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The Cochrane Database of Systematic... Sep 2013Benign masseter muscle hypertrophy is an uncommon clinical phenomenon of uncertain aetiology which is characterised by a soft swelling near the angle of the mandible.... (Review)
Review
BACKGROUND
Benign masseter muscle hypertrophy is an uncommon clinical phenomenon of uncertain aetiology which is characterised by a soft swelling near the angle of the mandible. The swelling may on occasion be associated with facial pain and can be prominent enough to be considered cosmetically disfiguring. Varying degrees of success have been reported for some of the treatment options for masseter hypertrophy, which range from simple pharmacotherapy to more invasive surgical reduction. Injection of botulinum toxin type A into the masseter muscle is generally considered a less invasive modality and has been advocated for cosmetic sculpting of the lower face. Botulinum toxin type A is a powerful neurotoxin which is produced by the anaerobic organism Clostridium botulinum and when injected into a muscle causes interference with the neurotransmitter mechanism producing selective paralysis and subsequent atrophy of the muscle.This review is an update of a previously published Cochrane review.
OBJECTIVES
To assess the efficacy and safety of botulinum toxin type A compared to placebo or no treatment, for the management of benign bilateral masseter hypertrophy.
SEARCH METHODS
We searched the following databases from inception to April 2013: the Cochrane Central Register of Controlled Trials (CENTRAL); MEDLINE (via PubMed); EMBASE (via embase.com); Web of Science; CINAHL; Academic Search Premier (via EBSCOhost); ScienceDirect; LILACS (via BIREME); PubMed Central and Google Scholar (from 1700 to 19 April 2013). We searched two bibliographic databases of regional journals (IndMED and Iranmedex) which were expected to contain relevant trials. We also searched reference lists of relevant articles and contacted investigators to identify additional published and unpublished studies.
SELECTION CRITERIA
Randomised controlled trials (RCTs) and controlled clinical trials (CCTs) comparing intra-masseteric injections of botulinum toxin versus placebo administered for cosmetic facial sculpting in individuals of any age with bilateral benign masseter hypertrophy, which had been self-evaluated and confirmed by clinical and radiological examination were considered for inclusion. We excluded participants with unilateral or compensatory contralateral masseter hypertrophy resulting from head and neck radiotherapy.
DATA COLLECTION AND ANALYSIS
Two review authors independently screened the search results. For future updates, two authors will independently extract data and assess trial quality using the Cochrane risk of bias tool. Risk ratios (RR) and corresponding 95% confidence intervals (CI) will be calculated for all dichotomous outcomes and the mean difference (MD) and 95% CI will be calculated for continuous outcomes.
MAIN RESULTS
We retrieved 683 unique references to studies. After screening these references 660 were excluded for being non-applicable. We assessed 23 full text articles for eligibility and all of these studies were excluded from the review.
AUTHORS' CONCLUSIONS
We were unable to identify any RCTs or CCTs assessing the efficacy and safety of intra-masseteric injections of botulinum toxin for people with bilateral benign masseter hypertrophy. The absence of high level evidence for the effectiveness of this intervention emphasises the need for well-designed, adequately powered RCTs.
Topics: Botulinum Toxins, Type A; Humans; Hypertrophy; Injections, Intramuscular; Masseter Muscle; Neuromuscular Agents
PubMed: 24018587
DOI: 10.1002/14651858.CD007510.pub3 -
Biochimica Et Biophysica Acta.... Sep 2020Skeletal muscle is a dynamic tissue with two unique abilities; one is its excellent regenerative ability, due to the activity of skeletal muscle-resident stem cells... (Review)
Review
Skeletal muscle is a dynamic tissue with two unique abilities; one is its excellent regenerative ability, due to the activity of skeletal muscle-resident stem cells named muscle satellite cells (MuSCs); and the other is the adaptation of myofiber size in response to external stimulation, intrinsic factors, or physical activity, which is known as plasticity. Low physical activity and some disease conditions lead to the reduction of myofiber size, called atrophy, whereas hypertrophy refers to the increase in myofiber size induced by high physical activity or anabolic hormones/drugs. MuSCs are essential for generating new myofibers during regeneration and the increase in new myonuclei during hypertrophy; however, there has been little investigation of the molecular mechanisms underlying MuSC activation, proliferation, and differentiation during hypertrophy compared to those of regeneration. One reason is that 'degenerative damage' to myofibers during muscle injury or upon hypertrophy (especially overloaded muscle) is believed to trigger similar activation/proliferation of MuSCs. However, evidence suggests that degenerative damage of myofibers is not necessary for MuSC activation/proliferation during hypertrophy. When considering MuSC-based therapy for atrophy, including sarcopenia, it will be indispensable to elucidate MuSC behaviors in muscles that exhibit non-degenerative damage, because degenerated myofibers are not present in the atrophied muscles. In this review, we summarize recent findings concerning the relationship between MuSCs and hypertrophy, and discuss what remains to be discovered to inform the development and application of relevant treatments for muscle atrophy.
