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Journal of Applied Physiology... Nov 2019We determined the effects of cold water immersion (CWI) on long-term adaptations and post-exercise molecular responses in skeletal muscle before and after resistance...
We determined the effects of cold water immersion (CWI) on long-term adaptations and post-exercise molecular responses in skeletal muscle before and after resistance training. Sixteen men (22.9 ± 4.6 y; 85.1 ± 17.9 kg; mean ± SD) performed resistance training (3 day/wk) for 7 wk, with each session followed by either CWI [15 min at 10°C, CWI (COLD) group, = 8] or passive recovery (15 min at 23°C, control group, = 8). Exercise performance [one-repetition maximum (1-RM) leg press and bench press, countermovement jump, squat jump, and ballistic push-up], body composition (dual X-ray absorptiometry), and post-exercise (i.e., +1 and +48 h) molecular responses were assessed before and after training. Improvements in 1-RM leg press were similar between groups [130 ± 69 kg, pooled effect size (ES): 1.53 ± 90% confidence interval (CI) 0.49], whereas increases in type II muscle fiber cross-sectional area were attenuated with CWI (-1,959 ± 1,675 µM ; ES: -1.37 ± 0.99). Post-exercise mechanistic target of rapamycin complex 1 signaling (rps6 phosphorylation) was blunted for COLD at post-training (POST) +1 h (-0.4-fold, ES: -0.69 ± 0.86) and POST +48 h (-0.2-fold, ES: -1.33 ± 0.82), whereas basal protein degradation markers (FOX-O1 protein content) were increased (1.3-fold, ES: 2.17 ± 2.22). Training-induced increases in heat shock protein (HSP) 27 protein content were attenuated for COLD (-0.8-fold, ES: -0.94 ± 0.82), which also reduced total HSP72 protein content (-0.7-fold, ES: -0.79 ± 0.57). CWI blunted resistance training-induced muscle fiber hypertrophy, but not maximal strength, potentially via reduced skeletal muscle protein anabolism and increased catabolism. Post-exercise CWI should therefore be avoided if muscle hypertrophy is desired. This study adds to existing evidence that post-exercise cold water immersion attenuates muscle fiber growth with resistance training, which is potentially mediated by attenuated post-exercise increases in markers of skeletal muscle anabolism coupled with increased catabolism and suggests that blunted muscle fiber growth with cold water immersion does not necessarily translate to impaired strength development.
Topics: Adolescent; Adult; Cold Temperature; Heat-Shock Proteins; Humans; Hypertrophy; Immersion; Male; Muscle Fibers, Skeletal; Muscle Strength; Recovery of Function; Resistance Training; Young Adult
PubMed: 31513450
DOI: 10.1152/japplphysiol.00127.2019 -
Circulation Oct 2020Cardiac fibrosis is a key antecedent to many types of cardiac dysfunction including heart failure. Physiological factors leading to cardiac fibrosis have been recognized...
BACKGROUND
Cardiac fibrosis is a key antecedent to many types of cardiac dysfunction including heart failure. Physiological factors leading to cardiac fibrosis have been recognized for decades. However, the specific cellular and molecular mediators that drive cardiac fibrosis, and the relative effect of disparate cell populations on cardiac fibrosis, remain unclear.
METHODS
We developed a novel cardiac single-cell transcriptomic strategy to characterize the cardiac cellulome, the network of cells that forms the heart. This method was used to profile the cardiac cellular ecosystem in response to 2 weeks of continuous administration of angiotensin II, a profibrotic stimulus that drives pathological cardiac remodeling.
