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Abstract Rationale Exacerbations of chronic obstructive pulmonary disease (COPD) acutely reduce skeletal muscle strength and result in long-term loss of functional capacity. Objectives To investigate whether resistance training is feasible and safe and can prevent deteriorating muscle function during exacerbations of COPD. Methods Forty patients (FEV1 49 ± 17% predicted) hospitalized with a severe COPD exacerbation were randomized to receive usual care or an additional resistance training program during the hospital admission. Patients were followed up for 1 month after discharge. Primary outcomes were quadriceps force and systemic inflammation. A muscle biopsy was taken in a subgroup of patients to assess anabolic and catabolic pathways. Measurements and Main Results Resistance training did not yield higher systemic inflammation as indicated by C-reactive protein levels and could be completed uneventfully. Enhanced quadriceps force was seen at discharge (+9.7 ± 16% in the training group; −1 ± 13% in control subjects; P = 0.05) and at 1 month follow-up in the patients who trained. The 6-minute walking distance improved after discharge only in the group who received resistance training (median 34; interquartile range, 14–61 m; P = 0.002). In a subgroup of patients a muscle biopsy showed a more anabolic status of skeletal muscle in patients who followed training. Myostatin was lower (P = 0.03) and the myogenin/MyoD ratio tended to be higher (P = 0.08) in the training group compared with control subjects. Conclusions Resistance training is safe, successfully counteracts skeletal muscle dysfunction during acute exacerbations of COPD, and may up-regulate the anabolic milieu in the skeletal muscle. Clinical trial registered with www.clinicaltrials.gov (NCT00877084).

Background: Short successive periods of physical inactivity occur throughout life and contribute considerably to the age-related loss of skeletal muscle mass. The maintenance of muscle mass during brief periods of disuse is required to prevent functional decline and maintain metabolic health. Objective: To assess whether daily leucine supplementation during a short period of disuse can attenuate subsequent muscle loss in vivo in humans. Methods: Thirty healthy (22 ± 1 y) young males were exposed to a 7-day unilateral knee immobilization intervention by means of a full leg cast with (LEU, n = 15) or without (CON, n = 15) daily leucine supplementation (2.5 g leucine, three times daily). Prior to and directly after immobilization, quadriceps muscle cross-sectional area (computed tomography (CT) scan) and leg strength (one-repetition maximum (1-RM)) were assessed. Furthermore, muscle biopsies were taken in both groups before and after immobilization to assess changes in type I and type II muscle fiber CSA. Results: Quadriceps muscle cross-sectional area (CSA) declined in the CON and LEU groups (p < 0.01), with no differences between the two groups (from 7712 ± 324 to 7287 ± 305 mm2 and from 7643 ± 317 to 7164 ± 328 mm2; p = 0.61, respectively). Leg muscle strength decreased from 56 ± 4 to 53 ± 4 kg in the CON group and from 63 ± 3 to 55 ± 2 kg in the LEU group (main effect of time p < 0.01), with no differences between the groups (p = 0.052). Type I and II muscle fiber size did not change significantly over time, in both groups (p > 0.05). Conclusions: Free leucine supplementation with each of the three main meals (7.5 g/d) does not attenuate the decline of muscle mass and strength during a 7-day limb immobilization intervention.

To examine whether combined testosterone replacement and exercise training (ET) therapies would potentiate the beneficial effects of isolated therapies on neurovascular control and muscle wasting in patients with heart failure (HF) with testosterone deficiency. From January 10, 2010, through July 25, 2013, 39 male patients with HF, New York Heart Association functional class III, total testosterone level less than 249 ng/dL (to convert to nmol/L, multiply by .03467), and free testosterone level less than 131 pmol/L were randomized to training (4-month cycloergometer training), testosterone (intramuscular injection of testosterone undecylate for 4 months), and training + testosterone groups. Muscle sympathetic nerve activity was measured using microneurography, forearm blood flow using plethysmography, body composition using dual X-ray absorptiometry, and functional capacity using cardiopulmonary test. Skeletal muscle biopsy was performed in the vastus lateralis. Muscle sympathetic nerve activity decreased in ET groups (training, P<.01; training + testosterone, P<.01), whereas no changes were observed in the testosterone group (P=.89). Forearm blood flow was similar in all groups. Lean mass increased in ET groups (training, P<.01; training + testosterone, P<.01), whereas lean mass decreased in the testosterone group (P<.01). The response of cross-sectional area of type I (P<.01) and type II (P<.05) fibers increased in the training + testosterone group as compared with the isolated testosterone group. Our findings provide evidence for a superior effect of combined ET and testosterone replacement therapies on muscle sympathetic nerve activity, muscle wasting, and functional capacity in patients with HF with testosterone deficiency.

