https://www.commed.vcu.edu/Chronic_Disease/2012/cochranrvwrschbias.pdf

The Cochrane Collaboration's tool for assessing risk of bias in randomised trials

Charge, Sophie B. P., and Michael A. Rudnicki. Cellular and Molecular Regulation of Muscle Regeneration. Physiol Rev 84: 209–238, 2004; 10.1152/physrev.00019.2003.—Under normal circumstances, mamma...

Cellular and Molecular Regulation of Muscle Regeneration

Mammalian skeletal muscle comprises different fiber types, whose identity is first established during embryonic development by intrinsic myogenic control mechanisms and is later modulated by neural and hormonal factors. The relative proportion of the different fiber types varies strikingly between species, and in humans shows significant variability between individuals. Myosin heavy chain isoforms, whose complete inventory and expression pattern are now available, provide a useful marker for fiber types, both for the four major forms present in trunk and limb muscles and the minor forms present in head and neck muscles. However, muscle fiber diversity involves all functional muscle cell compartments, including membrane excitation, excitation-contraction coupling, contractile machinery, cytoskeleton scaffold, and energy supply systems. Variations within each compartment are limited by the need of matching fiber type properties between different compartments. Nerve activity is a major control mechanism of the fiber type profile, and multiple signaling pathways are implicated in activity-dependent changes of muscle fibers. The characterization of these pathways is raising increasing interest in clinical medicine, given the potentially beneficial effects of muscle fiber type switching in the prevention and treatment of metabolic diseases.

Fiber types in mammalian skeletal muscles.

This review aims to summarize the latest developments with regard to physical fitness and several health outcomes in young people. The literature reviewed suggests that (1) cardiorespiratory fitness levels are associated with total and abdominal adiposity; (2) both cardiorespiratory and muscular fitness are shown to be associated with established and emerging cardiovascular disease risk factors; (3) improvements in muscular fitness and speed/agility, rather than cardiorespiratory fitness, seem to have a positive effect on skeletal health; (4) both cardiorespiratory and muscular fitness enhancements are recommended in pediatric cancer patients/survivors in order to attenuate fatigue and improve their quality of life; and (5) improvements in cardiorespiratory fitness have positive effects on depression, anxiety, mood status and self-esteem, and seem also to be associated with a higher academic performance. In conclusion, health promotion policies and physical activity programs should be designed to improve cardiorespiratory fitness, but also two other physical fitness components such us muscular fitness and speed/agility. Schools may play an important role by identifying children with low physical fitness and by promoting positive health behaviors such as encouraging children to be active, with special emphasis on the intensity of the activity.

Physical fitness in childhood and adolescence: a powerful marker of health

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Biomechanics And Motor Control Of Human Movement

The objective of this review is to evaluate the measurement tools currently used in the study of eccentric contraction-induced muscle injury, with emphasis on their usefulness for quantifying the magnitude and duration of the injury and as indicators of muscle functional deficits. In studies in humans, it was concluded that measurements of maximal voluntary contraction torque and range of motion provide the best methods for quantifying muscle injury. Similarly, in animal studies, the in vitro measurement of electrically elicited force under isometric conditions was considered to be the best of the measurement tools currently in use. For future studies, more effort should be put into measuring other contractile parameters (e.g. force/torque-velocity and force/torque-length relationships maximal shortening velocity and fatigue susceptibility) that may reflect injury-induced functional impairments. The use of histology, ratings of soreness and the measurement of blood or bath levels of myofibre proteins should be discouraged for purposes of quantifying muscle injury and/or functional impairment.