Topics: Animals; Biomarkers; Cell Proliferation; Humans; Hypertrophy; Muscle, Skeletal; Regeneration; Satellite Cells, Skeletal Muscle
PubMed: 32417255
DOI: 10.1016/j.bbamcr.2020.118742 -
Sports Medicine (Auckland, N.Z.) Aug 2021Hypertrophy and strength are two common long-term goals of resistance training that are mediated by the manipulation of numerous variables. One training variable that is... (Review)
Review
Hypertrophy and strength are two common long-term goals of resistance training that are mediated by the manipulation of numerous variables. One training variable that is often neglected but is essential to consider for achieving strength and hypertrophy gains is the movement tempo of particular repetitions. Although research has extensively investigated the effects of different intensities, volumes, and rest intervals on muscle growth, many of the present hypertrophy guidelines do not account for different movement tempos, likely only applying to volitional movement tempos. Changing the movement tempo during the eccentric and concentric phases can influence acute exercise variables, which form the basis for chronic adaptive changes to resistance training. To further elaborate on the already unclear anecdotal evidence of different movement tempos on muscle hypertrophy and strength development, one must acknowledge that the related scientific research does not provide equivocal evidence. Furthermore, there has been no assessment of the impact of duration of particular movement phases (eccentric vs. concentric) on chronic adaptations, making it difficult to draw definitive conclusions in terms of resistance-training recommendations. Therefore, the purpose of this review is to explain how variations in movement tempo can affect chronic adaptive changes. This article provides an overview of the available scientific data describing the impact of movement tempo on hypertrophy and strength development with a thorough analysis of changes in duration of particular phases of movement. Additionally, the review provides movement tempo-specific recommendations as well real training solutions for strength and conditioning coaches and athletes, depending on their goals.
Topics: Adaptation, Physiological; Exercise; Humans; Hypertrophy; Muscle Strength; Muscle, Skeletal; Resistance Training
PubMed: 34043184
DOI: 10.1007/s40279-021-01465-2 -
Journal of Applied Physiology... Jan 2007The onset of whole muscle hypertrophy in response to overloading is poorly documented. The purpose of this study was to assess the early changes in muscle size and... (Clinical Trial)
Clinical Trial
The onset of whole muscle hypertrophy in response to overloading is poorly documented. The purpose of this study was to assess the early changes in muscle size and architecture during a 35-day high-intensity resistance training (RT) program. Seven young healthy volunteers performed bilateral leg extension three times per week on a gravity-independent flywheel ergometer. Cross-sectional area (CSA) in the central (C) and distal (D) regions of the quadriceps femoris (QF), muscle architecture, maximal voluntary contraction (MVC), and electromyographic (EMG) activity were measured before and after 10, 20, and 35 days of RT. By the end of the training period, MVC and EMG activity increased by 38.9 +/- 5.7 and 34.8% +/- 4.7%, respectively. Significant increase in QF CSA (3.5 and 5.2% in the C and D regions, respectively) was observed after 20 days of training, along with a 2.4 +/- 0.7% increase in fascicle length from the 10th day of training. By the end of the 35-day training period, the total increase in QF CSA for regions C and D was 6.5 +/- 1.1 and 7.4 +/- 0.8%, respectively, and fascicle length and pennation angle increased by 9.9 +/- 1.2 and 7.7 +/- 1.3%, respectively. The results show for the first time that changes in muscle size are detectable after only 3 wk of RT and that remodeling of muscle architecture precedes gains in muscle CSA. Muscle hypertrophy seems to contribute to strength gains earlier than previously reported; flywheel training seems particularly effective for inducing these early structural adaptations.
