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The American Journal of Sports Medicine Aug 2020Anterior cruciate ligament (ACL) injuries and reconstruction (ACLR) promote quadriceps muscle atrophy and weakness that can persist for years, suggesting the need for... (Randomized Controlled Trial)
Randomized Controlled Trial
Utility of Neuromuscular Electrical Stimulation to Preserve Quadriceps Muscle Fiber Size and Contractility After Anterior Cruciate Ligament Injuries and Reconstruction: A Randomized, Sham-Controlled, Blinded Trial.
BACKGROUND
Anterior cruciate ligament (ACL) injuries and reconstruction (ACLR) promote quadriceps muscle atrophy and weakness that can persist for years, suggesting the need for more effective rehabilitation programs. Whether neuromuscular electrical stimulation (NMES) can be used to prevent maladaptations in skeletal muscle size and function is unclear.
PURPOSE
To examine whether early NMES use, started soon after an injury and maintained through 3 weeks after surgery, can preserve quadriceps muscle size and contractile function at the cellular (ie, fiber) level in the injured versus noninjured leg of patients undergoing ACLR.
STUDY DESIGN
Randomized controlled trial; Level of evidence, 1.
METHODS
Patients (n = 25; 12 men/13 women) with an acute, first-time ACL rupture were randomized to NMES (5 d/wk) or sham (simulated microcurrent electrical nerve stimulation; 5 d/wk) treatment to the quadriceps muscles of their injured leg. Bilateral biopsies of the vastus lateralis were performed 3 weeks after surgery to measure skeletal muscle fiber size and contractility. Quadriceps muscle size and strength were assessed 6 months after surgery.
RESULTS
A total of 21 patients (9 men/12 women) completed the trial. ACLR reduced single muscle fiber size and contractility across all fiber types ( < .01 to < .001) in the injured compared with noninjured leg 3 weeks after surgery. NMES reduced muscle fiber atrophy ( < .01) through effects on fast-twitch myosin heavy chain (MHC) II fibers ( < .01 to < .001). NMES preserved contractility in slow-twitch MHC I fibers ( < .01 to < .001), increasing maximal contractile velocity ( < .01) and preserving power output ( < .01), but not in MHC II fibers. Differences in whole muscle strength between groups were not discerned 6 months after surgery.
CONCLUSION
Early NMES use reduced skeletal muscle fiber atrophy in MHC II fibers and preserved contractility in MHC I fibers. These results provide seminal, cellular-level data demonstrating the utility of the early use of NMES to beneficially modify skeletal muscle maladaptations to ACLR.
CLINICAL RELEVANCE
Our results provide the first comprehensive, cellular-level evidence to show that the early use of NMES mitigates early skeletal muscle maladaptations to ACLR.
REGISTRATION
NCT02945553 (ClinicalTrials.gov identifier).
Topics: Anterior Cruciate Ligament Injuries; Anterior Cruciate Ligament Reconstruction; Electric Stimulation Therapy; Female; Humans; Male; Muscle Contraction; Muscle Fibers, Skeletal; Muscle Strength; Organ Size; Quadriceps Muscle
PubMed: 32631074
DOI: 10.1177/0363546520933622 -
Journal of Strength and Conditioning... Feb 2023Nuzzo, JL. Narrative review of sex differences in muscle strength, endurance, activation, size, fiber type, and strength training participation rates, preferences,... (Review)
Review
Narrative Review of Sex Differences in Muscle Strength, Endurance, Activation, Size, Fiber Type, and Strength Training Participation Rates, Preferences, Motivations, Injuries, and Neuromuscular Adaptations.
Nuzzo, JL. Narrative review of sex differences in muscle strength, endurance, activation, size, fiber type, and strength training participation rates, preferences, motivations, injuries, and neuromuscular adaptations. J Strength Cond Res 37(2): 494-536, 2023-Biological sex and its relation with exercise participation and sports performance continue to be discussed. Here, the purpose was to inform such discussions by summarizing the literature on sex differences in numerous strength training-related variables and outcomes-muscle strength and endurance, muscle mass and size, muscle fiber type, muscle twitch forces, and voluntary activation; strength training participation rates, motivations, preferences, and practices; and injuries and changes in muscle size and strength with strength training. Male subjects become notably stronger than female subjects around age 15 years. In adults, sex differences in strength are more pronounced in upper-body than lower-body muscles and in concentric than eccentric contractions. Greater male than female strength is not because of higher voluntary activation but to greater muscle mass and type II fiber areas. Men participate in strength training more frequently than women. Men are motivated more by challenge, competition, social recognition, and a desire to increase muscle size and strength. Men also have greater preference for competitive, high-intensity, and upper-body exercise. Women are motivated more by improved attractiveness, muscle "toning," and body mass management. Women have greater preference for supervised and lower-body exercise. Intrasexual competition, mate selection, and the drive for muscularity are likely fundamental causes of exercise behaviors in men and women. Men and women increase muscle size and strength after weeks of strength training, but women experience greater relative strength improvements depending on age and muscle group. Men exhibit higher strength training injury rates. No sex difference exists in strength loss and muscle soreness after muscle-damaging exercise.
