos AM, Moura FA, Santos SN, Freitas WM, Sposito AC. Therefore, the best means to build muscle mass, no matter your age, is progressive resistance training PRTsays Dr. Skeletal Muscle Mitochondrial Respiration and Exercise Intolerance in Patients With Heart Failure With Preserved Ejection Fraction. |
| Helpful Links | Patients were diagnosed and evaluated for sarcopenia regarding the diagnostic indicators of EWGSOP. The results showed that the prevalence of sarcopenia was The prevalence of sarcopenia was much higher in male patients than in female patients, and sarcopenia was associated with thrombolysis-related myocardial infarction scores The study assessed skeletal muscle mass in patients with ST-segment elevation acute myocardial infarction. All-cause death, non-fatal myocardial infarction, non-fatal ischemic stroke, hospitalization for congestive heart failure, and unplanned revascularization were used as the endpoints of long-term follow-up. The results showed that the lower limb skeletal muscle index was still independently associated with the high risk of primary complex events In addition, some studies have shown that muscle mass and muscle strength are negatively correlated with the increase of coronary artery calcification score. Furthermore, muscle mass is positively correlated with coronary artery diastolic ability, suggesting that sarcopenia is related to subclinical coronary atherosclerosis Loss of muscle mass correlates with coronary artery calcification, an independent risk factor for CHD. Decreased skeletal muscle mass also increases the risk of death in patients with CHD Reduced muscle mass diagnosed by CT is a strong predictor of poor prognosis in patients with CHD who undergo percutaneous coronary intervention The mechanism of the role of sarcopenia in CHD is currently unclear. Studies have shown that sarcopenia and obesity form a vicious circle in the body and then participate in the occurrence and development of CVDs led by CHD through a series of mechanisms such as insulin resistance, mitochondrial dysfunction, oxidative stress, adipokines, and inflammatory factors 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. Relationship between sarcopenia and mortality in elderly inpatients. Eurasian J Med. doi: PubMed Abstract CrossRef Full Text Google Scholar. Li J, Chan MC Yu Y, Bei Y, Chen P, Zhou Q, et al. miRb contributes to multiple types of muscle atrophy. Nat Commun. Lena A, Anker MS, Springer J. Muscle wasting and sarcopenia in heart failure-the current state of science. Int J Mol Sci. Han P, Yu H, Ma Y, Kang L, Fu L, Jia L, et al. The increased risk of sarcopenia in patients with cardiovascular risk factors in suburb-dwelling older Chinese using the AWGS definition. Sci Rep. Rosenberg IH. Sarcopenia: origins and clinical relevance. J Nutr. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, Boirie Y, Cederholm T, Landi F, et al. Sarcopenia: European consensus on definition and diagnosis: report of the European Working Group on sarcopenia in older people. Age Ageing. Fielding RA, Vellas B, Evans WJ, Bhasin S, Morley JE, Newman AB, et al. Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences International working group on sarcopenia. J Am Med Dir Assoc. Chen LK, Liu LK, Woo J, Assantachai P, Auyeung TW, Bahyah KS, et al. Sarcopenia in Asia: consensus report of the Asian Working Group for Sarcopenia. Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyere O, Cederholm T, et al. Sarcopenia: revised European consensus on definition and diagnosis. Chen LK, Woo J, Assantachai P, Auyeung TW, Chou MY, Iijima K, et al. Asian Working Group for Sarcopenia: consensus update on sarcopenia diagnosis and treatment. Cruz-Jentoft AJ, Landi F, Schneider SM, Zuniga C, Arai H, Boirie Y, et al. Prevalence of and interventions for sarcopenia in ageing adults: a systematic review. Report of the International Sarcopenia Initiative EWGSOP and IWGS. Studenski SA, Peters KW, Alley DE, Cawthon PM, McLean RR, Harris TB, et al. The FNIH sarcopenia project: rationale, study description, conference recommendations, and final estimates. J Gerontol A Biol Sci Med Sci. Zeng Y, Hu X, Xie L, Han Z, Zuo Y, Yang M. The prevalence of sarcopenia in chinese elderly nursing home residents: a comparison of 4 diagnostic criteria. Foley RN, Wang C, Ishani A, Collins AJ, Murray AM. Kidney function and sarcopenia in the United States general population: NHANES III. Am J Nephrol. von Haehling S. The wasting continuum in heart failure: from sarcopenia to cachexia. Proc Nutr Soc. Bouchard DR, Dionne IJ, Brochu M. Obesity Silver Spring. Woods JL, Iuliano-Burns S, King SJ, Strauss BJ, Walker KZ. Poor physical function in elderly women in low-level aged care is related to muscle strength rather than to measures of sarcopenia. Clin Interv Aging. Patel HP, Syddall HE, Jameson K, Robinson S, Denison H, Roberts HC, et al. Prevalence of sarcopenia in community-dwelling older people in the UK using the