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Free Radical Biology & Medicine Sep 2016The plasticity of skeletal muscle can be traced down to extensive metabolic, structural and molecular remodeling at the single fiber level. Skeletal muscle is comprised... (Review)
Review
The plasticity of skeletal muscle can be traced down to extensive metabolic, structural and molecular remodeling at the single fiber level. Skeletal muscle is comprised of different fiber types that are the basis of muscle plasticity in response to various functional demands. Resistance and endurance exercises are two external stimuli that differ in their duration and intensity of contraction and elicit markedly different responses in muscles adaptation. Further, eccentric contractions that are associated with exercise-induced injuries, elicit varied muscle adaptation and regenerative responses. Most adaptive changes are fiber type-specific and are highly influenced by diverse structural, metabolic and functional characteristics of individual fiber types. Regulation of signaling pathways by reactive oxygen species (ROS) and oxidative stress also plays an important role in muscle fiber adaptation during exercise. This review focuses on cellular and molecular responses that regulate the adaptation of skeletal muscle to exercise and exercise-related injuries.
Topics: Exercise; Humans; Mitochondria; Muscle Fibers, Skeletal; Muscle, Skeletal; Organelle Biogenesis; Physical Endurance; Reactive Oxygen Species; Regeneration; Resistance Training; Signal Transduction
PubMed: 27032709
DOI: 10.1016/j.freeradbiomed.2016.03.025 -
Ageing Research Reviews Nov 2018Age-related loss of skeletal muscle mass and function, sarcopenia, is associated with physical frailty and increased risk of morbidity (chronic diseases), in addition to... (Review)
Review
Age-related loss of skeletal muscle mass and function, sarcopenia, is associated with physical frailty and increased risk of morbidity (chronic diseases), in addition to all-cause mortality. The loss of muscle mass occurs incipiently from middle-age (∼1%/year), and in severe instances can lead to a loss of ∼50% by the 8-9th decade of life. This review will focus on muscle deterioration with ageing and highlight the two underpinning mechanisms regulating declines in muscle mass and function: muscle fibre atrophy and muscle fibre loss (hypoplasia) - and their measurement. The mechanisms of muscle fibre atrophy in humans relate to imbalances in muscle protein synthesis (MPS) and breakdown (MPB); however, since there is limited evidence for basal alterations in muscle protein turnover, it would appear that "anabolic resistance" to fundamental environmental cues regulating diurnal muscle homeostasis (namely physical activity and nutrition), underlie age-related catabolic perturbations in muscle proteostasis. While the 'upstream' drivers of the desensitization of aged muscle to anabolic stimuli are poorly defined, they most likely relate to impaired efficiency of the conversion of nutritional/exercise stimuli into signalling impacting mRNA translation and proteolysis. Additionally, loss of muscle fibres has been shown in cadaveric studies using anatomical fibre counts, and from iEMG studies demonstrating motor unit loss, albeit with few molecular investigations of this in humans. We suggest that defining countermeasures against sarcopenia requires improved understandings of the co-ordinated regulation of muscle fibre atrophy and fibre loss, which are likely to be inextricably linked.
Topics: Aging; Animals; Exercise; Humans; Muscle Fibers, Skeletal; Muscle Proteins; Muscle Strength; Muscle, Skeletal; Muscular Atrophy; Nutritional Status; Sarcopenia
PubMed: 30048806
DOI: 10.1016/j.arr.2018.07.005 -
The FEBS Journal Oct 2018Different forms of myosin heavy chains (MyHCs), coded by a large family of sarcomeric MYH genes, are expressed in striated muscles. The generation of specific anti-MyHC... (Review)
Review
Different forms of myosin heavy chains (MyHCs), coded by a large family of sarcomeric MYH genes, are expressed in striated muscles. The generation of specific anti-MyHC antibodies has provided a powerful tool to define the fiber types present in skeletal muscles, their functional properties, their response to conditions that affect muscle plasticity and their changes in muscle disorders. Cardiomyocyte heterogeneity has been revealed by the serendipitous observation that different MyHCs are present in atrial and ventricular myocardium and in heart conduction tissue. Developmental MyHCs present in embryonic and fetal/neonatal skeletal muscle are re-expressed during muscle regeneration and can be used to identify regenerating fibers in muscle diseases. MyHC isoforms provide cell type-specific markers to identify the signaling pathways that control muscle cell identity and are an essential reference to interpret the results of single-cell transcriptomics and proteomics.
