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Frontiers in Nutrition 2024It is unclear whether resistance training in combination with different timing of protein intake might have differential effects on muscle hypertrophy, strength, and...
BACKGROUND
It is unclear whether resistance training in combination with different timing of protein intake might have differential effects on muscle hypertrophy, strength, and performance. Therefore, we compared the effects of 8 weeks of resistance training combined with two different high-protein diet strategies (immediately pre-and after, or 3 h pre and after exercise) in resistance-trained males.
METHODS
Forty resistance-trained males (24 ± 4 years) performed 8 weeks of resistance training combined with 2 g kg d protein. Body composition, muscular performance, and biochemical markers were assessed pre and post-intervention.
RESULTS
Nine participants (four from 3 h group and five from the immediate group) withdrew from the study. Therefore, 31 participants completed the study. All measures of skeletal muscle mass, Australian pull-up, and muscle strength, significantly increased post-intervention in both groups ( < 0.05). The biochemical marker urea also significantly increased from pre to post in both groups ( < 0.05). There were no significant between-group differences ( > 0.05).
CONCLUSION
High-protein diet enhances muscular performance and skeletal muscle mass in resistance-trained males, irrespective of intake time. Consequently, the total daily protein intake appears to be the primary factor in facilitating muscle growth induced by exercise.
PubMed: 38846541
DOI: 10.3389/fnut.2024.1397090 -
Sports Medicine - Open Jun 2024Palmitoylethanolamide (PEA) has analgesic/anti-inflammatory properties that may be a suitable alternative to over-the-counter (OTC) non-steroidal...
The Effect of Palmitoylethanolamide (PEA) on Skeletal Muscle Hypertrophy, Strength, and Power in Response to Resistance Training in Healthy Active Adults: A Double-Blind Randomized Control Trial.
BACKGROUND
Palmitoylethanolamide (PEA) has analgesic/anti-inflammatory properties that may be a suitable alternative to over-the-counter (OTC) non-steroidal analgesics/anti-inflammatories. While OTC pain medications can impair strength training adaptations, the mechanism of action of PEA is distinct from these and it may not negatively affect skeletal muscle adaptations to strength training.
METHODS
The primary aim of this study was to investigate the effects of daily PEA supplementation (350 mg Levagen + equivalent to 300 mg PEA) combined with 8-weeks of resistance training on lean body mass with secondary aims addressing strength, power, sleep, and wellbeing compared to placebo (PLA) in young, healthy, active adults. In a randomized, controlled, double-blinded trial, 52 untrained, recreationally active participants aged 18-35 y were allocated to either the PEA or PLA groups. Participants consumed either 2 × 175 mg Levagen + PEA or identically matched maltodextrin capsules during an 8-week period of whole-body resistance training. This trial assessed the pre- to post- changes in total and regional lean body mass, muscular strength (1-RM bench, isometric mid-thigh pull), muscular power [countermovement jump (CMJ), bench throw], pain associated with exercise training, sleep, and wellbeing compared with the PEA or PLA condition.
RESULTS
48 Participants were included in the final intention to treat (ITT) analysis and we also conducted per protocol (PP) analysis (n = 42). There were no significant between-group differences for total or regional lean muscle mass post-intervention. There was a significantly higher jump height (CMJ) at week 10 in the PEA group compared to the PLA (Adjusted mean difference [95% CI] p-value; ITT: - 2.94 cm [- 5.15, - 0.74] p = 0.010; PP: - 2.93 cm [- 5.31, - 0.55] p = 0.017). The PLA group had higher 1-RM bench press post-intervention compared with the PEA group (ITT: 2.24 kg [0.12, 4.37] p = 0.039; PP: 2.73 kg [0.40, 5.06] p = 0.023). No significant treatment effects were noted for any of the other outcomes.
CONCLUSION
PEA supplementation, when combined with 8 weeks of strength training, did not impair lean mass gains and it resulted in significantly higher dynamic lower-body power when compared with the PLA condition.
