Effect of muscle mass decrease on age-related BMR changes.
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Adult↗
SEARCH · PubMed Health
Results for “Muscle mass”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
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Muscle mass and composition in malnourished infants and children and changes seen after recovery.
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Body Composition↗
Carcinoma of the lung occurring as a skeletal muscle mass.
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Carcinoma, Squamous Cell↗
Performance of conventional orthogonal and multiple-dipole electrocardiograms in estimating left ventricular muscle mass.
For estimating left ventricular mass (LVM), ECG criteria for left ventricular hypertrophy (LVH) were selected from conventional 12-lead ECGs, orthogonal three-lead ECGs, and multiple-dipole ECGs (MDECG). The three cardiograms were recorded in 139 patients for whom the degree of LVH was independently determined from biplane ventriculograms. Tested ECG criteria included Sokolow-Lyon measurements for the 12-lead ECG; for the orthogonal ECG, maximal QRS magnitude in the horizontal plane, R duration in the z-lead and Jxyz (spatial magnitude of point J); and for the 126 leads of the MDECG, the dipole activity (DA) of the septum and the free left ventricular wall. Correlation coefficients between LVM and the 12-lead ECG, three-lead ECG and MDECG were 0.61, 0.78 and 0.89, respectively, with corresponding errors of estimated LVM of 103, 82 and 60 g. More complex recording and analytic methods clearly led to increased accuracy in LVM estimates. However, the large error of estimate may limit practical applicability of such correlations. For classification of subjects into normal and above-normal categories, a likelihood ratio was also used and led to a maximum performance index of 86% with MDECG measurements.
Electrocardiography↗
Comparative skeletal mass and radial bone mineral content in black and white women.
The age-related changes in both skeletal mass and muscle mass were directly measured in normal black women ages 30-80 yr. The levels of total-body calcium (TBCa) were determined with the use of in vivo neutron activation. The muscle mass was measured by wholebody counting of 40K. In the same population, the bone mineral content of the radius was measured using a photon absorptiometric technique. Although there was no significant difference in stature, black women had a greater skeletal mass and bone mineral content of the radius than age-matched white female subjects. When the TBCa values were normalized for body size (i.e., corrected for height and lean body mass), the TBCa was still higher for the black women but not as high as the absolute TBCa values. Clearly, it is the larger muscle mass (as reflected by the 40K measure) in relation to weight and height that accounts for this difference. The lower prevalence of fracture and osteoporosis observed in black women relative to white women is due in part to this greater quantity of skeleton. American black women with a higher bone density (i.e., skeletal mass) maintain mechanical integrity of the skeleton longer than individuals with a lower bone density. It is suggested that the larger muscle mass in black women is, in part, a determinant of their increased skeletal mass and is partly responsible for their apparent resistance to osteoporosis and fracture of the skeleton.
Adult↗
Gaining and losing weight in athletics.
Participants in many sports, such as wrestling, gymnastics, and light-weight crew, attempt to reduce body weight to achieve a maximum ratio of muscle strength to body weight. Such weight reduction should result only from reduction in excess body fat. In most instances, weight reduction should be achieved at a rate of no more than 1 kg a week, through a modest reduction in diet and a moderate increase in exercise. More rapid weight reduction by starvation and dehydration compromises strength and endurance. Athletes attempting to gain weight should increase weight as muscle mass, not fat. Muscle mass is increased only through muscle work supported by an appropriate increase in food intake. No food, vitamin, drug, or hormone will increase muscle mass. It is recommended that the high caloric diet required to support muscle growth from increased work should be low in animal fats and cholesterol.
Adipose Tissue↗
The distribution of motoneurones supplying chick hind limb muscles.
