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This study tested the hypothesis that changes in indirect markers of muscle damage following maximal eccentric exercise would be smaller for the knee extensors (KE) and flexors (KF) compared with the elbow flexors (EF) and extensors (EE). A total of 17 sedentary men performed five sets of six maximal isokinetic (90° s −1 ) eccentric contractions of EF (range of motion, ROM: 90°–0°, 0 = full extension), EE (55°–145°), KF (90°–0°), and KE (30°–120°) using a different limb with a 4–5-week interval in a counterbalanced order. Changes in maximal isometric and concentric isokinetic strength, optimum angle, limb circumference, ROM, plasma creatine kinase activity and myoglobin concentration, muscle soreness, and echo-intensity of B-mode ultrasound images before and for 5 days following exercise were compared amongst the four exercises using two-way repeated-measures ANOVA. All variables changed significantly following EF, EE, and KF exercises, but KE exercise did not change the optimum angle, limb circumference, and echo-intensity. Compared with KF and KE, EF and EE showed significantly greater changes in all variables, without significant differences between EF and EE. Changes in all variables were significantly greater for KF than KE. For the same subjects, the magnitude of change in the dependent variables following exercise varied among the exercises. These results suggest that the two arm muscles are equally more susceptible to muscle damage than leg muscles, but KF is more susceptible to muscle damage than KE. The difference in the susceptibility to muscle damage seems to be associated with the use of muscles in daily activities.

Potency is a quantitative measure of the desired biological function of an advanced therapy medicinal product (ATMP) and is a prerequisite for market approval application (MAA). To assess the potency of human skeletal muscle-derived cells (SMDCs), which are currently investigated in clinical trials for the regeneration of skeletal muscle defects, we evaluated acetylcholinesterase (AChE), which is expressed in skeletal muscle and nervous tissue of all mammals. CD56+ SMDCs were separated from CD56- SMDCs by magnetic activated cell sorting (MACS) and both differentiated in skeletal muscle differentiation medium. AChE activity of in vitro differentiated SMDCs was correlated with CD56 expression, fusion index, cell number, cell doubling numbers, differentiation markers and compared to the clinical efficacy in patients treated with SMDCs against fecal incontinence. CD56- SMDCs did not form multinucleated myotubes and remained low in AChE activity during differentiation. CD56+ SMDCs generated myotubes and increased in AChE activity during differentiation. AChE activity was found to accurately reflect the number of CD56+ SMDCs in culture, their fusion competence, and cell doubling number. In patients with fecal incontinence responding to SMDCs treatment, the improvement of clinical symptoms was positively linked with the AChE activity of the SMDCs injected. AChE activity was found to truly reflect the in vitro differentiation status of SMDCs and to be superior to the mere use of surface markers as it reflects not only the number of myogenic SMDCs in culture but also their fusion competence and population doubling number, thus combining cell quality and quantification of the expected mode of action (MoA) of SMDCs. Moreover, the successful in vitro validation of the assay proves its suitability for routine use. Most convincingly, our results demonstrate a link between clinical efficacy and the AChE activity of the SMDCs preparations used for the treatment of fecal incontinence. Thus, we recommend using AChE activity of in vitro differentiated SMDCs as a potency measure in end stage (phase III) clinical trials using SMDCs for skeletal muscle regeneration and subsequent market approval application (MAA).

Muscle symptoms in patients who are treated with statins and have normal creatine kinase levels are not well understood. To report biopsy-confirmed myopathy and normal creatine kinase levels associated with statin use. Case reports from preliminary analysis of an ongoing clinical trial. Clinical research center in a community hospital. Four patients with muscle symptoms that developed during statin therapy and reversed during placebo use. 1) Patients' ability to identify blinded statin therapy and 2) standard measures of functional capacity and muscle strength. All four patients repeatedly distinguished blinded statin therapy from placebo. Strength testing confirmed weakness during statin therapy that reversed during placebo use. Muscle biopsies showed evidence of mitochondrial dysfunction, including abnormally increased lipid stores, fibers that did not stain for cytochrome oxidase activity, and ragged red fibers. These findings reversed in the three patients who had repeated biopsy when they were not receiving statins. Creatine kinase levels were normal in all four patients despite the presence of significant myopathy. Some patients who develop muscle symptoms while receiving statin therapy have demonstrable weakness and histopathologic findings of myopathy despite normal serum creatine kinase levels.