Topics: Adolescent; Adult; Electromyography; Ergometry; Exercise; Female; Humans; Hypertrophy; Magnetic Resonance Imaging; Male; Muscle Contraction; Muscle, Skeletal; Time Factors; Weight Lifting
PubMed: 17053104
DOI: 10.1152/japplphysiol.00789.2006 -
International Journal of Molecular... May 2019Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detrimental stimuli. Nevertheless, long-term stimuli incite chronic... (Review)
Review
Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detrimental stimuli. Nevertheless, long-term stimuli incite chronic hypertrophy and may lead to heart failure. In this review, we analyze the recent literature regarding the role of ERK (extracellular signal-regulated kinase) activity in cardiac hypertrophy. ERK signaling produces beneficial effects during the early phase of chronic pressure overload in response to G protein-coupled receptors (GPCRs) and integrin stimulation. These functions comprise (i) adaptive concentric hypertrophy and (ii) cell death prevention. On the other hand, ERK participates in maladaptive hypertrophy during hypertension and chemotherapy-mediated cardiac side effects. Specific ERK-associated scaffold proteins are implicated in either cardioprotective or detrimental hypertrophic functions. Interestingly, ERK phosphorylated at threonine 188 and activated ERK5 (the big MAPK 1) are associated with pathological forms of hypertrophy. Finally, we examine the connection between ERK activation and hypertrophy in (i) transgenic mice overexpressing constitutively activated RTKs (receptor tyrosine kinases), (ii) animal models with mutated sarcomeric proteins characteristic of inherited hypertrophic cardiomyopathies (HCMs), and (iii) mice reproducing syndromic genetic RASopathies. Overall, the scientific literature suggests that during cardiac hypertrophy, ERK could be a "good" player to be stimulated or a "bad" actor to be mitigated, depending on the pathophysiological context.
Topics: Animals; Cardiomegaly; Humans; MAP Kinase Signaling System; Myocardium
PubMed: 31052420
DOI: 10.3390/ijms20092164 -
Acta Physiologica (Oxford, England) Jul 2020Within the current paradigm of the myonuclear domain theory, it is postulated that a linear relationship exists between muscle fibre size and myonuclear content. The... (Review)
Review
Within the current paradigm of the myonuclear domain theory, it is postulated that a linear relationship exists between muscle fibre size and myonuclear content. The myonuclear domain is kept (relatively) constant by adding additional nuclei (supplied by muscle satellite cells) during muscle fibre hypertrophy and nuclear loss (by apoptosis) during muscle fibre atrophy. However, data from recent animal studies suggest that myonuclei that are added to support muscle fibre hypertrophy are not lost within various muscle atrophy models. Such myonuclear permanence has been suggested to constitute a mechanism allowing the muscle fibre to (re)grow more efficiently during retraining, a phenomenon referred to as "muscle memory." The concept of "muscle memory by myonuclear permanence" has mainly been based on data attained from rodent experimental models. Whether the postulated mechanism also holds true in humans remains largely ambiguous. Nevertheless, there are several studies in humans that provide evidence to potentially support or contradict (parts of) the muscle memory hypothesis. The goal of the present review was to discuss the evidence for the existence of "muscle memory" in both animal and human models of muscle fibre hypertrophy as well as atrophy. Furthermore, to provide additional insight in the potential presence of muscle memory by myonuclear permanence in humans, we present new data on previously performed exercise training studies. Finally, suggestions for future research are provided to establish whether muscle memory really exists in humans.
Topics: Animals; Cell Nucleus; Humans; Hypertrophy; Muscle Fibers, Skeletal; Muscle, Skeletal; Muscular Atrophy; Satellite Cells, Skeletal Muscle
PubMed: 32175681
DOI: 10.1111/apha.13465 -
International Journal of Sport... Jan 2022The acute response of muscle protein synthesis (MPS) to resistance exercise and nutrition is often used to inform recommendations for exercise programming and dietary...
The acute response of muscle protein synthesis (MPS) to resistance exercise and nutrition is often used to inform recommendations for exercise programming and dietary interventions, particularly protein nutrition, to support and enhance muscle growth with training. Those recommendations are worthwhile only if there is a predictive relationship between the acute response of MPS and subsequent muscle hypertrophy during resistance exercise training. The metabolic basis for muscle hypertrophy is the dynamic balance between the synthesis and degradation of myofibrillar proteins in muscle. There is ample evidence that the process of MPS is much more responsive to exercise and nutrition interventions than muscle protein breakdown. Thus, it is intuitively satisfying to translate the acute changes in MPS to muscle hypertrophy with training over a longer time frame. Our aim is to examine and critically evaluate the strength and nature of this relationship. Moreover, we examine the methodological and physiological factors related to measurement of MPS and changes in muscle hypertrophy that contribute to uncertainty regarding this relationship. Finally, we attempt to offer recommendations for practical and contextually relevant application of the information available from studies of the acute response of MPS to optimize muscle hypertrophy with training.