1. The motor nuclei supplying many of the hind limb muscles were localized in late chick embryos (stage 36-37; 10-11 days) by utilizing the technique of retrograde transport of horseradish peroxidase. 2. Each nucleus was found to be localized in a characteristic position in both the rostro-caudal and transverse plane of the spinal cord with only slight individual variation. 3. Each motor nucleus consisted of an elongate, coherent cluster of labelled cells, with few cells occurring outside the cluster. Thus, there did not appear to be extensive overlap of nuclei nor extensive intermingling of motoneurones projecting to different muscles. 4. The position of a motor nucleus in the transverse plane was not correlated with whether its muscle was used as an extensor or flexor; nor were adjacent nuclei necessarily co-activated during normal unrestrained walking movements as deduced from e.m.g. recordings. The position of a motor nucleus also was not correlated in a topographical manner with the adult position in the limb of the muscle to which it projected. 5. Further, while no correlation was found between the rostrocaudal position of a motor nucleus and the embryonic muscle mass from which its muscle was derived, such a relationship existed for the medio-lateral position; all muscles arising from the dorsal muscle mass, regardless of their function or adult position, were innervated by laterally situated motoneurones, all muscles arising from the ventral muscle mass by medially situated motoneurones. 6. It is concluded that motoneurone position is most closely correlated with ontogenetic events presumaeriphery. It can also be inferred that the central connexions onto motoneurones, responsible for their proper activation, cannot be achieved by a simple mechanism based largely on the position of the motoneurone soma.
Action Potentials↗
Celery seed extract attenuates sarcopenic obesity and age-related sarcopenia by reducing intramuscular lipid accumulation in mice.
BACKGROUND & AIMS: Sarcopenia is characterized by progressive loss of skeletal muscle mass and function and is increasingly recognized to be influenced by metabolic disturbances associated with aging and obesity. Intramuscular lipid accumulation has emerged as a key pathological feature linking metabolic dysfunction to skeletal muscle deterioration. Celery seed extract (CSE) possesses anti-obesity, anti-inflammatory, and antioxidant properties; however, its potential role in skeletal muscle metabolism has not been well investigated. This study aimed to determine whether CSE attenuates skeletal muscle deterioration associated with obesity and aging through modulation of intramuscular lipid accumulation and related metabolic pathways. METHODS: Diet-induced obese mice and naturally aged mice were used to evaluate the effects of CSE supplementation. Skeletal muscle mass, grip strength, muscle morphology, intramuscular lipid content, mitochondrial metabolic signaling, inflammatory responses, and muscle protein turnover pathways were assessed using biochemical, molecular, and histological analyses. RESULTS: CSE supplementation significantly improved skeletal muscle mass, grip strength, and muscle fiber cross-sectional area in both obese and aged mice. These improvements were accompanied by reduced intramuscular triglyceride and cholesterol accumulation. Mechanistically, CSE improved mitochondrial metabolic signaling by activating the AMPK-PGC-1α pathway and increasing mitochondrial oxidative phosphorylation proteins. In addition, CSE suppressed inflammatory signaling pathways, including MAPK activation and NLRP3 inflammasome signaling, and improved muscle proteostasis by enhancing myogenic regulators while reducing the expression of proteolytic factors such as MuRF1, Atrogin-1, and myostatin. Correlation analyses further indicated that intramuscular lipid accumulation was closely associated with mitochondrial dysfunction, inflammatory activation, and muscle atrophy. CONCLUSIONS: These findings demonstrate that CSE alleviates skeletal muscle deterioration in both obesity- and aging-associated sarcopenia by reducing intramuscular lipid accumulation and improving mitochondrial metabolism, inflammatory responses, and muscle protein turnover. Targeting intramuscular lipid accumulation may therefore represent a promising nutritional strategy for preventing sarcopenia associated with metabolic and aging-related stress.
AMPK–PGC-1α↗
Comparative Analysis of Primary Sarcopenia and End-Stage Renal Disease-Related Muscle Wasting Using Multi-Omics Approaches.
