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Critical Reviews in Oncology/hematology Jul 2021Muscle wasting has a negative effect on treatment toxicity and cancer prognosis. Resistance training appears to be a promising approach to counteract the loss of muscle... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Muscle wasting has a negative effect on treatment toxicity and cancer prognosis. Resistance training appears to be a promising approach to counteract the loss of muscle mass.
METHODS
Pubmed, Cochrane Library, SportDiscus and CINAHL. Randomized controlled resistance training trials with cancer survivros where eligible if lean body mass (LBM) or muscle mass were assessed.
RESULTS
A total of 34 trials were included into the primary analysis. Compared to the control individuals, the intervention groups show a superiority in LBM of 0.85 kg (95 % CI = 0.26-1.43, p = .004). Isolated, the participants in the intervention groups show an increase in LBM of 0.51 kg (95 % CI = -0.05-1.06, p = .072); the control groups displayed a decrease of -0.59 kg (95 % CI= -1.04 to 0.06, p = .078). Supervision displayed an mediating role.
CONCLUSIONS
Resistance training can counteract the loss of muscle mass in cancer patients. Especially in a supervised setting.
Topics: Humans; Hypertrophy; Muscle Strength; Muscle, Skeletal; Muscles; Neoplasms; Resistance Training; Survivors
PubMed: 34062243
DOI: 10.1016/j.critrevonc.2021.103371 -
The Journal of Hand Surgery, European... Sep 2018Congenital muscle hypertrophy of the upper limb is a very rare condition with unknown aetiology. This descriptive observational and retrospective series included eight... (Observational Study)
Observational Study
UNLABELLED
Congenital muscle hypertrophy of the upper limb is a very rare condition with unknown aetiology. This descriptive observational and retrospective series included eight children followed by a multidisciplinary team from 2005 to 2017. The diagnosis was based on a cluster of clinical and radiological characteristics after elimination of differential diagnoses. Patients were categorized according to: anomalies of the wrist, anomalies of long fingers of intrinsic or extrinsic origin; and anomalies of the thumb with or without first web space contracture. Treatment begins in young children with hand orthoses to limit muscle contraction and joint malposition. The purpose of surgical treatment was to release contractures and to restore muscle balance through, in the main, finger intrinsic releases and first web releases. At the 2-year follow-up, we found that limited surgical procedures improved finger, thumb and wrist positions. We conclude that muscle hypertrophy is the main cause of deformity and that selective releases of contracted musculo-tendinous units and skin lengthening are effective.
LEVEL OF EVIDENCE
IV.
Topics: Adolescent; Child; Child, Preschool; Contracture; Female; Humans; Hypertrophy; Magnetic Resonance Imaging; Male; Muscle, Skeletal; Orthopedic Procedures; Radiography; Retrospective Studies; Upper Extremity Deformities, Congenital
PubMed: 29759027
DOI: 10.1177/1753193418774459 -
Journal of Bodywork and Movement... Oct 2022Neuromuscular electrical stimulation (NMES) with kiloHertz currents (kHz) is a resource used in rehabilitation for producing muscle contractions with functional... (Review)
Review
BACKGROUND
Neuromuscular electrical stimulation (NMES) with kiloHertz currents (kHz) is a resource used in rehabilitation for producing muscle contractions with functional objectives, resulting from the optimization of the performance of aspects of muscle function (AOMF). However, parameters such as inadequate frequency, phase duration, amplitude, and therapy time may limit the effectiveness of NMES by the absence of adequate stimuli to generate positive adaptations in the AOMF. This study aimed to present an overview of the effectiveness and dosimetry of NMES by kHz on AOMF, such as torque and hypertrophy, in healthy people.
METHODS
The study was outlined as a scoping review. From the search, 3892 studies were found of which were incorporated into Rayyan software for exclusion of duplicates and further selection by titles and abstracts, which resulted in 33 articles for this review.
RESULTS
According to the included studies, kHz can increase torque and generate hypertrophy. Only the studies with Russian current showed hypertrophy gains. Dosimetry was not always detailed in the studies, which hinders stipulating optimal parameters for kHz.
CONCLUSION
From this review, it is concluded that NMSC by kHz is a valid resource to optimize AOMF, although the dosimetric parameters are still inconsistent.
Topics: Electric Stimulation Therapy; Humans; Hypertrophy; Muscle Contraction; Muscle, Skeletal; Muscles; Torque
PubMed: 36180136
DOI: 10.1016/j.jbmt.2022.05.015 -
Dermatologic Therapy Nov 2021With the increasing demand for body contouring, botulinum toxin (BTX) injection is being widely used off-label for muscular hypertrophy. However, to the best of our...