RESULTS
Our analysis provides a comprehensive map of the cardiac cellular landscape uncovering multiple cell populations that contribute to pathological remodeling of the extracellular matrix of the heart. Two phenotypically distinct fibroblast populations, Fibroblast- and Fibroblast-, emerged after induction of tissue stress to promote fibrosis in the absence of smooth muscle actin-expressing myofibroblasts, a key profibrotic cell population. After angiotensin II treatment, Fibroblast- develops as the most abundant fibroblast subpopulation and the predominant fibrogenic cell type. Mapping intercellular communication networks within the heart, we identified key intercellular trophic relationships and shifts in cellular communication after angiotensin II treatment that promote the development of a profibrotic cellular microenvironment. Furthermore, the cellular responses to angiotensin II and the relative abundance of fibrogenic cells were sexually dimorphic.
CONCLUSIONS
These results offer a valuable resource for exploring the cardiac cellular landscape in health and after chronic cardiovascular stress. These data provide insights into the cellular and molecular mechanisms that promote pathological remodeling of the mammalian heart, highlighting early transcriptional changes that precede chronic cardiac fibrosis.
Topics: Animals; Cardiomegaly; Fibroblasts; Fibrosis; Gene Expression Profiling; Mice; Myocardium; Pyrophosphatases; Single-Cell Analysis; Stress, Physiological; Thrombospondins
PubMed: 32795101
DOI: 10.1161/CIRCULATIONAHA.119.045115 -
Sports Medicine (Auckland, N.Z.) Jan 2024Resistance exercise training is widely used by general and athletic populations to increase skeletal muscle hypertrophy, power and strength. Endogenous sex hormones... (Meta-Analysis)
Meta-Analysis
The Effect of Hormonal Contraceptive Use on Skeletal Muscle Hypertrophy, Power and Strength Adaptations to Resistance Exercise Training: A Systematic Review and Multilevel Meta-analysis.
BACKGROUND
Resistance exercise training is widely used by general and athletic populations to increase skeletal muscle hypertrophy, power and strength. Endogenous sex hormones influence various bodily functions, including possibly exercise performance, and may influence adaptive changes in response to exercise training. Hormonal contraceptive (HC) use modulates the profile of endogenous sex hormones, and therefore, there is increasing interest in the impact, if any, of HC use on adaptive responses to resistance exercise training.
OBJECTIVE
Our aim is to provide a quantitative synthesis of the effect of HC use on skeletal muscle hypertrophy, power and strength adaptations in response to resistance exercise training.
METHODS
A systematic review with meta-analysis was conducted on experimental studies which directly compared skeletal muscle hypertrophy, power and strength adaptations following resistance exercise training in hormonal contraceptive users and non-users conducted before July 2023. The search using the online databases PUBMED, SPORTDiscus, Web of Science, Embase and other supplementary search strategies yielded 4669 articles, with 8 articles (54 effects and 325 participants) meeting the inclusion criteria. The methodological quality of the included studies was assessed using the "Tool for the assessment of study quality and reporting in exercise".
RESULTS
All included studies investigated the influence of oral contraceptive pills (OCP), with no study including participants using other forms of HC. The articles were analysed using a meta-analytic multilevel maximum likelihood estimator model. The results indicate that OCP use does not have a significant effect on hypertrophy [0.01, 95% confidence interval (CI) [- 0.11, 0.13], t = 0.14, p = 0.90), power (- 0.04, 95% CI [- 0.93, 0.84], t = - 0.29, p = 0.80) or strength (0.10, 95% CI [- 0.08, 0.28], t = 1.48, p = 0.20).
DISCUSSION
Based on the present analysis, there is no evidence-based rationale to advocate for or against the use of OCPs in females partaking in resistance exercise training to increase hypertrophy, power and/or strength. Rather, an individualised approach considering an individual's response to OCPs, their reasons for use and menstrual cycle history may be more appropriate.
REGISTRATION
The review protocol was registered on PROSPERO (ID number and hyperlink: CRD42022365677).