BACKGROUND: Age-related primary sarcopenia and end-stage renal disease (ESRD)-related muscle wasting are discrete entities; however, both manifest as a decline in skeletal muscle mass and strength. The etiological pathways differ, with aging factors implicated in sarcopenia and a combination of uremic factors, including haemodialysis, contributing to ESRD-related muscle wasting. Understanding these molecular nuances is imperative for targeted interventions, and the integration of proteomic and metabolomic data elucidate these intricate processes. METHODS: We generated detailed clinical data and multi-omics data (plasma proteomics and metabolomics) for 78 participants to characterise sarcopenia (n = 28; mean age, 72.6 ± 7.0 years) or ESRD (n = 22; 61.6 ± 5.5 years) compared with controls (n = 28; 69.3 ± 5.7 years). Muscle mass was measured using bioelectrical impedance analysis and handgrip strength. Five-times sit-to-stand test performance was measured for all participants. Sarcopenia was diagnosed in accordance with the 2019 Consensus Guidelines from the Asian Working Group for Sarcopenia. An abundance of 234 metabolites and 722 protein groups was quantified in all plasma samples using liquid chromatography with tandem mass spectrometry. RESULTS: Muscle mass, handgrip strength and lower limb muscle function significantly lower in the sarcopenia group and the ESRD group compared with those in the control group. Metabolomics revealed altered metabolites, highlighting exclusive differences in ESRD-related muscle wasting. Metabolite set enrichment analysis revealed the involvement of numerous metabolic intermediates associated with urea cycle, amino acid metabolism and nucleic acid metabolism. Catecholamines, including epinephrine, dopamine and serotonin, are significantly elevated in the plasma of patients within the ESRD group. Proteomics data exhibited a clearer distinction among the three groups compared with the metabolomics data, particularly in distinguishing the control group from the sarcopenia group. The ciliary neurotrophic factor receptor was top-ranked in terms of the variable importance of projection scores. Plasma AHNAK protein levels was higher in the sarcopenia group but was lower in the ESRD group. Proteomic set enrichment analysis revealed enrichment of several pathways related to sarcopenia, such as hemopexin, defence response and cell differentiation, in sarcopenia group. Multi-omic integration analysis revealed associations between relevant metabolites, including catecholamines, and a group of annotated proteins in extracellular exosomes. CONCLUSIONS: We identified distinct multi-omic signatures in individuals with ESRD or sarcopenia, providing new insights into the mechanisms underlying ESRD-related muscle wasting, which differ from primary sarcopenia. These findings may support interventions for context-dependent muscle loss and contribute to the development of targeted treatments and preventive strategies for muscle wasting.
Humans↗
The effect of low birth weight as an intrauterine exposure on the early onset of sarcopenia through possible molecular pathways.
Sarcopenia, a musculoskeletal disease characterized by the progressive loss of skeletal muscle mass, strength, and physical performance, presents significant challenges to global public health due to its adverse effects on mobility, morbidity, mortality, and healthcare costs. This comprehensive review explores the intricate connections between sarcopenia and low birth weight (LBW), emphasizing the developmental origins of health and disease (DOHaD) hypothesis, inflammatory processes (inflammaging), mitochondrial dysfunction, circadian rhythm disruptions, epigenetic mechanisms, and genetic variations revealed through genome-wide studies (GWAS). A systematic search strategy was developed using PubMed to identify relevant English-language publications on sarcopenia, LBW, DOHaD, inflammaging, mitochondrial dysfunction, circadian disruption, epigenetic mechanisms, and GWAS. The publications consist of 46.2% reviews, 21.2% cohort studies, 4.8% systematic reviews, 1.9% cross-sectional studies, 13.4% animal studies, 4.8% genome-wide studies, 5.8% epigenome-wide studies, and 1.9% book chapters. The review identified key factors contributing to sarcopenia development, including the DOHaD hypothesis, LBW impact