Topics: Animals; Antibodies, Monoclonal; Gene Expression Regulation, Developmental; Humans; Muscle Fibers, Skeletal; Muscle, Skeletal; Myosin Heavy Chains; Protein Isoforms
PubMed: 29761627
DOI: 10.1111/febs.14502 -
Wiley Interdisciplinary Reviews.... Jul 2016Skeletal muscle fibers are classified into fiber types, in particular, slow twitch versus fast twitch. Muscle fiber types are generally defined by the particular myosin... (Review)
Review
Skeletal muscle fibers are classified into fiber types, in particular, slow twitch versus fast twitch. Muscle fiber types are generally defined by the particular myosin heavy chain isoforms that they express, but many other components contribute to a fiber's physiological characteristics. Skeletal muscle fiber type can have a profound impact on muscle diseases, including certain muscular dystrophies and sarcopenia, the aging-induced loss of muscle mass and strength. These findings suggest that some muscle diseases may be treated by shifting fiber type characteristics either from slow to fast, or fast to slow phenotypes, depending on the disease. Recent studies have begun to address which components of muscle fiber types mediate their susceptibility or resistance to muscle disease. However, for many diseases it remains largely unclear why certain fiber types are affected. A substantial body of work has revealed molecular pathways that regulate muscle fiber type plasticity and early developmental muscle fiber identity. For instance, recent studies have revealed many factors that regulate muscle fiber type through modulating the activity of the muscle regulatory transcription factor MYOD1. Future studies of muscle fiber type development in animal models will continue to enhance our understanding of factors and pathways that may provide therapeutic targets to treat muscle diseases. WIREs Dev Biol 2016, 5:518-534. doi: 10.1002/wdev.230 For further resources related to this article, please visit the WIREs website.
Topics: Animals; Developmental Biology; Humans; Muscle Fibers, Skeletal; Muscular Diseases; Myosin Heavy Chains
PubMed: 27199166
DOI: 10.1002/wdev.230 -
Clinical Neurophysiology : Official... May 2021Describe and evaluate the concepts of near fiber electromyography (NFEMG), the features used, including near fiber motor unit potential (NFMUP) duration and dispersion,...
OBJECTIVE
Describe and evaluate the concepts of near fiber electromyography (NFEMG), the features used, including near fiber motor unit potential (NFMUP) duration and dispersion, which relate to motor unit distal axonal branch and muscle fiber conduction time dispersion, and NFMUP segment jitter, a new measure of the temporal variability of neuromuscular junction transmission (NMJ), and axonal branch and muscle fibre conduction for the near fibres (i.e. NF jitter), and the methods for obtaining their values.
METHODS
Trains of high-pass filtered motor unit potentials (MUPs) (i.e. NFMUP trains) were extracted from needle-detected EMG signals to assess changes in motor unit (MU) morphology and electrophysiology caused by neuromuscular disorders or ageing. Evaluations using simulated needle-detected EMG data were completed and example human data are presented.
RESULTS
NFEMG feature values can be used to detect axonal sprouting, conduction slowing and NMJ transmission delay as well as changes in MU fiber diameter variability, and NF jitter. These changes can be detected prior to alterations of MU size or numbers.
CONCLUSIONS
The evaluations clearly demonstrate and the example data support that NFMUP duration and dispersion reflect MU distal axonal branching, conduction slowing and NMJ transmission delay and/or MU fiber diameter variability and that NFMUP jiggle and segment jitter reflect NF jitter.
SIGNIFICANCE
NFEMG can detect early changes in MU morphology and/or electrophysiology and has the potential to augment clinical diagnosis and tracking of neuromuscular disorders.
Topics: Axons; Electromyography; Evoked Potentials, Motor; Humans; Muscle Fibers, Skeletal
PubMed: 33774377
DOI: 10.1016/j.clinph.2021.02.008 -
Advances in Experimental Medicine and... 2018Muscle tissue is a highly specialized type of tissue, made up of cells that have as their fundamental properties excitability and contractility. The cellular elements... (Review)
Review
Muscle tissue is a highly specialized type of tissue, made up of cells that have as their fundamental properties excitability and contractility. The cellular elements that make up this type of tissue are called muscle fibers, or myofibers, because of the elongated shape they have. Contractility is due to the presence of myofibrils in the muscle fiber cytoplasm, as large cellular assemblies. Also, myofibers are responsible for the force that the muscle generates which represents a countless aspect of human life. Movements due to muscles are based on the ability of muscle fibers to use the chemical energy procured in metabolic processes, to shorten and then to return to the original dimensions. We describe in detail the levels of organization for the myofiber, and we correlate the structural aspects with the functional ones, beginning with neuromuscular transmission down to the biochemical reactions achieved in the sarcoplasmic reticulum by the release of Ca and the cycling of crossbridges. Furthermore, we are reviewing the types of muscle contractions and the fiber-type classification.
Topics: Animals; Humans; Muscle Contraction; Muscles; Myofibrils; Sarcoplasmic Reticulum
PubMed: 30390246
DOI: 10.1007/978-981-13-1435-3_2 -
The Journal of Physiology Sep 2019Performing resistance exercise with heavier loads is often proposed to be necessary for the recruitment of larger motor units and activation of type II muscle fibres,... (Clinical Trial)
Clinical Trial
KEY POINTS
Performing resistance exercise with heavier loads is often proposed to be necessary for the recruitment of larger motor units and activation of type II muscle fibres, leading to type II fibre hypertrophy. Indirect measures [surface electromyography (EMG)] have been used to support this thesis, although we propose that lighter loads lifted to task failure (i.e. volitional fatigue) result in the similar activation of type II fibres. In the present study, participants performed resistance exercise to task failure with heavier and lighter loads with both a normal and longer repetition duration (i.e. time under tension). Type I and type II muscle fibre glycogen depletion was determined by neither load, nor repetition duration during resistance exercise performed to task failure. Surface EMG amplitude was not related to muscle fibre glycogen depletion or anabolic signalling; however, muscle fibre glycogen depletion and anabolic signalling were related. Performing resistance exercise to task failure, regardless of load lifted or repetition duration, necessitates the activation of type II muscle fibres.
