. PubMed ID: 23626925 doi:10.1515/plm-2012-0032 10.1515/plm-2012-0032 23626925 2. Alves AN , Fernandes KPS , Deana AM , Bussadori SK , Mesquita-Ferrari RA . Effects of low-level laser therapy on skeletal muscle repair: a systematic review . Am J Phys Med Rehabil . 2014 ; 93 ( 12 ): 1073
Stephan R. Fisher, Justin H. Rigby, Joni A. Mettler and Kevin W. McCurdy
Jeffrey J. Dueweke, Tariq M. Awan and Christopher L. Mendias
Eccentric-contraction-induced skeletal muscle injuries, included in what is clinically referred to as muscle strains, are among the most common injuries treated in the sports medicine setting. Although patients with mild injuries often fully recover to their preinjury levels, patients who suffer moderate or severe injuries can have a persistent weakness and loss of function that is refractory to rehabilitation exercises and currently available therapeutic interventions. The objectives of this review were to describe the fundamental biophysics of force transmission in muscle and the mechanism of muscle-strain injuries, as well as the cellular and molecular processes that underlie the repair and regeneration of injured muscle tissue. The review also summarizes how commonly used therapeutic modalities affect muscle regeneration and opportunities to further improve our treatment of skeletal muscle strain injuries.
Walter Herzog, Timothy Koh, Evelyne Hasler and Tim Leonard
We hypothesize that the neuromuscular system is designed to function effectively in accomplishing everyday movement tasks. Since everyday movement tasks may vary substantially in terms of speed and resistance, we speculate that agonistic muscles contribute differently to varying movement tasks such that the mechanical, structural, and physiological properties of the system are optimized at all times. We further hypothesize that a mechanical perturbation to the musculoskeletal system, such as the loss of an important joint ligament or the change of a muscle’s line of action, causes an adaptation of the system aimed at reestablishing effective function. Here. we demonstrate how the specificity of the cat ankle extensors is used to accommodate different locomotor tasks. We then illustrate how the loss of an important ligament in the cat knee leads to neuromuscular adaptation. Finally, we discuss the adaptability of skeletal muscle following an intervention that changes a muscle’s line of action, moment arm, and excursion.
Emily Arentson-Lantz, Elfego Galvan, Adam Wacher, Christopher S. Fry and Douglas Paddon-Jones
et al., 2011 ). To mimic the overt physical inactivity experienced during hospitalization, while separating the catabolic, disease-related effects from the intrinsic effects of skeletal muscle disuse, we subjected a cohort of healthy, community-dwelling older adults to a 7-day bed rest (BR) protocol
David T. Corr, Ray Vanderby Jr. and Thomas M. Best
An existing rheological model of skeletal muscle (Forcinito et al., 1998) was modified with a nonlinear Maxwell fluid element to provide a phenomenological model capable of analyzing the strain-stiffening behavior typically found in passive, and occasionally observed in active, skeletal muscle. This new model describes both active and passive muscular behavior as a combination of the behavior of each model component, without requiring prior knowledge of the force-length or force-velocity characteristics of the muscle.
Brent A. Baker
Even though chronological aging is an inevitable phenomenological consequence occurring in every living organism, it is biological aging that may be the most significant factor challenging our quality of life. Development of functional limitations, resulting from improper maintenance and restoration of various organ systems, ultimately leads to reduced health and independence. Skeletal muscle is an organ system that, when challenged, is often injured in response to varying stimuli. Overt muscle-strain injury can be traumatic, clinically diagnosable, properly managed, and a remarkably common event, yet our contemporary understanding of how age and environmental stressors affect the initial and subsequent induction of injury and how the biological processes resulting from this event are modifiable and, eventually, lead to functional restoration and healing of skeletal muscle and adjacent tissues is presently unclear. Even though the secondary injury response to and recovery from "contraction-induced" skeletal-muscle injury are impaired with aging, there is no scientific consensus as to the exact mechanism responsible for this event. Given the multitude of investigative approaches, particular consideration given to the appropriateness of the muscle-injury model, or research paradigm, is critical so that outcomes may be physiologically relevant and translational. In this case, methods implementing stretch-shortening contractions, the most common form of muscle movements used by all mammals during physical movement, work, and activity, are highlighted.
Understanding the fundamental evidence regarding how aging influences the responsivity of skeletal muscle to strain injury is vital for informing how clinicians approach and implement preventive strategies, as well as therapeutic interventions. From a practical perspective, maintaining or improving the overall health and tissue quality of skeletal muscle as one ages will positively affect skeletal muscle’s safety threshold and responsivity, which may reduce incidence of injury, improve recovery time, and lessen overall fiscal burdens.
Lothar Stein, Constanze Pacht, Sibylle Junge, Tobias S. Kaeding, Momme Kück, Norbert Maassen, Torge Wittke and Vladimir Shushakov
Defects in the gene encoding the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) cause CF. Absence of the CFTR may result in skeletal muscle dysfunction. Here, we tested skeletal muscle function in male adolescent patients with CF.
Ten CF and 10 control participants (age: 16.8 ± 0.6 years) performed 7 repetitive sets of maximum voluntary contractions (MVCs) and underwent an isometric fatigue test of the knee extensors. Electromyography (EMG) activity was recorded from the m. vastus lateralis (VL) and m. vastus medialis (VM).