Purpose Recent data suggest diminished post-operative quadriceps muscle strength after tourniquet application during total knee arthroplasty (TKA). The metabolic effects of the commonly utilized intraoperative tourniquet with consecutive ischaemia on the skeletal muscle cells were unknown. Ubiquitin proteasome system represents one of the main pathways involved in muscle protein breakdown contributing to muscle atrophy. Therefore, the purpose of the present study was to quantify the acute effects of the tourniquet application during TKA on the (1) concentrations of free/conjugated ubiquitin, (2) total ubiquitin-protein ligase activity, (3) proteasome-dependent and (4) proteasome-independent peptidase activities in the cells of vastus medialis. Methods The randomized, controlled, monocentric trial included 34 patients scheduled to undergo primary TKA. Each patient was randomly assigned to the tourniquet ( n  = 17) or non-tourniquet group ( n  = 17) after receiving a written consent. Muscle biopsies of (5 × 5 × 5 mm) 125 mm 3 were obtained from vastus medialis immediately after performing the surgical approach and exactly 60 min later. After preparation of the muscle tissue specimen, the concentrations of the free/conjugated ubiquitin (Ub) were measured by western blot analyses. The ubiquitination was determined as biotinylated Ub incorporated into the sum of the cytosolic proteins and expressed as total ubiquitin-protein ligase activity (tUbPL). The quantification of the proteasome-dependent and proteasome-independent peptidase activities was performed with peptidase assays. Results Tourniquet application did not influence the concentration of the free/conjugated Ub. There were no differences in tUbPL activities between groups and time points. Tourniquet-induced ischaemia resulted in statistically significant higher proteasome-dependent (caspase-like p  = 0.0034; chymotryptic-like p  = 0.0013; tryptic-like p  = 0.0036) and proteasome-independent (caspase-like p  = 0.03; chymotryptic-like p  = 0.0001; tryptic-like p  = 0.0062) peptidase activities. Conclusion Tourniquet application did not affect the free/conjugated Ub as well as tUbPL significantly, emphasizing the sophisticated regulation of ubiquitination. The proteasome-dependent peptidase activities were significantly upregulated during tourniquet application, suggesting an increase in protein degradation, which in turn might explain the skeletal muscle atrophy occurring after TKA. These findings add further knowledge and should raise the awareness of surgeons about the effects of tourniquet-induced ischaemia at the molecular level. Additional high-quality research may be warranted to examine the short- and long-term clinical significance of the present data. Level of evidence I.

The authors previously reported that focused eccentric resistance training during the first 15 weeks following anterior cruciate ligament reconstruction (ACL-R) induced greater short-term increases in muscle volume, strength, and measures of function relative to standard rehabilitation. The purpose of this study was to evaluate the effects of early progressive eccentric exercise on muscle volume and function at 1 year after ACL-R. Forty patients who had undergone an ACL-R were randomly assigned to 1 of 2 groups: a group that received early progressive eccentric exercise (n=20) and a group that received standard rehabilitation (n=20). Seventeen participants in the eccentric exercise group and 15 participants in the standard rehabilitation group completed a 1-year follow-up. Magnetic resonance images of the thighs were acquired 1 year after ACL-R and compared with images acquired 3 weeks after surgery. Likewise, routine knee examinations, self-report assessments, and strength and functional testing were completed 1 year after surgery and compared with previous evaluations. A 2-factor analysis of variance for repeated measures (group x time) was used to analyze the data. Compared with the standard rehabilitation group, improvements in quadriceps femoris and gluteus maximus muscle volume in the involved lower extremity from 3 weeks to 1 year following ACL-R were significantly greater in the eccentric exercise group. Improvements in quadriceps femoris and gluteus maximus muscle volume were 23.3% (SD=14.1%) and 20.6% (SD=12.9%), respectively, in the eccentric exercise group and 13.4% (SD=10.3%) and 11.6% (SD=10.4%), respectively, in the standard rehabilitation group. Improvements in quadriceps femoris muscle strength and hopping distance also were significantly greater in the eccentric exercise group 1 year postsurgery. A 12-week focused eccentric resistance training program, implemented 3 weeks after ACL-R, resulted in greater increases in quadriceps femoris and gluteus maximus muscle volume and function compared with standard rehabilitation at 1 year following ACL-R.