Measurement Tools Used in the Study of Eccentric Contraction-Induced Injury

Exercise for which a skeletal muscle is not adequately conditioned results in focal sites of injury distributed within and among the fibres. Exercise with eccentric contractions is particularly damaging. The injury process can be hypothesised to occur in several stages. First, an initial phase serves to inaugurate the sequence. Hypotheses for the initial event can be categorised as either physical or metabolic in nature. We argue that the initial event is physical, that stresses imposed on sarcolemma by sarcomere length inhomogeneities occurring during eccentric contractions cause disruption of the normal permeability barrier provided by the cell membrane and basal lamina. This structural disturbance allows Ca++ to enter the fibre down its electrochemical gradient, precipitating the Ca++ overload phase. If the breaks in the sarcolemma are relatively minor, the entering Ca++ may be adequately handled by ATPase pumps that sequester and extrude Ca++ from the cytoplasm ('reversible' injury). However, if the Ca++ influx overwhelms the Ca++ pumps and free cytosolic Ca++ concentration rises, the injury becomes 'irreversible'. Elevations in intracellular Ca++ levels activate a number of Ca(++)-dependent proteolytic and phospholipolytic pathways that are indigenous to the muscle fibres, which respectively degrade structural and contractile proteins and membrane phospholipids; for instance, it has been demonstrated that elevation of intracellular Ca++ levels with Ca++ ionophores results in loss of creatine kinase activity from the fibres through activation of phospholipase A2 and subsequent production of leukotrienes. This autogenetic phase occurs prior to arrival of phagocytic cells, and continues during the inflammatory period when macrophages and other phagocytic cells are active at the damage site. The phagocytic phase is in evidence by 2 to 6 hours after the injury, and proceeds for several days. The regenerative phase then restores the muscle fibre to its normal condition. Repair of the muscle fibres appears to be complete; the fibres adapt during this process so that future bouts of exercise of similar type, intensity, and duration cause less injury to the muscle.

Mechanisms of exercise-induced muscle fibre injury

Higbie, Elizabeth J., Kirk J. Cureton, Gordon L. Warren III, and Barry M. Prior. Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation.J. Appl...

/pdf/effects-of-concentric-and-eccentric-training-on-muscle-kwjdtuiao7.pdf

Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation

WARREN, G.L., C.P. INGALLS, D.A. LOWE, and R.B. ARMSTRONG. Excitation-contraction uncoupling: major role in contraction-induced muscle injury. Exerc. Sports Sci. Rev., Vol. 29, No. 2, pp. 82-87, 2001. The mechanisms that account for the strength loss after contraction-induced muscle injury remain co

Excitation-Contraction Uncoupling: Major Role in Contraction-Induced Muscle Injury

The objectives of this research were to determine the contribution of excitation-contraction (E-C) coupling failure to the decrement in maximal isometric tetanic force (Po) in mouse extensor digitorum longus (EDL) muscles after eccentric contractions and to elucidate possible mechanisms. The left anterior crural muscles of female ICR mice (n = 164) were injured in vivo with 150 eccentric contractions. Po, caffeine-, 4-chloro-m-cresol-, and K+-induced contracture forces, sarcoplasmic reticulum (SR) Ca2+ release and uptake rates, and intracellular Ca2+ concentration ([Ca2+]i) were then measured in vitro in injured and contralateral control EDL muscles at various times after injury up to 14 days. On the basis of the disproportional reduction in Po (approximately 51%) compared with caffeine-induced force (approximately 11-21%), we estimate that E-C coupling failure can explain 57-75% of the Po decrement from 0 to 5 days postinjury. Comparable reductions in Po and K+-induced force (51%), and minor reductions (0-6%) in the maximal SR Ca2+ release rate, suggest that the E-C coupling defect site is located at the t tubule-SR interface immediately after injury. Confocal laser scanning microscopy indicated that resting [Ca2+]i was elevated and peak tetanic [Ca2+]i was reduced, whereas peak 4-chloro-m-cresol-induced [Ca2+]i was unchanged immediately after injury. By 3 days postinjury, 4-chloro-m-cresol-induced [Ca2+]i became depressed, probably because of decreased SR Ca2+ release and uptake rates (17-31%). These data indicate that the decrease in Po during the first several days after injury primarily stems from a failure in the E-C coupling process.

Gordon L. Warren

Papers

Measurement Tools Used in the Study of Eccentric Contraction-Induced Injury

Mechanisms of exercise-induced muscle fibre injury

Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation

Excitation-Contraction Uncoupling: Major Role in Contraction-Induced Muscle Injury

E-C coupling failure in mouse EDL muscle after in vivo eccentric contractions