European Working Group on Sarcopenia in Older People EWGSOP definition: findings from the Hertfordshire Cohort Study HCS. Hsu YH, Liang CK, Chou MY, Liao MC, Lin YT, Chen LK, et al. Association of cognitive impairment, depressive symptoms and sarcopenia among healthy older men in the veterans retirement community in Southern Taiwan: a cross-sectional study. Geriatr Gerontol Int. Chen LK, Lee WJ, Peng LN, Liu LK, Arai H, Akishita M. Recent advances in sarcopenia research in asia: update from the Asian Working Group for sarcopenia. Srikanthan P, Karlamangla AS. Relative muscle mass is inversely associated with insulin resistance and prediabetes. Findings from the third National Health and Nutrition Examination Survey. J Clin Endocrinol Metab. But when further more detailed analysis was carried out, muscle volume remained significantly associated with lower cardiovascular disease risk, irrespective of diet, household income, and educational attainment, as well as known risk factors, such as diabetes among those aged 45 and older, but only among men. The gender disparity may be partly explained by higher muscle volume in men to start with and hormonal differences between the sexes in the ageing process, suggest the researchers. And they suggest that periodic physical activity, including resistance training, and a diet rich in protein, may help preserve lean muscle mass as people age. Research: Skeletal muscle mass in relation to 10 year cardiovascular disease incidence among middle aged and older adults: the ATTICA study doi pdf Peer Reviewed? Yes Evidence type: Observational Subjects: People. If you are a journalist who would like to receive our press releases, please provide your details. Middle aged muscle mass linked to future heart disease risk. BMJ Expert Media Panel If you are a journalist needing to speak to an expert, please click here. Bring the resistance tubing up behind your shoulders so that you are holding the handles on top of your shoulders with your palms facing forward. Movement: Hinge forward at the hips and bend your knees to lower your buttocks toward the floor as if sitting down in a chair. Throughout the movement, press your weight back into your heels and keep the handles on top of your shoulders. Return to the starting position. Starting position: Stand with the resistance tubing under your feet. Position your feet hip-width apart and place your hands at your sides with thumbs pointing forward as you hold the handles. Movement: Squeeze your shoulder blades together while you slowly lift your arms toward the two front corners of the room, creating a V as you raise the resistance tubing. Go no higher than your shoulders. Slowly return to the starting position. As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician. Thanks for visiting. Don't miss your FREE gift. The Best Diets for Cognitive Fitness , is yours absolutely FREE when you sign up to receive Health Alerts from Harvard Medical School. Sign up to get tips for living a healthy lifestyle, with ways to fight inflammation and improve cognitive health , plus the latest advances in preventative medicine, diet and exercise , pain relief, blood pressure and cholesterol management, and more. Get helpful tips and guidance for everything from fighting inflammation to finding the best diets for weight loss from exercises to build a stronger core to advice on treating cataracts. PLUS, the latest news on medical advances and breakthroughs from Harvard Medical School experts. Sign up now and get a FREE copy of the Best Diets for Cognitive Fitness. 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| Can stronger muscles pump up your heart health? - Harvard Health | Determinants of exercise intolerance in elderly Nad failure patients with preserved ejection Preservatjon. This constant challenging builds Antioxidant drinks for hydration Musclee keeps you away from plateaus where you stop making gains. Senescent cells: a therapeutic target for cardiovascular disease. The power of protein Your diet also plays a role in building muscle mass. Beta-hydroxy-beta-methylbutyrate HMB supplementation in humans is safe and may decrease cardiovascular risk factors. |
| Relationship Between Sarcopenia and Cardiovascular Diseases in the Elderly: An Overview | Position your feet hip-width apart and place your hands at your sides with thumbs pointing forward as you hold the handles. Movement: Squeeze your shoulder blades together while you slowly lift your arms toward the two front corners of the room, creating a V as you raise the resistance tubing. Go no higher than your shoulders. Slowly return to the starting position. As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician. Thanks for visiting. Don't miss your FREE gift. The Best Diets for Cognitive Fitness , is yours absolutely FREE when you sign up to receive Health Alerts from Harvard Medical School. Sign up to get tips for living a healthy lifestyle, with ways