Rowers regularly undertake rowing training within 24 h of performing bouts of strength training; however, the effect of this practice has not been investigated. This study evaluated the impact of a bout of high-intensity strength training on 2,000 m rowing ergometer performance and rowing-specific maximal power. Eight highly trained male club rowers performed baseline measures of five separate, static squat jumps (SSJ) and countermovement jumps (CMJ), maximal rowing ergometer power strokes (PS) and a single 2,000 m rowing ergometer test (2,000 m). Subsequently, participants performed a high-intensity strength training session consisting of various multi-joint barbell exercises. The 2,000 m test was repeated at 24 and 48 h post-ST, in addition SSJ, CMJ and PS tests were performed at these time points and also at 2 h post-ST. Muscle soreness, serum creatine kinase (CK) and lactate dehydrogenase (LDH) were assessed pre-ST and 2, 24 and 48 h post-ST. Following the ST, there were significant elevations in muscle soreness (2 and 24 h, P < 0.01), CK (2, 24 and 48 h, P < 0.01), and LDH (2 h, P < 0.05) in comparison to baseline values. There were significant decrements across all time points for SSJ, CMJ and PS, which ranged between 3 and 10% ( P < 0.05). However, 2,000 m performance and related measurements of heart rate and blood lactate were not significantly affected by ST. In summary, a bout of high-intensity strength training resulted in symptoms of muscle damage and decrements in rowing-specific maximal power, but this did not affect 2,000 m rowing ergometer performance in highly trained rowers.

The aim of the study was to determine if Panax notoginseng is effective in reducing pain, indicators of inflammation and muscle damage, and in turn improve performance in well trained males who underwent a bout of eccentric exercise designed to induce delayed onset muscle soreness (DOMS). A double blind randomised placebo controlled trial. Twenty well trained male volunteers, matched by maximum aerobic capacity were randomly assigned to consume a regime of 4000mg of P. notoginseng capsules or an indistinguishable placebo before and after a downhill treadmill running episode designed to induce DOMS. Performance measures (Kin–Com, counter movement and squat jump), pain assessments (visual analogue scale (VAS), algometer) and blood analyses (interleukin-1, interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), C-reactive protein, myoglobin, creatine kinase) were assessed at 7 time points over 5 days (pre, post, 4, 24, 48, 72 and 96h after the downhill run). The placebo group demonstrated a significant decrease in squat jump performance immediately post the downhill run, with a mean change±95% confidence interval (CI) of 0.8cm (−3.53 to 1.93). The placebo group also experienced increased pain in the quadriceps 96h after the downhill run, with a mean VAS change±95% CI of −0.32cm (−0.34 to 0.98).The serum concentration of IL-6 and TNF-α were significantly lower in the placebo group 24h after the downhill run. Mean IL-6 change±95% CI of 0.50pg/mL (−1.59 to 0.59), and mean TNF-α change±95% CI was 0.98pg/mL (−2.04 to 0.09). No other significant differences were identified between the groups for any other outcome measure. Considering all data from this study, P. notoginseng did not convincingly have an effect on performance, muscular pain or assessed blood markers in well-trained males after an intense bout of eccentric exercise that induced DOMS.

It is plausible that multiple muscle biopsies following a muscle damaging intervention can exacerbate the inflammatory and subsequent satellite cell responses. To elucidate confounding effects of muscle biopsy procedure on satellite cell number, indirect markers of damage and the inflammatory response following acute downhill running (DHR) were investigated. 10 healthy male participant were divided into a non-exercising control ( n  = 4) and DHR (12 × 5min bouts, 10 % decline at 85 % VO 2 max) ( n  = 6) group. Blood samples were taken pre, post and every 24 h for 9 days. Serum was analysed for creatine kinase (CK), myoglobin (Mb), lactate dehydrogenase (LDH), TNF-α, IL-6 and IL-10. Muscle biopsies taken on days 1 and 2 post intervention from opposing legs were analysed for Pax7 + satellite cells. In the DHR group, Mb (536 ± 277 ng mL −1 ), IL-6 (12.6 ± 4.7 pg mL −1 ) and IL-10 (27.3 ± 11.5 pg mL −1 ) peaked immediately post DHR, while CK (2651 ± 1911 U L −1 ), LDH (202 ± 47 U L −1 ) and TNF-α (25.1 ± 8.7 pg mL −1 ) peaked on day 1. A 30 % increase in Pax7 + satellite cells on day 1 in the DHR group was no longer apparent on day 2. H&E staining show evidence of phagocytosis in the DHR group. No significant changes over time were observed in the control group for any of the variables measured. Events observed in the DHR group were as a result of the intervention protocol and subsequent muscle damage. The relationship between SC proliferation and pro-inflammatory cytokine release appears to be complex since the IL-6/IL-10 response time differs significantly from the TNF-α response.