on muscle mass, inflammaging, mitochondrial dysfunction, the influence of clock genes, the role of epigenetic mechanisms, and genetic variations revealed through GWAS. The DOHaD theory suggests that LBW induces epigenetic alterations during foetal development, impacting long-term health outcomes, including the early onset of sarcopenia. LBW correlates with reduced muscle mass, grip strength, and lean body mass in adulthood, increasing the risk of sarcopenia. Chronic inflammation (inflammaging) and mitochondrial dysfunction contribute to sarcopenia, with LBW linked to increased oxidative stress and dysfunction. Disrupted circadian rhythms, regulated by genes such as BMAL1 and CLOCK, are associated with both LBW and sarcopenia, impacting lipid metabolism, muscle mass, and the ageing process. Early-life exposures, including LBW, induce epigenetic modifications like DNA methylation (DNAm) and histone changes, playing a pivotal role in sarcopenia development. Genome-wide studies have identified candidate genes and variants associated with lean body mass, muscle weakness, and sarcopenia, providing insights into genetic factors contributing to the disorder. LBW emerges as a potential early predictor of sarcopenia development, reflecting the impact of intrauterine exposures on long-term health outcomes. Understanding the complex interplay between LBW with inflammaging, mitochondrial dysfunction, circadian disruption, and epigenetic factors is essential for elucidating the pathogenesis of sarcopenia and developing targeted interventions. Future research on GWAS and the underlying mechanisms of LBW-associated sarcopenia is warranted to inform preventive strategies and improve public health outcomes.
Humans↗
Limb volume, composition, and maximum aerobic power output in relation to habitual 'preference' in young male subjects.
Anthropometric data are presented for the preferred and non-preferred limbs of normal subjects together with measurements of one-limb maximum aerobic power output (V O2 max). The habitually preferred arms and legs were significantly larger in total volume (LV) when compared with the contralateral limbs (5 per cent, P less than 0-01; and 2 per cent, P less than 0-01 respectively). These differences were mainly attributable to variation in the size of the muscle component. Expressed in absolute terms, V O2 max achieved in exercise with the preferred legs was significantly larger than the non-preferred legs (2-84 cf. 2-74 l/min; P less than 0-01) and a similar but non-significant difference was found between the arms (1-10 cf. 1-05 l/min). If, however, V O2 max is standardized for the size of the active muscle mass (LV, muscle plus bone) these differences between the preferred and non-preferred limbs disappear. The implications of these observations are discussed.
Adult↗
Effects of specific muscle training on VO2 on-response and early blood lactate.
The relationship between half time of the O2 uptake on-response (t1/2 VO2on, seconds) and early blood lactate accumulation (delta Lab, mmol.1(-1) at the onset of submaximal arm and/or leg exercise was the object of a cross-sectional study of sedentary subjects (S,n = 3), and kayakers (K, n = 8), and of a longitudinal study on 11 untrained subjects of specific arm vs. leg training. In supine arm cranking (W = 125 watts) S had an average t1/2 VO2on of 82 s and a delta Aab of 9.2 mmol.1(-1) compared to 47 +/- 7 s and 4 +/- 1.4 mmol.1(-1), respectively, for K. In longitudinal trainees shorter t1/2 VO2on was accompanied by lower Lab for the trained limbs. Specific limb conditioning in swimmers and runners resulted in shorter t1/2 VO2on. A linear relationship was observed between delta Lab and t1/2 VO2on having an intercept on the time axis at congruent to 20 s and a slope proportional to muscle mass. Trained muscles were grouped closest to the intercept indicating local acceleration of the rate of O2 transfer approaching the t1/2 VO2on for isolated perfused muscle at the onset of work. Since t1/2 VO2on, we conclude that factors distal to the capillary are specifically involved in the local training response.
Adenosine Triphosphate↗
Impact of creatine supplementation alone or combined with exercise on inflammatory and clinical outcomes in chronic musculoskeletal pain treated in the rheumatological field: a systematic review.