TRIAL REGISTRATION
Australian New Zealand Clinical Trials Registry (ANZCTR: ACTRN12621001726842p).
PubMed: 38844675
DOI: 10.1186/s40798-024-00732-6 -
European Journal of Pharmacology Aug 2024Cardiac Hypertrophy is an adaptive response of the body to physiological and pathological stimuli, which increases cardiomyocyte size, thickening of cardiac muscles and...
Cardiac Hypertrophy is an adaptive response of the body to physiological and pathological stimuli, which increases cardiomyocyte size, thickening of cardiac muscles and progresses to heart failure. Downregulation of SIRT1 in cardiomyocytes has been linked with the pathogenesis of cardiac hypertrophy. The present study aimed to investigate the effect of Artesunate against isoprenaline induced cardiac hypertrophy in rats via SIRT1 inhibiting NF-κB activation. Experimental cardiac hypertrophy was induced in rats by subcutaneous administration of isoprenaline (5 mg/kg) for 14 days. Artesunate was administered simultaneously for 14 days at a dose of 25 mg/kg and 50 mg/kg. Artesunate administration showed significant dose dependent attenuation in mean arterial pressure, electrocardiogram, hypertrophy index and left ventricular wall thickness compared to the disease control group. It also alleviated cardiac injury biomarkers and oxidative stress. Histological observation showed amelioration of tissue injury in the artesunate treated groups compared to the disease control group. Further, artesunate treatment increased SIRT1 expression and decreased NF-kB expression in the heart. The results of the study show the cardioprotective effect of artesunate via SIRT1 inhibiting NF-κB activation in cardiomyocytes.
Topics: Animals; Artesunate; Sirtuin 1; Isoproterenol; NF-kappa B; Male; Cardiomegaly; Rats; Oxidative Stress; Artemisinins; Myocytes, Cardiac; Cardiotonic Agents; Rats, Sprague-Dawley
PubMed: 38843948
DOI: 10.1016/j.ejphar.2024.176709 -
Journal of the American Heart... Jun 2024The mineralocorticoid receptor plays a significant role in the development of chronic kidney disease (CKD) and associated cardiovascular complications. Classic steroidal...
BACKGROUND
The mineralocorticoid receptor plays a significant role in the development of chronic kidney disease (CKD) and associated cardiovascular complications. Classic steroidal mineralocorticoid receptor antagonists are a therapeutic option, but their use in the clinic is limited due to the associated risk of hyperkalemia in patients with CKD. Finerenone is a nonsteroidal mineralocorticoid receptor antagonist that has been recently investigated in 2 large phase III clinical trials (FIDELIO-DKD [Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease] and FIGARO-DKD [Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease]), showing reductions in kidney and cardiovascular outcomes.
METHODS AND RESULTS
We tested whether finerenone improves renal and cardiac function in a preclinical nondiabetic CKD model. Twelve weeks after 5/6 nephrectomy, the rats showed classic signs of CKD characterized by a reduced glomerular filtration rate and increased kidney weight, associated with left ventricular (LV) diastolic dysfunction and decreased LV perfusion. These changes were associated with increased cardiac fibrosis and reduced endothelial nitric oxide synthase activating phosphorylation (ser 1177). Treatment with finerenone prevented LV diastolic dysfunction and increased LV tissue perfusion associated with a reduction in cardiac fibrosis and increased endothelial nitric oxide synthase phosphorylation. Curative treatment with finerenone improves nondiabetic CKD-related LV diastolic function associated with a reduction in cardiac fibrosis and increased cardiac phosphorylated endothelial nitric oxide synthase independently from changes in kidney function. Short-term finerenone treatment decreased LV end-diastolic pressure volume relationship and increased phosphorylated endothelial nitric oxide synthase and nitric oxide synthase activity.