to fight inflammation and improve cognitive health , plus the latest advances in preventative medicine, diet and exercise , pain relief, blood pressure and cholesterol management, and more. Get helpful tips and guidance for everything from fighting inflammation to finding the best diets for weight loss from exercises to build a stronger core to advice on treating cataracts. PLUS, the latest news on medical advances and breakthroughs from Harvard Medical School experts. Sign up now and get a FREE copy of the Best Diets for Cognitive Fitness. Stay on top of latest health news from Harvard Medical School. Recent Blog Articles. Flowers, chocolates, organ donation — are you in? What is a tongue-tie? What parents need to know. Which migraine medications are most helpful? How well do you score on brain health? Shining light on night blindness. Can watching sports be bad for your health? Beyond the usual suspects for healthy resolutions. My podcast changed me Can 'biological race' explain disparities in health? Why Parkinson's research is zooming in on the gut Tools General Health Drugs A-Z Health Hubs Health Tools Find a Doctor BMI Calculators and Charts Blood Pressure Chart: Ranges and Guide Breast Cancer: Self-Examination Guide Sleep Calculator Quizzes RA Myths vs Facts Type 2 Diabetes: Managing Blood Sugar Ankylosing Spondylitis Pain: Fact or Fiction Connect About Medical News Today Who We Are Our Editorial Process Content Integrity Conscious Language Newsletters Sign Up Follow Us. Medical News Today. Health Conditions Health Products Discover Tools Connect. Human Biology. Nervous system Cardiovascular system Respiratory system Digestive system Immune system. Is there a link between muscle mass and cardiovascular risk? By Maria Cohut, Ph. on November 13, — Fact checked by Jasmin Collier. Share on Pinterest Muscle mass loss is linked to a higher risk of cardiovascular problems in males aged 45 and over. Muscle mass loss may increase heart risks. Share this article. Latest news Ovarian tissue freezing may help delay, and even prevent menopause. RSV vaccine errors in babies, pregnant people: Should you be worried? Scientists discover biological mechanism of hearing loss caused by loud noise — and find a way to prevent it. How gastric bypass surgery can help with type 2 diabetes remission. Atlantic diet may help prevent metabolic syndrome. Related Coverage. But just because you lose muscle mass does not mean it is gone forever. Thomas W. Storer, director of the exercise physiology and physical function lab at Harvard-affiliated Brigham and Women's Hospital. One possible contributor to sarcopenia is the natural decline of testosterone, the hormone that stimulates protein synthesis and muscle growth. Think of testosterone as the fuel for your muscle-building fire. Some research has shown that supplemental testosterone can add lean body mass—that is, muscle—in older men, but there can be adverse effects. Plus, the FDA has not approved these supplements specifically for increasing muscle mass in men. Therefore, the best means to build muscle mass, no matter your age, is progressive resistance training PRT , says Dr. With PRT, you gradually amp up your workout volume—weight, reps, and sets—as your strength and endurance improve. This constant challenging builds muscle and keeps you away from plateaus where you stop making gains. See "Working on a PRT program. Your diet also plays a role in building muscle mass. Protein is the king of muscle food. The body breaks it down into amino acids, which it uses to build muscle. However, older men often experience a phenomenon called anabolic resistance, which lowers their bodies' ability to break down and synthesize protein. Therefore, as with PRT, if you are older, you need more. A recent study in the journal Nutrients suggests a daily intake of 1 to 1. For example, a pound man would need about 79 g to g a day. If possible, divide your protein equally among your daily meals to maximize muscle protein synthesis. This is a high amount compared with the average diet, but there are many ways to get the extra protein you need. Animal sources meat, eggs, and milk are considered the best, as they provide the proper ratios of all the essential amino acids. Yet, you want to stay away from red and processed meat because of high levels of saturated fat and additives. Instead, opt for healthier choices, such as. Protein powders can offer about 30 g per scoop and can be added to all kinds of meals like oatmeal, shakes, and yogurt. Also, to maximize muscle growth and improve recovery, he suggests consuming a drink or meal with a carbohydrate-to-protein ratio of about three-to-one or four-to-one within 30 minutes after your workout. For example, a good choice is 8 ounces of chocolate milk, which has about 22 g of carbs and 8 g of protein. Building muscle is not all about strength, says Dr. You also need power. |
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