Persistent muscle weakness after anterior cruciate ligament (ACL) reconstruction may be due to underlying activation failure and arthrogenic muscle inhibition (AMI). Knee-joint cryotherapy has been shown to improve quadriceps function transiently in those with AMI, thereby providing an opportunity to improve quadriceps muscle activation and strength in patients with a reconstructed ACL. To compare quadriceps muscle function in patients with a reconstructed ACL who completed a 2-week intervention including daily cryotherapy (ice bag), daily exercises, or both. Cross-sectional study. Laboratory. A total of 30 patients with reconstructed ACLs who were at least 6 months post-index surgery and had measurable quadriceps AMI. The patients attended 4 supervised visits over a 2-week period. They were randomly assigned to receive 20 minutes of knee-joint cryotherapy, 1 hour of therapeutic rehabilitation exercises, or cryotherapy followed by exercises. We measured quadriceps Hoffmann reflex, normalized maximal voluntary isometric contraction torque, central activation ratio using the superimposed-burst technique, and patient-reported outcomes before and after the intervention period. After the 2-week intervention period, patients who performed rehabilitation exercises immediately after cryotherapy had higher normalized maximal voluntary isometric contraction torques (P = .002, Cohen d effect size = 1.4) compared with those who received cryotherapy alone (P = .16, d = 0.58) or performed exercise alone (P = .16, d = 0.30). After ACL reconstruction, patients with AMI who performed rehabilitation exercises immediately after cryotherapy experienced greater strength gains than those who performed cryotherapy or exercises alone.

Background Muscle satellite cells (SCs) are crucial for muscle regeneration following muscle trauma. Acute skeletal muscle damage results in inflammation and the production of reactive oxygen species (ROS) which may be implicated in SCs activation. Protection of these cells from oxidative damage is essential to ensure sufficient muscle regeneration. The aim of this study is to determine whether SCs activity under conditions of aseptic skeletal muscle trauma induced by exercise is redox-dependent. Methods/design Based on the SCs content in their vastus lateralis skeletal muscle, participants will be classified as either high or low respondents. In a randomized, double-blind, crossover, repeated-measures design, participants will then receive either placebo or N -acetylcysteine (alters redox potential in muscle) during a preliminary 7-day loading phase, and for eight consecutive days following a single bout of intense muscle-damaging exercise. In both trials, blood samples and muscle biopsies will be collected, and muscle performance and soreness will be measured at baseline, pre-exercise, 2 and 8 days post exercise. Biological samples will be analyzed for redox status and SCs activity. Between trials, a 4-week washout period will be implemented. Discussion This study is designed to investigate the impact of redox status on SCs mobilization and thus skeletal muscle potential for regeneration under conditions of aseptic inflammation induced by exercise. Findings of this trial should provide insight into (1) molecular pathways involved in SCs recruitment and muscle healing under conditions of aseptic skeletal muscle trauma present in numerous catabolic conditions and (2) whether skeletal muscle’s potential for regeneration depends on its basal SCs content. Trial registration ClinicalTrials.gov, ID: NCT03711838 . Registered on 19 Oct 2018.