Topics: Adult; Humans; Male; Female; Adolescent; Muscle, Skeletal; Motivation; Resistance Training; Muscle Strength; Muscle Fibers, Skeletal
PubMed: 36696264
DOI: 10.1519/JSC.0000000000004329 -
Sports Medicine (Auckland, N.Z.) Sep 2021Muscle glycogen is the main substrate during high-intensity exercise and large reductions can occur after relatively short durations. Moreover, muscle glycogen is stored... (Review)
Review
Muscle glycogen is the main substrate during high-intensity exercise and large reductions can occur after relatively short durations. Moreover, muscle glycogen is stored heterogeneously and similarly displays a heterogeneous and fiber-type specific depletion pattern with utilization in both fast- and slow-twitch fibers during high-intensity exercise, with a higher degradation rate in the former. Thus, depletion of individual fast- and slow-twitch fibers has been demonstrated despite muscle glycogen at the whole-muscle level only being moderately lowered. In addition, muscle glycogen is stored in specific subcellular compartments, which have been demonstrated to be important for muscle function and should be considered as well as global muscle glycogen availability. In the present review, we discuss the importance of glycogen metabolism for single and intermittent bouts of high-intensity exercise and outline possible underlying mechanisms for a relationship between muscle glycogen and fatigue during these types of exercise. Traditionally this relationship has been attributed to a decreased ATP resynthesis rate due to inadequate substrate availability at the whole-muscle level, but emerging evidence points to a direct coupling between muscle glycogen and steps in the excitation-contraction coupling including altered muscle excitability and calcium kinetics.
Topics: Exercise; Fatigue; Glycogen; Humans; Muscle, Skeletal; Muscles
PubMed: 33900579
DOI: 10.1007/s40279-021-01475-0 -
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 -
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 -
Proceedings of the National Academy of... Jan 2023Sarcopenia is distinct from normal muscle atrophy in that it is closely related to a shift in the muscle fiber type. Deficiency of the anabolic action of androgen on...
Sarcopenia is distinct from normal muscle atrophy in that it is closely related to a shift in the muscle fiber type. Deficiency of the anabolic action of androgen on skeletal muscles is associated with sarcopenia; however, the function of the androgen receptor (AR) pathway in sarcopenia remains poorly understood. We generated a mouse model (fast-twitch muscle-specific AR knockout [fmARKO] mice) in which the AR was selectively deleted in the fast-twitch muscle fibers. In young male mice, the deletion caused no change in muscle mass, but it reduced muscle strength and fatigue resistance and induced a shift in the soleus muscles from fast-twitch fibers to slow-twitch fibers (14% increase, = 0.02). After middle age, with the control mice, the male fmARKO mice showed much less muscle function, accompanied by lower hindlimb muscle mass; this phenotype was similar to the progression of sarcopenia. The bone mineral density of the femur was significantly reduced in the fmARKO mice, indicating possible osteosarcopenia. Microarray and gene ontology analyses revealed that in male fmARKO mice, there was downregulation of polyamine biosynthesis-related geneswhich was confirmed by liquid chromatography-tandem mass spectrometry assay and the primary cultured myofibers. None of the AR deletion-related phenotypes were observed in female fmARKO mice. Our findings showed that the AR pathway had essential muscle type- and sex-specific roles in the differentiation toward fast-twitch fibers and in the maintenance of muscle composition and function. The AR in fast-twitch muscles was the dominant regulator of muscle fiber-type composition and muscle function, including the muscle-bone relationship.
Topics: Mice; Male; Female; Animals; Sarcopenia; Receptors, Androgen; Muscle Fibers, Slow-Twitch; Muscle, Skeletal; Muscle Fibers, Fast-Twitch; Muscular Diseases; Phenotype; Mice, Knockout
PubMed: 36669097
DOI: 10.1073/pnas.2218032120 -
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 -
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 -
Redox Biology Aug 2020Endurance exercise training promotes numerous biochemical adaptations within skeletal muscle fibers culminating into a phenotype that is safeguarded against numerous... (Review)
Review
Endurance exercise training promotes numerous biochemical adaptations within skeletal muscle fibers culminating into a phenotype that is safeguarded against numerous perils including doxorubicin-induced myopathy and inactivity-induced muscle atrophy. This exercise-induced protection of skeletal muscle fibers is commonly termed "exercise preconditioning". This review will discuss the biochemical mechanisms responsible for exercise-induced protection of skeletal muscle fibers against these harmful events. The first segment of this report highlights the evidence that endurance exercise training provides cytoprotection to skeletal muscle fibers against several potentially damaging insults. The second and third sections of the review will discuss the cellular adaptations responsible for exercise-induced protection of skeletal muscle fibers against doxorubicin-provoked damage and inactivity-induced fiber atrophy, respectively. Importantly, we also identify gaps in our understanding of exercise preconditioning in hopes of stimulating future research.
Topics: Adaptation, Physiological; Exercise; Humans; Muscle Fibers, Skeletal; Muscle, Skeletal; Muscular Atrophy
PubMed: 32089451
DOI: 10.1016/j.redox.2020.101462 -
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