With the increasing demand for body contouring, botulinum toxin (BTX) injection is being widely used off-label for muscular hypertrophy. However, to the best of our knowledge, no study has investigated the clinical efficacy of BTX type A (BTX-A) in deltoid muscle hypertrophy. This study was conducted to evaluate the efficacy and safety of intramuscular injection of BTX in reducing deltoid muscle hypertrophy. Overall, 10 patients with bilateral deltoid muscle hypertrophy were treated with an intramuscular injection of prabotulinum toxin A, with a total of 50 units [U] administered per patient. As measured by ultrasonography, the thickness of the deltoid muscles was significantly decreased at weeks 2 and 12. In addition, the clinical assessment score by blinded investigators was improved after the treatment; however, patients' satisfaction scores were relatively low. No major complications were reported. Therefore, intramuscular injection of BTX-A seems to be a candidate for novel treatment option for deltoid muscle hypertrophy. Further larger clinical studies are warranted to confirm the efficacy of BTX-A.
Topics: Botulinum Toxins, Type A; Deltoid Muscle; Humans; Hypertrophy; Injections, Intramuscular; Treatment Outcome
PubMed: 34676643
DOI: 10.1111/dth.15168 -
Revista de Neurologia May 2016
Topics: Electromyography; Humans; Hypertrophy; Muscle, Skeletal
PubMed: 27113071
DOI: No ID Found -
Scandinavian Journal of Medicine &... Mar 2024The aim of this study was to determine whether a 9-week resistance training program based on high load (HL) versus low load combined with blood flow restriction (LL-BFR)... (Randomized Controlled Trial)
Randomized Controlled Trial
PURPOSE
The aim of this study was to determine whether a 9-week resistance training program based on high load (HL) versus low load combined with blood flow restriction (LL-BFR) induced a similar (i) distribution of muscle hypertrophy among hamstring heads (semimembranosus, SM; semitendinosus, ST; and biceps femoris long head, BF) and (ii) magnitude of tendon hypertrophy of ST, using a parallel randomized controlled trial.
METHODS
A total of 45 participants were randomly allocated to one of three groups: HL, LL-BFR, and control (CON). Both HL and LL-BFR performed a 9-week resistance training program composed of seated leg curl and stiff-leg deadlift exercises. Freehand 3D ultrasound was used to assess the changes in muscle and tendon volume.
RESULTS
The increase in ST volume was greater in HL (26.5 ± 25.5%) compared to CON (p = 0.004). No difference was found between CON and LL-BFR for the ST muscle volume (p = 0.627). The change in SM muscle volume was greater for LL-BFR (21.6 ± 27.8%) compared to CON (p = 0.025). No difference was found between HL and CON for the SM muscle volume (p = 0.178).There was no change in BF muscle volume in LL-BFR (14.0 ± 16.5%; p = 0.436) compared to CON group. No difference was found between HL and CON for the BF muscle volume (p = 1.0). Regarding ST tendon volume, we did not report an effect of training regimens (p = 0.411).
CONCLUSION
These results provide evidence that the HL program induced a selective hypertrophy of the ST while LL-BFR induced hypertrophy of SM. The magnitude of the selective hypertrophy observed within each group varied greatly between individuals. This finding suggests that it is very difficult to early determine the location of the hypertrophy among a muscle group.
Topics: Humans; Hamstring Muscles; Muscle Strength; Hypertrophy; Tendons; Resistance Training; Regional Blood Flow; Muscle, Skeletal
PubMed: 38515303
DOI: 10.1111/sms.14608 -
Current Opinion in Clinical Nutrition... Jul 2023Heart failure is one of the major causes of death worldwide and continues to increase despite therapeutics and pharmacology advances. Fatty acids and glucose are used as... (Review)
Review
PURPOSE OF REVIEW
Heart failure is one of the major causes of death worldwide and continues to increase despite therapeutics and pharmacology advances. Fatty acids and glucose are used as ATP-producing fuels in heart to meet its energy demands. However, dysregulation of metabolites' use plays a pivotal role in cardiac diseases. How glucose becomes toxic or drives cardiac dysfunction is incompletely understood. In the present review, we summarize the recent findings on cardiac cellular and molecular events that are driven by glucose during pathologic conditions and potential therapeutic strategies to tackle hyperglycemia-mediated cardiac dysfunction.
RECENT FINDINGS
Several studies have emerged recently, demonstrating that excessive glucose utilization has been correlated with impairment of cellular metabolic homeostasis primarily driven by mitochondrial dysfunction and damage, oxidative stress, and abnormal redox signaling. This disturbance is associated with cardiac remodeling, hypertrophy, and systolic and diastolic dysfunction. Both human and animal heart failure studies, report that glucose is a preferable fuel at the expense of fatty acid oxidation during ischemia and hypertrophy, but the opposite happens in diabetic hearts, which warrants further investigation.
SUMMARY
A better understanding of glucose metabolism and its fate during distinct types of heart disease will contribute to developing novel therapeutic options for the prevention and treatment of heart failure.
Topics: Animals; Humans; Glucose; Energy Metabolism; Myocardium; Oxidation-Reduction; Heart Failure; Fatty Acids; Hypertrophy
PubMed: 37144457
DOI: 10.1097/MCO.0000000000000943 -
GeroScience Aug 2022With aging, skeletal muscle plasticity is attenuated in response to exercise. Here, we report that senescent cells, identified using senescence-associated...