Topics: Female; Humans; Contraceptives, Oral; Gonadal Steroid Hormones; Hypertrophy; Muscle Strength; Muscle, Skeletal; Resistance Training
PubMed: 37755666
DOI: 10.1007/s40279-023-01911-3 -
Graefe's Archive For Clinical and... Nov 2022Extraocular muscle enlargement can occur secondary to a range of orbital and systemic diseases. Although the most common cause of extraocular muscle enlargement is... (Review)
Review
Extraocular muscle enlargement can occur secondary to a range of orbital and systemic diseases. Although the most common cause of extraocular muscle enlargement is thyroid eye disease, a range of other inflammatory, infective, neoplastic, and vascular conditions can alter the size and shape of the extraocular muscles. Imaging with computed tomography and magnetic resonance imaging plays an essential role in the workup of these conditions. This article provides an image-rich review of the wide range of pathology that can cause enlargement of the extraocular muscles.
Topics: Humans; Oculomotor Muscles; Tomography, X-Ray Computed; Graves Ophthalmopathy; Magnetic Resonance Imaging; Hypertrophy
PubMed: 35713708
DOI: 10.1007/s00417-022-05727-1 -
The Journal of Experimental Medicine May 2021Meteorin-like/Meteorin-β (Metrnl/Metrnβ) is a secreted protein produced by skeletal muscle and adipose tissue that exerts metabolic actions that improve glucose...
Meteorin-like/Meteorin-β (Metrnl/Metrnβ) is a secreted protein produced by skeletal muscle and adipose tissue that exerts metabolic actions that improve glucose metabolism. The role of Metrnβ in cardiac disease is completely unknown. Here, we show that Metrnβ-null mice exhibit asymmetrical cardiac hypertrophy, fibrosis, and enhanced signs of cardiac dysfunction in response to isoproterenol-induced cardiac hypertrophy and aging. Conversely, adeno-associated virus-mediated specific overexpression of Metrnβ in the heart prevents the development of cardiac remodeling. Furthermore, Metrnβ inhibits cardiac hypertrophy development in cardiomyocytes in vitro, indicating a direct effect on cardiac cells. Antibody-mediated blockage of Metrnβ in cardiomyocyte cell cultures indicated an autocrine action of Metrnβ on the heart, in addition to an endocrine action. Moreover, Metrnβ is highly produced in the heart, and analysis of circulating Metrnβ concentrations in a large cohort of patients reveals that it is a new biomarker of heart failure with an independent prognostic value.
Topics: Animals; Animals, Newborn; Blood Pressure; Cardiomegaly; Cardiotonic Agents; Cells, Cultured; Disease Models, Animal; Echocardiography; Gene Expression Regulation; Heart Failure; Humans; Male; Mice, Inbred C57BL; Mice, Knockout; Muscle, Skeletal; Myocytes, Cardiac; Nerve Growth Factors; PPAR alpha; Mice
PubMed: 33635944
DOI: 10.1084/jem.20201206 -
Circulation Research Jan 2020
Topics: Aspartic Acid; Cardiomegaly; Glucose; Humans; Myocardium
PubMed: 31944916
DOI: 10.1161/CIRCRESAHA.119.316358 -
PloS One 2022Several studies comparing resistance training (RT) frequencies may have been affected by the large between-subject variability. This study aimed to compare the changes... (Randomized Controlled Trial)
Randomized Controlled Trial
Several studies comparing resistance training (RT) frequencies may have been affected by the large between-subject variability. This study aimed to compare the changes in lower limbs maximal dynamic strength (1RM) and quadriceps femoris cross-sectional area (CSA) after a RT with different weekly frequencies in strength-trained individuals using a within-subject design. Twenty-four men participated in a 9-week RT program, being randomly divided into two conditions: resistance training with equalized total training volume (RTEV) and with unequalized total training volume (RTUV). The RT protocol used the unilateral leg press 45° exercise and each subject's lower limb executed one of the proposed frequencies (one and three times/week). All conditions effectively increased 1RM and CSA (p<0.001); however, no significant differences were observed in the values of 1RM (p = 0.454) and CSA (p = 0.310) between the RT frequencies in the RTEV and RTUV conditions. Therefore, RT performed three times a week showed similar increases in 1RM and CSA to the program performed once a week, regardless of training volume equalization. Nevertheless, when the higher RT frequency allowed the application of a greater TTV (i.e., RTUV), higher effect size (ES) values (0.51 and 0.63, 1RM and CSA, respectively) were observed for the adaptations.