CONCLUSIONS
We showed that the nonsteroidal mineralocorticoid receptor antagonist finerenone reduces renal hypertrophy and albuminuria, attenuates cardiac diastolic dysfunction and cardiac fibrosis, and improves cardiac perfusion in a preclinical nondiabetic CKD model.
Topics: Animals; Mineralocorticoid Receptor Antagonists; Renal Insufficiency, Chronic; Naphthyridines; Ventricular Dysfunction, Left; Male; Disease Models, Animal; Fibrosis; Nitric Oxide Synthase Type III; Glomerular Filtration Rate; Ventricular Function, Left; Diastole; Kidney; Phosphorylation; Myocardium; Rats, Sprague-Dawley; Rats; Nephrectomy
PubMed: 38842271
DOI: 10.1161/JAHA.123.032971 -
IScience Jun 2024The routine need for myonuclear turnover in skeletal muscle, together with more sporadic demands for hypertrophy and repair, are performed by resident muscle stem cells...
The routine need for myonuclear turnover in skeletal muscle, together with more sporadic demands for hypertrophy and repair, are performed by resident muscle stem cells called satellite cells. Muscular dystrophies are characterized by muscle wasting, stimulating chronic repair/regeneration by satellite cells. Here, we derived and validated transcriptomic signatures for satellite cells, myoblasts/myocytes, and myonuclei using publicly available murine single cell RNA-Sequencing data. Our signatures distinguished disease from control in transcriptomic data from several muscular dystrophies including facioscapulohumeral muscular dystrophy (FSHD), Duchenne muscular dystrophy, and myotonic dystrophy type I. For FSHD, the expression of our gene signatures correlated with direct counts of satellite cells on muscle sections, as well as with increasing clinical and pathological severity. Thus, our gene signatures enable the investigation of myogenesis in bulk transcriptomic data from muscle biopsies. They also facilitate study of muscle regeneration in transcriptomic data from human muscle across health and disease.
PubMed: 38840844
DOI: 10.1016/j.isci.2024.109947 -
International Journal of Dermatology Jun 2024Masseter muscle hypertrophy is characterized by a symmetrical or asymmetrical increase in muscle volume. Although it can be asymptomatic, it may be associated with...
BACKGROUND
Masseter muscle hypertrophy is characterized by a symmetrical or asymmetrical increase in muscle volume. Although it can be asymptomatic, it may be associated with bruxism. Therefore, patients may seek intervention for esthetic and/or functional concerns. This study aimed to establish patient characteristics, purpose of undergoing botulinum toxin injection into the masseter muscles, efficacy, and side effects of the procedure at a dermatology clinic.
METHODS
A retrospective chart review was carried out over a period of one year from January 2022 to January 2023 for the patients who underwent botulinum toxin injection into the masseter muscles. The general characteristics of patients, the purpose of botulinum toxin treatment, relief levels regarding bruxism according to the Visual Analog Scale (VAS), side effects, and complications were recorded.
RESULTS
The study group comprised 74 female and 6 male patients with a mean age of 31.20 ± 6.71 years. Eighteen (22.5%) patients were treated only for narrowing the lower face contour, 28 (35%) patients were treated only for the relief of bruxism, and 34 (42.5%) patients were treated for both indications. Fifteen (18.8%) patients experienced 16 treatment-related side effects, including two (2.5%) with smile asymmetry and two (2.5%) with paradoxical bulging.
CONCLUSIONS
Botulinum toxin injection into the masseter muscles with the intention of lower face contouring and/or relieving bruxism offers a minimally invasive, safe, and effective treatment option. Although it has a favorable safety profile, the risks of significant side effects or complications remain.
PubMed: 38837386
DOI: 10.1111/ijd.17282 -
Cellular and Molecular Biology... Jun 2024Nur77 is a member of the NR4A subfamily of orphan nuclear receptors that is expressed and has a function within the immune system. This study aimed to investigate the...