In CF, the MVC torque was lower and correlated with the predicted forced expiratory volume in one second (r = .73, p = .012, n = 10). The M-wave in the VL was shorter in CF than in controls (18.6 ± 0.5 vs. 20.3 ± 0.5 ms, p < .028). In the VM, both the M-wave (4.96 ± 0.61 vs. 7.97 ± 0.60 mV, p = .001) and the EMG (0.29 ± 0.04 vs. 0.47 ± 0.04 mV, p = .004) amplitudes were smaller in CF.
The differences in the VL and VM EMG signals between the groups indicate that the lower MVC torque in CF did not result from the direct impact of a CFTR defect on the sarcolemmal excitability; the differences more likely resulted from the less developed musculature in the patients with CF.
Ildus I. Ahmetov, Olga L. Vinogradova and Alun G. Williams
The ability to perform aerobic or anaerobic exercise varies widely among individuals, partially depending on their muscle-fiber composition. Variability in the proportion of skeletal-muscle fiber types may also explain marked differences in aspects of certain chronic disease states including obesity, insulin resistance, and hypertension. In untrained individuals, the proportion of slow-twitch (Type I) fibers in the vastus lateralis muscle is typically around 50% (range 5–90%), and it is unusual for them to undergo conversion to fast-twitch fibers. It has been suggested that the genetic component for the observed variability in the proportion of Type I fibers in human muscles is on the order of 40–50%, indicating that muscle fiber-type composition is determined by both genotype and environment. This article briefly reviews current progress in the understanding of genetic determinism of fiber-type proportion in human skeletal muscle. Several polymorphisms of genes involved in the calcineurin–NFAT pathway, mitochondrial biogenesis, glucose and lipid metabolism, cytoskeletal function, hypoxia and angiogenesis, and circulatory homeostasis have been associated with fiber-type composition. As muscle is a major contributor to metabolism and physical strength and can readily adapt, it is not surprising that many of these gene variants have been associated with physical performance and athlete status, as well as metabolic and cardiovascular diseases. Genetic variants associated with fiber-type proportions have important implications for our understanding of muscle function in both health and disease.
Stefan M. Pasiakos, Holly L. McClung, James P. McClung, Maria L. Urso, Matthew A. Pikosky, Gregory J. Cloutier, Roger A. Fielding and Andrew J. Young
This study examined alterations in skeletal-muscle growth and atrophy-related molecular events after a single bout of moderate-intensity endurance exercise. Muscle biopsies were obtained from 10 men (23 ± 1 yr, body mass 80 ± 2 kg, and VO2peak 45 ± 1 ml · kg−1 · min−1) immediately (0 hr) and 3 hr after a 60-min bout of cycle exercise (60% ± 5% VO2peak). Corresponding muscle biopsies were also obtained under resting conditions. The phosphorylation status of insulin/IGF-PI3K molecular-signaling proteins, ubiquitin-proteasome-related gene expression, FOXO transcription factors, and myogenic regulatory factors in muscle samples was analyzed using multiplex analysis, Western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR). A condition–time interaction was observed for Akt phosphorylation (p < .05) with multiplexing. Regardless of endurance exercise, Akt phosphorylation decreased and ERK phosphorylation increased at 3 hr compared with 0 hr (p < .05). Levels of p70S6K phosphorylation were 110% greater (p < .05) at 3 hr than at 0 hr using Western blots. MuRF mRNA expression postexercise increased; levels were 4.7- and 5.7-fold greater (p < .05) at 0 hr and 3 hr, respectively, than at rest with qRT-PCR. Atrogin mRNA expression was up-regulated 3.2-fold 3 hr postexercise compared with rest. These findings demonstrate modest changes in the molecular responses to moderate endurance exercise in the absence of nutrition. This study provides the groundwork for future investigations designed to optimize the metabolic conditions necessary to positively influence the cellular mechanisms specific to skeletal-muscle protein turnover during recovery from endurance exercise.
Martin J. Gibala
The contribution of amino acid oxidation to total energy expenditure is negligible during short-term intense exercise and accounts for 3–6% of the total adenosine triphosphate supplied during prolonged exercise in humans. While not quantitatively important in terms of energy supply, the intermediary metabolism of several amino acids—notably glutamate, alanine, and the branched-chain amino acids—afreets other metabolites .including the intermediates within the tricarboxylic acid (TCA) cycle. Glutamate appears to be a key substrate for the rapid increase in muscle TCA cycle intermediates (TCAI) that occurs at the onset of moderate to intense exercise, due to a rightward shift of the reaction catalyzed by alanine aminotransferase (glutamate + pyruvate <-> alanine + 2-oxoglutarate). The pool of muscle TCAI declines during prolonged exercise, and this has been attributed to an increase in leucine oxidation that relies on one of the TCAI. However, this mechanism does not appear to be quantitatively important due of the relatively low maximal activity of branched-chain oxoacid dehydrogenase, the key enzyme involved. It has been suggested that an increase in TCAI is necessary to attain high rates of aerobic energy production and that a decline in TCAI may be a causative factor in local muscle fatigue. These topics remain controversial, but recent evidence suggests that changes in TCAI during exercise are unrelated to oxidative energy provision in skeletal muscle.