ABSTRACT
Heavier loads (>60% of maximal strength) are considered to be necessary during resistance exercise (RE) to activate and stimulate hypertrophy of type II fibres. Support for this proposition comes from observation of higher surface electromyography (EMG) amplitudes during RE when lifting heavier vs. lighter loads. We aimed to determine the effect of RE, to task failure, with heavier vs. lighter loads and shorter or longer repetition durations on: EMG-derived variables, muscle fibre activation, and anabolic signalling. Ten recreationally-trained young men performed four unilateral RE conditions randomly on two occasions (two conditions, one per leg per visit). Muscle biopsies were taken from the vastus lateralis before and one hour after RE. Broadly, total time under load, number of repetitions, exercise volume, EMG amplitude (at the beginning and end of each set) and total EMG activity were significantly different between conditions (P < 0.05); however, neither glycogen depletion (in both type I and type II fibres), nor phosphorylation of relevant signalling proteins showed any difference between conditions. We conclude that muscle fibre activation and subsequent anabolic signalling are independent of load, repetition duration and surface EMG amplitude when RE is performed to task failure. The results of the present study provide evidence indicating that type I and type II fibres are activated when heavier and lighter loads are lifted to task failure. We propose that our results explain why RE training with higher or lower loads, when loads are lifted to task failure, leads to equivalent muscle hypertrophy and occurs in both type I and type II fibres.
Topics: Adult; Electromyography; Exercise; Humans; Male; Muscle Contraction; Muscle Fibers, Fast-Twitch; Muscle Fibers, Slow-Twitch; Muscle Strength; Resistance Training; Young Adult
PubMed: 31294822
DOI: 10.1113/JP278056 -
Oncotarget Mar 2017
Topics: Animals; Electromyography; Electrophysiological Phenomena; Humans; Muscle Denervation; Muscle Fibers, Skeletal; Muscles; Nerve Regeneration; Neurons
PubMed: 28407699
DOI: 10.18632/oncotarget.15757 -
Advances in Neurobiology 2022Extraocular motoneurons are located in three brainstem nuclei: the abducens, trochlear and oculomotor. They control all types of eye movements by innervating three pairs...
Extraocular motoneurons are located in three brainstem nuclei: the abducens, trochlear and oculomotor. They control all types of eye movements by innervating three pairs of agonistic/antagonistic extraocular muscles. They exhibit a tonic-phasic discharge pattern, demonstrating sensitivity to eye position and sensitivity to eye velocity. According to their innervation pattern, extraocular muscle fibers can be classified as singly innervated muscle fiber (SIF), or the peculiar multiply innervated muscle fiber (MIF). SIF motoneurons show anatomical and physiological differences with MIF motoneurons. The latter are smaller and display lower eye position and velocity sensitivities as compared with SIF motoneurons.
Topics: Eye Movements; Humans; Motor Neurons; Oculomotor Muscles
PubMed: 36066830
DOI: 10.1007/978-3-031-07167-6_12 -
The Journal of Physiology Dec 2022Ageing is accompanied by decrements in the size and function of skeletal muscle that compromise independence and quality of life in older adults. Developing therapeutic... (Review)
Review
Ageing is accompanied by decrements in the size and function of skeletal muscle that compromise independence and quality of life in older adults. Developing therapeutic strategies to ameliorate these changes is critical but requires an in-depth mechanistic understanding of the underlying physiology. Over the past 25 years, studies on the contractile mechanics of isolated human muscle fibres have been instrumental in facilitating our understanding of the cellular mechanisms contributing to age-related skeletal muscle dysfunction. The purpose of this review is to characterize the changes that occur in single muscle fibre size and contractile function with ageing and identify key areas for future research. Surprisingly, most studies observe that the size and contractile function of fibres expressing slow myosin heavy chain (MHC) I are well-preserved with ageing. In contrast, there are profound age-related decrements in the size and contractile function of the fibres expressing the MHC II isoforms. Notably, lifelong aerobic exercise training is unable to prevent most of the decrements in fast fibre contractile function, which have been implicated as a primary mechanism for the age-related loss in whole-muscle power output. These findings reveal a critical need to investigate the effectiveness of other nutritional, pharmaceutical or exercise strategies, such as lifelong resistance training, to preserve fast fibre size and function with ageing. Moreover, integrating single fibre contractile mechanics with the molecular profile and other parameters important to contractile function (e.g. phosphorylation of regulatory proteins, innervation status, mitochondrial function, fibre economy) is necessary to comprehensively understand the ageing skeletal muscle phenotype.
Topics: Humans; Aged; Quality of Life; Muscle Contraction; Muscle Fibers, Skeletal; Muscle, Skeletal; Aging; Myosin Heavy Chains
PubMed: 36268622
DOI: 10.1113/JP282298