Topics: Exercise; Humans; Hypertrophy; Muscle Proteins; Muscle, Skeletal; Resistance Training
PubMed: 34697259
DOI: 10.1123/ijsnem.2021-0139 -
The Journal of Physiology Sep 2016Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown. We show that changes...
KEY POINTS
Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown. We show that changes in myofibrillar protein synthesis (MyoPS) after an initial resistance exercise (RE) bout in the first week of RT (T1) were greater than those seen post-RE at the third (T2) and tenth week (T3) of RT, with values being similar at T2 and T3. Muscle damage (Z-band streaming) was the highest during post-RE recovery at T1, lower at T2 and minimal at T3. When muscle damage was the highest, so was the integrated MyoPS (at T1), but neither were related to hypertrophy; however, integrated MyoPS at T2 and T3 were correlated with hypertrophy. We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive attenuation of muscle damage.
ABSTRACT
Skeletal muscle hypertrophy is one of the main outcomes of resistance training (RT), but how hypertrophy is modulated and the mechanisms regulating it are still unknown. To investigate how muscle hypertrophy is modulated through RT, we measured day-to-day integrated myofibrillar protein synthesis (MyoPS) using deuterium oxide and assessed muscle damage at the beginning (T1), at 3 weeks (T2) and at 10 weeks of RT (T3). Ten young men (27 (1) years, mean (SEM)) had muscle biopsies (vastus lateralis) taken to measure integrated MyoPS and muscle damage (Z-band streaming and indirect parameters) before, and 24 h and 48 h post resistance exercise (post-RE) at T1, T2 and T3. Fibre cross-sectional area (fCSA) was evaluated using biopsies at T1, T2 and T3. Increases in fCSA were observed only at T3 (P = 0.017). Changes in MyoPS post-RE at T1, T2 and T3 were greater at T1 (P < 0.03) than at T2 and T3 (similar values between T2 and T3). Muscle damage was the highest during post-RE recovery at T1, attenuated at T2 and further attenuated at T3. The change in MyoPS post-RE at both T2 and T3, but not at T1, was strongly correlated (r ≈ 0.9, P < 0.04) with muscle hypertrophy. Initial MyoPS response post-RE in an RT programme is not directed to support muscle hypertrophy, coinciding with the greatest muscle damage. However, integrated MyoPS is quickly 'refined' by 3 weeks of RT, and is related to muscle hypertrophy. We conclude that muscle hypertrophy is the result of accumulated intermittent changes in MyoPS post-RE in RT, which coincides with progressive attenuation of muscle damage.
Topics: Adult; Humans; Hypertrophy; Male; Muscle Proteins; Muscular Diseases; Myofibrils; Protein Biosynthesis; Resistance Training
PubMed: 27219125
DOI: 10.1113/JP272472 -
JCI Insight Aug 2023The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic...
The growth of skeletal muscle relies on a delicate equilibrium between protein synthesis and degradation; however, how proteostasis is managed in the endoplasmic reticulum (ER) is largely unknown. Here, we report that the SEL1L-HRD1 ER-associated degradation (ERAD) complex, the primary molecular machinery that degrades misfolded proteins in the ER, is vital to maintain postnatal muscle growth and systemic energy balance. Myocyte-specific SEL1L deletion blunts the hypertrophic phase of muscle growth, resulting in a net zero gain of muscle mass during this developmental period and a 30% reduction in overall body growth. In addition, myocyte-specific SEL1L deletion triggered a systemic reprogramming of metabolism characterized by improved glucose sensitivity, enhanced beigeing of adipocytes, and resistance to diet-induced obesity. These effects were partially mediated by the upregulation of the myokine FGF21. These findings highlight the pivotal role of SEL1L-HRD1 ERAD activity in skeletal myocytes for postnatal muscle growth, and its physiological integration in maintaining whole-body energy balance.
Topics: Humans; Endoplasmic Reticulum-Associated Degradation; Ubiquitin-Protein Ligases; Proteins; Muscles; Energy Metabolism; Hypertrophy
PubMed: 37535424
DOI: 10.1172/jci.insight.170387 -
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