Creatine supplementation has demonstrated ergogenic and anabolic effects in healthy and clinical populations. However, its potential therapeutic role in individuals with chronic musculoskeletal pain treated in rheumatological contexts remains unclear. The aim was to evaluate the efficacy and safety of creatine supplementation on pain, physical function/disability, quality of life, muscle strength, skeletal muscle mass, and inflammatory markers in people with chronic musculoskeletal pain usually treated from the rheumatological field. A systematic review was conducted following PRISMA guidelines. Searches were performed in MEDLINE, Web of Science, CINAHL, Scopus, and EMBASE up to July 2026. Eligible studies were randomized or nonrandomized clinical trials that provided creatine supplementation alone or in combination with exercise as a treatment compared to a control or placebo group. Eight studies (n = 189) were included, encompassing fibromyalgia, osteoarthritis, rheumatoid arthritis, and juvenile idiopathic arthritis. Creatine dosages varied from chronic low-dose to loading protocols (20 g/d, 2-5 g/d). Combined creatine plus resistance training may improve strength, skeletal muscle mass, and quality of life beyond exercise alone in osteoarthritis. Trials on fibromyalgia suggest an increase in muscle strength, but inconsistent effects on pain. Rheumatoid arthritis studies suggest gains in skeletal muscle mass and, in pilot studies, reduced disease activity. No major adverse events were reported. In conclusion, creatine supplementation alone may be insufficient to obtain clinical benefits, while combined with resistance exercise it could offer potential benefits for muscle strength, skeletal muscle mass and certain aspects of quality of life in these clinical conditions. However, evidence on pain and inflammation remains limited; Furthermore, the response across different clinical conditions is heterogeneous, highlighting the need for larger, high-quality trials.
Humans↗
COVID-19 multi-omics reveal organ-specific responses and biomarkers.
OBJECTIVE: Post-COVID-19 syndrome is characterised by persistent immune dysfunction and multi-organ sequelae. This study aimed to characterise the systemic blood molecular landscape induced by SARS-CoV-2 infection and identify prognostic markers linked to skeletal muscle mass loss, a key driver of poor outcomes. METHODS: We enrolled 30 healthy controls and 307 COVID-19 patients, collecting 422 plasma samples for integrated proteomic and metabolomic profiling to investigate organ-specific molecular alterations in COVID-19. RESULTS: We comprehensively mapped the molecular landscape of COVID-19, encompassing immune, tissue-specific, and metabolic perturbations, and delineated their interactions. Focusing on organ-damage-related molecular patterns associated with disease progression and mortality, we found that skeletal muscle mass loss contributed to poor clinical outcomes of COVID-19 (p < 0.0001). Dysregulated arginine metabolism emerged as a key metabolic signature in fatal COVID-19 cases, with GLUL, GOT1, and citrulline showing significant correlation with skeletal muscle mass loss. Longitudinal analyses further revealed that reduced citrulline levels underlie the poor outcome of COVID-19 patients with muscle mass loss. These findings were robustly supported through multiple approaches: Mendelian randomization confirmed causal relationships between citrulline depletion, sarcopenia/fat-free mass loss, and COVID-19 mortality (p < 0.05), transcriptomic analyses of SARS-CoV-2-infected golden hamsters (GSE231910) provided additional support in enrichment of arginine biosynthesis (FDR < 0.05), and in vitro experiments further demonstrated that citrulline depletion promotes pro-inflammatory M1 macrophage polarisation — a key immunological feature of critical COVID-19. Leveraging these insights, we developed a skeletal muscle loss-specific prognostic prediction model for COVID-19 using GLUL, GOT1, and citrulline. This model effectively stratified patients into high- and low-risk groups (p = 0.035). CONCLUSION: Our study advances the understanding of COVID-19-induced organ pathophysiology and provides a foundation for developing targeted therapeutic strategies for post-COVID sequelae.
COVID-19↗
[Function and reserve of the hypertrophic left ventricle in aortic valve disease].