Nur77 is a member of the NR4A subfamily of orphan nuclear receptors that is expressed and has a function within the immune system. This study aimed to investigate the role of Nur77 in hypoxic pulmonary hypertension. SPF male SD rats were exposed in hypobaric chamber simulating 5000 m high altitude for 0, 3, 7, 14, 21 or 28 days. Rat pulmonary artery smooth muscle cells (RPASMCs) were cultured under normoxic conditions (5% CO2-95% ambient air) or hypoxic conditions (5% O2 for 6 h, 12 h, 24 h, 48 h). Hypoxic rats developed pulmonary arterial remodeling and right ventricular hypertrophy with significantly increased pulmonary arterial pressure. The levels of Nur77, HIF-1α and PNCA were upregulated in pulmonary arterial smooth muscle from hypoxic rats. Silencing of either Nur77 or HIF-1α attenuated hypoxia-induced proliferation. Silencing of HIF-1α down-regulated Nur77 protein level, but Nur77 silence did not reduce HIF-1α. Nur77 was not con-immunoprecipitated with HIF-1α. This study demonstrated that Nur77 acted as a downstream regulator of HIF-1α under hypoxia, and plays a critical role in the hypoxia-induced pulmonary vascular remodeling, which is regulated by HIF-1α. Nur77 maybe a novel target of HPH therapy.
Topics: Animals; Nuclear Receptor Subfamily 4, Group A, Member 1; Vascular Remodeling; Hypoxia-Inducible Factor 1, alpha Subunit; Male; Rats, Sprague-Dawley; Hypertension, Pulmonary; Pulmonary Artery; Hypoxia; Cell Proliferation; Myocytes, Smooth Muscle; Rats; Hypertrophy, Right Ventricular; Cells, Cultured
PubMed: 38836656
DOI: 10.14715/cmb/2024.70.6.35 -
Channels (Austin, Tex.) Dec 2024Alterations in ion channel expression and function known as "electrical remodeling" contribute to the development of hypertrophy and to the emergence of arrhythmias and...
Alterations in ion channel expression and function known as "electrical remodeling" contribute to the development of hypertrophy and to the emergence of arrhythmias and sudden cardiac death. However, comparing current density values - an electrophysiological parameter commonly utilized to assess ion channel function - between normal and hypertrophied cells may be flawed when current amplitude does not scale with cell size. Even more, common routines to study equally sized cells or to discard measurements when large currents do not allow proper voltage-clamp control may introduce a selection bias and thereby confound direct comparison. To test a possible dependence of current density on cell size and shape, we employed whole-cell patch-clamp recording of voltage-gated sodium and calcium currents in Langendorff-isolated ventricular cardiomyocytes and Purkinje myocytes, as well as in cardiomyocytes derived from trans-aortic constriction operated mice. Here, we describe a distinct inverse relationship between voltage-gated sodium and calcium current densities and cell capacitance both in normal and hypertrophied cells. This inverse relationship was well fit by an exponential function and may be due to physiological adaptations that do not scale proportionally with cell size or may be explained by a selection bias. Our study emphasizes the need to consider cell size bias when comparing current densities in cardiomyocytes of different sizes, particularly in hypertrophic cells. Conventional comparisons based solely on mean current density may be inadequate for groups with unequal cell size or non-proportional current amplitude and cell size scaling.
Topics: Myocytes, Cardiac; Animals; Cell Size; Cardiomegaly; Mice; Male; Patch-Clamp Techniques
PubMed: 38836323
DOI: 10.1080/19336950.2024.2361416 -
International Journal of Sports... 2024The rotator cuff (RC) plays a pivotal role in the performance and health of the shoulder and upper extremity. Blood flow restriction training (BFRT) is a modality to...