Topics: Humans; Hypertrophy; Male; Muscle Strength; Muscle, Skeletal; Quadriceps Muscle; Resistance Training; Weight Lifting
PubMed: 36228016
DOI: 10.1371/journal.pone.0276154 -
JACC. Cardiovascular Imaging Nov 2019Pathological left ventricular hypertrophy is a common feature of many cardiac diseases. It results from both myocyte hypertrophy and interstitial expansion. Interstitial... (Review)
Review
Pathological left ventricular hypertrophy is a common feature of many cardiac diseases. It results from both myocyte hypertrophy and interstitial expansion. Interstitial expansion is most commonly secondary to the accumulation of mature cross-linked collagen fibers due to dysregulated metabolism, known as interstitial fibrosis. This occurs secondary to a variety of stimuli including ischemic, toxic, metabolic, infective, genetic, and hemodynamic factors. Less commonly, interstitial expansion may occur because of the accumulation of misfolded amyloid protein or interstitial edema. It is now well recognized that the presence and extent of interstitial disease are associated with adverse outcomes. There is therefore interest in the development of novel therapies that target the pathways that drive these disease processes. With the emergence of such therapies, it is becoming increasingly important to be able to characterize the type and extent of interstitial disease to enable the use of such targeted therapies in a personalized manner.
Topics: Biopsy; Extracellular Space; Fibrosis; Humans; Hypertrophy, Left Ventricular; Magnetic Resonance Imaging; Myocardium; Tomography, Emission-Computed; Ventricular Function, Left; Ventricular Remodeling
PubMed: 31542527
DOI: 10.1016/j.jcmg.2019.05.033 -
Clinical Orthopaedics and Related... Mar 2020Blood flow restriction (BFR) is a process of using inflatable cuffs to create vascular occlusion within a limb during exercise. The technique can stimulate muscle...
BACKGROUND
Blood flow restriction (BFR) is a process of using inflatable cuffs to create vascular occlusion within a limb during exercise. The technique can stimulate muscle hypertrophy and improve physical function; however, most of these studies have enrolled healthy, young men with a focus on athletic performance. Furthermore, much of the information on BFR comes from studies with small samples sizes, limited follow-up time, and varied research designs resulting in greater design, selection, and sampling bias. Despite these limitations, BFR's popularity is increasing as a clinical rehabilitation tool for aging patients. It is important for practitioners to have a clear understanding of the reported effects of BFR specifically in older adults while simultaneously critically evaluating the available literature before deciding to employ the technique.
QUESTIONS/PURPOSES
(1) Does BFR induce skeletal muscle hypertrophy in adults older than 50 years of age? (2) Does BFR improve muscle strength and/or physical function in adults older than 50 years?
METHODS
Using PubMed, Google Scholar, Web of Science, and Science Direct, we conducted a systematic review of articles using Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to assess the reported effects of BFR on skeletal muscle in older adults. Included articles enrolled participants 50 years of age or older and used BFR in conjunction with exercise to study the effects of BFR on musculoskeletal outcomes and functionality. The following search terms were used: "blood flow restriction" OR "KAATSU" OR "ischemic training" AND "clinical" AND "elderly." After duplicates were removed, 1574 articles were reviewed for eligibility, and 30 articles were retained with interventions duration ranging from cross-sectional to 16 weeks. Sample sizes ranged from 6 to 56 participants, and exercise tasks included passive mobilization or electrical stimulation; walking; resistance training using machines, free weights, body weight, or elastic bands; and water-based activities. Furthermore, healthy participants and those with cardiovascular disease, osteoarthritis, osteoporosis, sporadic inclusion body myositis, spinal cord injuries, and current coma patients were studied. Lastly, retained articles were assigned a risk of bias score using aspects of the Risk of Bias in Nonrandomized Studies of Interventions and the Cochrane Collaboration's tool for assessing the risk of bias in randomized trials.