Left ventricular function was analyzed by angiography in 31 patients with aortic valve disease and in 12 patients without heart disease (control group). Ejection fraction, percentage shortening of minor equator, mean velocity of fiber shortening and men left atrial pressure were considered as parameters of left ventricular function. Contractile reserve was tested by a single postextrasystolic beat. Patients with pure aortic stenosis and an increase of left ventricular muscle mass to 220% of the normal value showed no impairment of left ventricular function. Patients with pure aortic regurgitation and a left ventricular muscle mass of 260% of normal showed no significantly impaired function. Both groups increased ejection fraction and percentage shortening of the minor equator after premature beat comparable to the control group. Patients with combined lesions of the aortic valve had a left ventricular muscle mass of 360% of normal. This group showed decreased ejection fraction, percentage shortening of minor equator and mean velocity of fiber shortening as compared to the control group while mean left atrial pressure was significantly elevated. After premature beat all parameters remained depressed as compared to control group. We conclude that the degree of hypertrophy determinates cardiac function in aortic valve disease. Moderate hypertrophy shows normal function at rest, while severe hypertrophy shows impaired function.
Adult↗
Left ventricular ejection power in coronary artery disease during atrial pacing.
Peak and mean left ventricular ejection power were measured during atrial pacing in 6 normal subjects (group I), 6 patients with coronary artery disease without myocardial infarction (group IIa), and 10 patients with coronary artery disease after myocardial infarction (group IIb). Pacing rates were 80 and 120/min. Power was determined by computer analysis of pressure, volume, and time. Data were normalised by end-diastolic volume and left ventricular muscle mass. Peak left ventricular ejection power normalised by end-diastolic volume values at a pacing rate of 120 min were significantly lower in group IIa and IIb than in normal subjects. Mean muscle mass in normal subjects was 179 g and in group IIa 216 g (P smaller than 0.05). Peak power normalised by muscle mass in normal subjects tended to increase at 120/min whereas in group IIa it declined by 26 per cent (P less than 0.001). These data indicate that the energy output of the left ventricle at rest may be the same in patients with significant coronary artery disease as in normal subjects. Increasing the heart rate from 80 to 120/min in a normal myocardium augments power but in coronary artery disease it remains static or falls.
Adult↗
The influence of hypertrophy on myocardial function.
In patients with hypertrophy from long-standing left ventricle pressure (PL) and volume overload (VL) as well as in a group of controls basal left ventricular contractility was assessed by peak measured isovolumic velocity of shortening (Vpm), mean velocity of circumferential fiber shortening (mean VCF) and mean normalized systolic ejection rate (MNSER). The angiographically determined left ventricular muscle mass was elevated to a similar extent in PL and VL. As compared to the control group both hypertrophy had decreased contractile indexes. No significant differences of contractility existed between the groups with PL and VL. Hence it appears that in chronic mechanical overloading the extent of hypertrophy is probably more important for the decrease of contractility than the nature of the stimulis to hypertrophy. In 15 patients with aortic stenosis left ventricular muscle mass and isovolumic and ejection phase contractile indexes were determined preoperatively and 13.5 months after successful valve replacement by a tilting disc prosthesis. Postoperatively there was a significant (P less than 0.001) decrease of muscle mass from 182 to 114 g/m2. Mean VCF increased from 1.07 to 1.52 circ/sec (P less than 0.01); MNSER from 1.92 to 2.59 enddiastolic volumes/sec (P less than 0.01); Vpm from 1.17 to 1.60 ML/sec (P less than 0.001) and total pressure Vmax from 1.61 to 2.09 ML/sec (P less than 0.01). In 9 of 13 patients an abnormal or pathologic response to handgrip at the preoperative study became normal postoperatively. It is concluded that in aortic stenosis removal of the chronic pressure burden leads to regression of left ventricular hypertrophy associated with an improvement of resting and exercise contractile function. Pressure-deprived contractile indexes; ejection phase contractile indexes; chronic pressure load; chronic volume load; aortic valve replacement; postoperative hemodynamics.
Cardiomyopathy, Hypertrophic↗
An analysis of acetylcholine in frog muscle by mass fragmentography.
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Acetylcholine↗