Background Chronic Obstructive Pulmonary Disease (COPD) has significant systemic effects beyond the lungs amongst which muscle wasting is a prominent contributor to exercise limitation and an independent predictor of morbidity and mortality. The molecular mechanisms leading to skeletal muscle dysfunction/wasting are not fully understood and are likely to be multi-factorial. The need to develop therapeutic strategies aimed at improving skeletal muscle dysfunction/wasting requires a better understanding of the molecular mechanisms responsible for these abnormalities. Microarrays are powerful tools that allow the investigation of the expression of thousands of genes, virtually the whole genome, simultaneously. We aim at identifying genes and molecular pathways involved in skeletal muscle wasting in COPD. Methods We assessed and compared the vastus lateralis transcriptome of COPD patients with low fat free mass index (FFMI) as a surrogate of muscle mass (COPD L ) (FEV 1 30 ± 3.6%pred, FFMI 15 ± 0.2 Kg.m −2 ) with patients with COPD and normal FFMI (COPD N ) (FEV 1 44 ± 5.8%pred, FFMI 19 ± 0.5 Kg.m −2 ) and a group of age and sex matched healthy controls (C) (FEV 1 95 ± 3.9%pred, FFMI 20 ± 0.8 Kg.m −2 ) using Agilent Human Whole Genome 4x44K microarrays. The altered expression of several of these genes was confirmed by real time TaqMan PCR. Protein levels of P21 were assessed by immunoblotting. Results A subset of 42 genes was differentially expressed in COPD L in comparison to both COPD N and C (PFP < 0.05; −1.5 ≥ FC ≥ 1.5). The altered expression of several of these genes was confirmed by real time TaqMan PCR and correlated with different functional and structural muscle parameters. Five of these genes (CDKN1A, GADD45A, PMP22, BEX2, CGREF1, CYR61), were associated with cell cycle arrest and growth regulation and had been previously identified in studies relating muscle wasting and ageing. Protein levels of CDKN1A, a recognized marker of premature ageing/cell cycle arrest, were also found to be increased in COPD L . Conclusions This study provides evidence of differentially expressed genes in peripheral muscle in COPD patients corresponding to relevant biological processes associated with skeletal muscle wasting and provides potential targets for future therapeutic interventions to prevent loss of muscle function and mass in COPD.

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.

This study examined the effect of resistance exercise on the production, recruitment, percentage, and adhesion characteristics of granulocytes with and without polyphenol (PPB) supplementation. Thirty‐eight untrained men were randomized into three groups: PPB (n = 13, 21.8 ± 2.5 years, 171.2 ± 5.5 cm, 71.2 ± 8.2 kg), placebo (PL; n = 15, 21.6 ± 2.5 years, 176.5 ± 4.9 cm, 84.0 ± 15.7 kg), or control (CON; n = 10, 23.3 ± 4.3 years, 173.7 ± 12.6 cm, 77.3 ± 16.3 kg). Blood samples were obtained pre (PRE), immediately (IP), 1 h (1H), 5 h (5H), 24 h (24H), 48 h (48H), and 96 h (96H) postresistance exercise (PPB/PL) or rest (CON). Fine‐needle biopsies were obtained from the vastus lateralis at PRE, 1H, 5H, and 48H. Plasma concentrations and intramuscular content of interleukin‐8 (IL‐8), granulocyte (G‐CSF), and granulocyte–macrophage colony stimulating factor (GM‐CSF) were analyzed via multiplex assays. Changes in relative number of circulating granulocytes and adhesion receptor (CD11b) were assessed using flow cytometry. Intramuscular IL‐8 was significantly elevated at 1H, 5H, and 48H (P < 0.001). Area under the curve analysis indicated a greater intramuscular IL‐8 content in PL than PPB (P = 0.011). Across groups, circulating G‐CSF was elevated from PRE at IP (P < 0.001), 1H (P = 0.011), and 5H (P = 0.025), while GM‐CSF was elevated at IP (P < 0.001) and 1H (P = 0.007). Relative number of granulocytes was elevated at 1H (P < 0.001), 5H (P < 0.001), and 24H (P = 0.005, P = 0.006) in PPB and PL, respectively. Across groups, granulocyte CD11b expression was upregulated from PRE to IP (P < 0.001) and 1H (P = 0.015). Results indicated an increase in circulating CD11b on granulocytes, and IL‐8 within the muscle following intense resistance exercise. Polyphenol supplementation may attenuate the IL‐8 response, however, did not affect granulocyte percentage and adhesion molecule expression in peripheral blood following resistance exercise. Resistance exercise elicits an increase in intramuscular IL‐8 content. Chronic polyphenol supplementation, however, appears to blunt this increase in IL‐8 content.