Statins are widely used and lower the risk of death from cardiovascular causes. In a fraction of patients, an autoimmune myopathy may develop, characterized by the development of autoantibodies to the target enzyme, HMG-CoA reductase. Statins significantly reduce the incidence of cardiovascular disease, are generally safe, and have an acceptable side-effect profile. Indeed, a recent meta-analysis confirmed that mild musculoskeletal problems, such as myalgia, occur in approximately equal numbers of persons treated with statins and those given placebo. 1 Only in rare cases, in approximately 1 of 10,000 treated persons per year, 2 do statins cause serious muscle damage, with weakness and elevated levels of creatine kinase. In the majority of such cases, the patients recover spontaneously after the statin treatment is discontinued. 3 , 4 It is now recognized, however, that in very rare cases, an autoimmune myopathy . . .

The dynamic coordination of processes controlling the quality of the mitochondrial network is crucial to maintain the function of mitochondria in skeletal muscle. Changes of mitochondrial proteolytic system, dynamics (fusion/fission), and mitophagy induce pathways that affect muscle mass and performance. When muscle mass is lost, the risk of disease onset and premature death is dramatically increased. For instance, poor quality of muscles correlates with the onset progression of several age-related disorders such as diabetes, obesity, cancer, and aging sarcopenia. To date, there are no drug therapies to reverse muscle loss, and exercise remains the best approach to improve mitochondrial health and to slow atrophy in several diseases. This review will describe the principal mechanisms that control mitochondrial quality and the pathways that link mitochondrial dysfunction to muscle mass regulation.

Moderate, acute alcohol consumption after eccentric exercise has been shown to magnify the muscular weakness that is typically associated with exercise-induced muscle damage (EIMD). As it is not known whether this effect is dose-dependent, the aim of this study was to investigate the effect of a low dose of alcohol on EIMD-related losses in muscular performance. Ten healthy males performed 300 maximal eccentric contractions of the quadriceps muscles of one leg on an isokinetic dynamometer. They then consumed either a beverage containing 0.5 g of alcohol per kg bodyweight (as vodka and orange juice) or an isocaloric, isovolumetric non-alcoholic beverage. At least 2 weeks later, they performed an equivalent bout of eccentric exercise on the contralateral leg after which they consumed the other beverage. Measurement of peak and average peak isokinetic (concentric and eccentric) and isometric torque produced by the quadriceps was made before and 36 and 60 h post-exercise. Significant decreases in all measures of muscular performance were observed over time under both conditions (all P  < 0.05); however, no difference between treatments was evident at any of the measured time points (all P  > 0.05). Therefore, consumption of a low dose of alcohol after damaging exercise appears to have no effect on the loss of force associated with strenuous eccentric exercise.

This study investigated the hypothesis that muscle damage would be attenuated in muscles subjected to passive hyperthermia 1 day prior to exercise. Fifteen male students performed 24 maximal eccentric actions of the elbow flexors with one arm; the opposite arm performed the same exercise 2-4 weeks later. The elbow flexors of one arm received a microwave diathermy treatment that increased muscle temperature to over 40 degrees C, 16-20 h prior to the exercise. The contralateral arm acted as an untreated control. Maximal voluntary isometric contraction strength (MVC), range of motion (ROM), upper arm circumference, muscle soreness, plasma creatine kinase activity and myoglobin concentration were measured 1 day prior to exercise, immediately before and after exercise, and daily for 4 days following exercise. Changes in the criterion measures were compared between conditions (treatment vs. control) using a two-way repeated measures ANOVA with a significance level of P < 0.05. All measures changed significantly following exercise, but the treatment arm showed a significantly faster recovery of MVC, a smaller change in ROM, and less muscle soreness compared with the control arm. However, the protective effect conferred by the diathermy treatment was significantly less effective compared with that seen in the second bout performed 4-6 weeks after the initial bout by a subgroup of the subjects (n = 11) using the control arm. These results suggest that passive hyperthermia treatment 1 day prior to eccentric exercise-induced muscle damage has a prophylactic effect, but the effect is not as strong as the repeated bout effect.