BACKGROUND
The rotator cuff (RC) plays a pivotal role in the performance and health of the shoulder and upper extremity. Blood flow restriction training (BFRT) is a modality to improve strength and muscle hypertrophy with even low-load training in healthy and injured individuals. There is minimal evidence examining its effect proximal to the occluded area, and particularly on the RC.
HYPOTHESIS & PURPOSE
The purpose of this case series is to explore the effects of low-load BFRT on RC strength, hypertrophy, and tendon thickness in asymptomatic individuals.
STUDY DESIGN
Case series.
METHODS
Fourteen participants with asymptomatic, untrained shoulders were recruited to participate. They performed an eight-week low-load shoulder exercise regimen where BFR was applied to the dominant arm only during exercise. The dependent variables were maximal isometric strength of the shoulder external rotators(ER) and elevators (in the scapular plane in full can position) (FC) measured via handheld dynamometry, cross sectional area (CSA) of the supraspinatus and infraspinatus muscles, and supraspinatus tendon thickness measured via ultrasound imaging (US). Mean changes within and between arms were compared after training using paired t-tests. Cohen's d was used to determine effect sizes.
RESULTS
All participants were able to complete the BFRT regimen without adverse effects. Mean strength and CSA increased for all variables in both arms, however this increase was only significant (p\<0.01) for FC strength bilaterally and CSA for the supraspinatus and infraspinatus on the BFRT side. The effect sizes for increased supraspinatus and infraspinatus CSA on the BFRT side were 0.40 (9.8% increase) and 0.46 (11.7% increase) respectively. There were no significant differences when comparing the mean changes of the BFRT side to the non-BFRT side for strength or muscle CSA. There were no significant changes to supraspinatus tendon thickness.
CONCLUSION
These results suggest variability in response of the RC musculature to low-load BFRT in asymptomatic individuals. The potential for a confounding systemic response in the study design makes determining whether low-load BFRT is more beneficial than low-load non-BFRT difficult. The hypertrophy seen on the BFRT side warrants further study.
LEVEL OF EVIDENCE
4.
PubMed: 38835981
DOI: 10.26603/001c.118143 -
Nature Communications Jun 2024Semaglutide, a glucagon-like peptide-1 receptor agonist, is clinically used as a glucose-lowering and weight loss medication due to its effects on energy metabolism. In...
Semaglutide, a glucagon-like peptide-1 receptor agonist, is clinically used as a glucose-lowering and weight loss medication due to its effects on energy metabolism. In heart failure, energy production is impaired due to altered mitochondrial function and increased glycolysis. However, the impact of semaglutide on cardiomyocyte metabolism under pressure overload remains unclear. Here we demonstrate that semaglutide improves cardiac function and reduces hypertrophy and fibrosis in a mouse model of pressure overload-induced heart failure. Semaglutide preserves mitochondrial structure and function under chronic stress. Metabolomics reveals that semaglutide reduces mitochondrial damage, lipid accumulation, and ATP deficiency by promoting pyruvate entry into the tricarboxylic acid cycle and increasing fatty acid oxidation. Transcriptional analysis shows that semaglutide regulates myocardial energy metabolism through the Creb5/NR4a1 axis in the PI3K/AKT pathway, reducing NR4a1 expression and its translocation to mitochondria. NR4a1 knockdown ameliorates mitochondrial dysfunction and abnormal glucose and lipid metabolism in the heart. These findings suggest that semaglutide may be a therapeutic agent for improving cardiac remodeling by modulating energy metabolism.
Topics: Animals; Male; Nuclear Receptor Subfamily 4, Group A, Member 1; Energy Metabolism; Mice; Glucagon-Like Peptides; Heart Failure; Mice, Inbred C57BL; Ventricular Remodeling; Lipid Metabolism; Myocytes, Cardiac; Cyclic AMP Response Element-Binding Protein; Disease Models, Animal; Myocardium; Signal Transduction; Mitochondria; Cardiomegaly
PubMed: 38834564
DOI: 10.1038/s41467-024-48970-2