RESULTS
BFR, in combination with a variety of exercises, was found to result in muscle hypertrophy as measured by muscle cross-sectional area, thickness, volume, mass, or circumference. Effect sizes for BFR's ability to induce muscle hypertrophy were calculated for 16 of the 30 papers and averaged 0.75. BFR was also shown to improve muscle strength and functional performance. Effect sizes were calculated for 21 of the 30 papers averaging 1.15.
CONCLUSIONS
Available evidence suggests BFR may demonstrate utility in aiding rehabilitation efforts in adults older than 50 years of age, especially for inducing muscle hypertrophy, combating muscle atrophy, increasing muscle strength, and improving muscle function. However, most studies in this systematic review were at moderate or high risk of bias; that being so, the findings in this systematic review should be confirmed, ideally using greater sample sizes, randomization of participants, and extended follow-up durations.
LEVEL OF EVIDENCE
Level II, systematic review.
Topics: Aged; Exercise Therapy; Female; Humans; Hypertrophy; Male; Middle Aged; Muscle Strength; Muscle, Skeletal; Orthopedic Procedures; Regional Blood Flow; Vasoconstriction
PubMed: 31860546
DOI: 10.1097/CORR.0000000000001090 -
Biomedicine & Pharmacotherapy =... May 2020Pathological cardiac hypertrophy is characterized by myocyte enlargement and cardiac dysfunction. However, the pathogenesis for this disease is still poorly understood....
Pathological cardiac hypertrophy is characterized by myocyte enlargement and cardiac dysfunction. However, the pathogenesis for this disease is still poorly understood. Stimulator of interferon genes (STING) could meditate inflammation and immune response in various kinds of diseases. In this work, we demonstrated that STING was critical for pressure overload-induced cardiac hypertrophy. Results showed that STING expression was up-regulated in human and mouse hypertrophic hearts. STING knockout attenuated cardiac hypertrophy induced by aortic banding (AB). The effects of STING deficiency on the improvement of cardiac hypertrophy and dysfunction were associated with the restrained macrophage infiltration, inflammatory response and fibrosis. Moreover, ER stress was detected in hearts of AB-operated mice, as evidenced by the increased expression of phospho-protein kinase RNA-like endoplasmic reticulum kinase (PERK), phospho-eukaryotic initiation factor 2 alpha (eIF2α) and phospho-inositol-requiring kinase (IRE)-1α. Importantly, these proteins were restrained in mice with STING knockout after AB surgery. What's more, angiotensin II (Ang II)-induced STING could be accelerated by ER stress activator, while being markedly abolished by the ER stress inhibitor. We then found that whether co-treated with or without transforming growth factor-beta 1 (TGF-β1), cardiac fibroblasts cultured in the conditional medium (CM) from Ang II-incubated cardiomyocytes with STING knockdown exhibited significantly reduced fibrosis, as displayed by the clearly down-regulated expression of α-SMA, Collagen type I (Col I) and Collagen type III (Col III). Therefore, we defined STING as an important signal contributing to cardiac hypertrophy closely associated with ER stress.
Topics: Angiotensin II; Animals; Biomarkers; Cardiomegaly; Disease Models, Animal; Disease Susceptibility; Echocardiography; Endoplasmic Reticulum Stress; Fibrosis; Gene Expression; Gene Knockdown Techniques; Immunohistochemistry; Inflammation; Male; Membrane Proteins; Mice; Myocytes, Cardiac; Rats; Signal Transduction
PubMed: 32106379
DOI: 10.1016/j.biopha.2020.110022