With aging, skeletal muscle plasticity is attenuated in response to exercise. Here, we report that senescent cells, identified using senescence-associated β-galactosidase (SA β-Gal) activity and p21 immunohistochemistry, are very infrequent in resting muscle, but emerge approximately 2 weeks after a bout of resistance exercise in humans. We hypothesized that these cells contribute to blunted hypertrophic potential in old age. Using synergist ablation-induced mechanical overload (MOV) of the plantaris muscle to model resistance training in adult (5-6-month) and old (23-24-month) male C57BL/6 J mice, we found increased senescent cells in both age groups during hypertrophy. Consistent with the human data, there were negligible senescent cells in plantaris muscle from adult and old sham controls, but old mice had significantly more senescent cells 7 and 14 days following MOV relative to young. Old mice had blunted whole-muscle hypertrophy when compared to adult mice, along with smaller muscle fibers, specifically glycolytic type 2x + 2b fibers. To ablate senescent cells using a hit-and-run approach, old mice were treated with vehicle or a senolytic cocktail consisting of 5 mg/kg dasatinib and 50 mg/kg quercetin (D + Q) on days 7 and 10 during 14 days of MOV; control mice underwent sham surgery with or without senolytic treatment. Old mice given D + Q had larger muscles and muscle fibers after 14 days of MOV, fewer senescent cells when compared to vehicle-treated old mice, and changes in the expression of genes (i.e., Igf1, Ddit4, Mmp14) that are associated with hypertrophic growth. Our data collectively show that senescent cells emerge in human and mouse skeletal muscle following a hypertrophic stimulus and that D + Q improves muscle growth in old mice.
Topics: Animals; Humans; Male; Mice; Hypertrophy; Mice, Inbred C57BL; Muscle, Skeletal; Senotherapeutics
PubMed: 35325353
DOI: 10.1007/s11357-022-00542-2 -
Biochemical and Biophysical Research... Dec 2022Mild heat stimulation is defined as a stimulation that occurs several degrees above optimal cell culture or body temperatures. Muscle hypertrophy in C2C12 cells is...
Mild heat stimulation is defined as a stimulation that occurs several degrees above optimal cell culture or body temperatures. Muscle hypertrophy in C2C12 cells is reportedly facilitated by 39 °C mild heat stimulation. However, the underlying molecular mechanisms by which 39 °C mild heat stimulation promotes muscle hypertrophy remains elusive. In this study, we aimed at understanding the details of these mechanisms. First, we found that 39 °C mild heat stimulation has little or no effect on Myogenesis-Related Factor (MRF) expression both in C2C12 and mouse primary satellite cells. Therefore, we hypothesized that 39 °C mild heat stimulation promotes muscle hypertrophy through myokines, essential components in myogenesis. Interestingly, we observed muscle hypertrophy in the group cultured at 37 °C in conditioned medium from 39 °C compared to the group cultured at 37 °C in conditioned medium from 37 °C in the case of both C2C12 and mouse primary satellite cells. These results suggest that 39 °C mild heat stimulation promotes muscle hypertrophy through myokines, once released in the culture medium. Finally, we identified Decorin as a hypertrophy-inducing myokine candidate. Therefore, in this study, we demonstrated that 39 °C mild heat stimulation contributes to muscle hypertrophy through enhancing Decorin gene expression in C2C12 and mouse primary satellite cells.
Topics: Mice; Animals; Hot Temperature; Culture Media, Conditioned; Decorin; Hypertrophy; Muscles; Muscle, Skeletal
PubMed: 36274366
DOI: 10.1016/j.bbrc.2022.10.018 -
Journal of Proteome Research Oct 2017Skeletal muscle, the most abundant body tissue, plays vital roles in locomotion and metabolism. Myostatin is a negative regulator of skeletal muscle mass. In addition to...
Skeletal muscle, the most abundant body tissue, plays vital roles in locomotion and metabolism. Myostatin is a negative regulator of skeletal muscle mass. In addition to increasing muscle mass, Myostatin inhibition impacts muscle contractility and energy metabolism. To decipher the mechanisms of action of the Myostatin inhibitors, we used proteomic and transcriptomic approaches to investigate the changes induced in skeletal muscles of transgenic mice overexpressing Follistatin, a physiological Myostatin inhibitor. Our proteomic workflow included a fractionation step to identify weakly expressed proteins and a comparison of fast versus slow muscles. Functional annotation of altered proteins supports the phenotypic changes induced by Myostatin inhibition, including modifications in energy metabolism, fiber type, insulin and calcium signaling, as well as membrane repair and regeneration. Less than 10% of the differentially expressed proteins were found to be also regulated at the mRNA level but the Biological Process annotation, and the KEGG pathways analysis of transcriptomic results shows a great concordance with the proteomic data. Thus this study describes the most extensive omics analysis of muscle overexpressing Follistatin, providing molecular-level insights to explain the observed muscle phenotypic changes.
Topics: Animals; Disease Models, Animal; Follistatin; Gene Expression Profiling; Gene Expression Regulation; Humans; Hypertrophy; Mice; Mice, Transgenic; Muscle, Skeletal; Muscular Diseases; Myostatin; Proteomics; Regeneration; Transcriptome
PubMed: 28810121
DOI: 10.1021/acs.jproteome.7b00069