Search

Intensive physical training may have a sport-dependent effect on bone mass acquisition. This cross-sectional study evaluated bone mass acquisition in girls practicing sports that put different mechanical loads on bone.Eighty girls from 10.7 to 18.0 years old (mean 13.83 ± 1.97) were recruited: 20 artistic gymnasts (AG; high-impact activity), 20 rhythmic gymnasts (RG; medium-impact activity), 20 swimmers (SW, no-impact activity), and 20 age-matched controls (CON; leisure physical activity3h/wk). Areal bone mineral density (aBMD) was determined using DEXA. Hip structural analysis applied at the femur evaluated cross-sectional area (CSA, cm(2)), section modulus (Z, cm(3)), and buckling ratio. Bone turnover markers and OPG/RANKL levels were analyzed.AG had higher aBMD than SW and CON at all bone sites and higher values than RG in the lumbar spine and radius. RG had higher aBMD than SW and CON only in the femoral region. CSA and mean cortical thickness were significantly higher and the buckling ratio was significantly lower in both gymnast groups compared with SW and CON. In RG only, endocortical diameter and width were reduced, while Z was only increased in AG compared with SW and CON. Reduced bone remodeling was observed in RG compared with AG only when groups were subdivided according to menarcheal status. All groups showed similar OPG concentrations, while RANKL concentrations increased with age and were decreased in SW.High-impact activity clearly had a favorable effect on aBMD and bone geometry during the growth period, although the bone health benefits seem to be more marked after menarche.

Background Obese patients are at risk for developing atelectasis and ARDS. Prone position (PP) may reduce atelectasis, and it improves oxygenation and outcome in severe hypoxemic patients with ARDS, but little is known about its effect in obese patients with ARDS. Methods Morbidly obese patients (BMI ≥ 35 kg/m 2 ) with ARDS (Pao 2 /Fio 2 ratio ≤ 200 mm Hg) were matched to nonobese (BMI 2 ) patients with ARDS in a case-control clinical study. The primary end points were safety and complications of PP; the secondary end points were the effect on oxygenation (Pao 2 /Fio 2 ratio at the end of PP), length of mechanical ventilation and ICU stay, nosocomial infections, and mortality. Results Between January 2005 and December 2009, 149 patients were admitted for ARDS. Thirty-three obese patients were matched with 33 nonobese patients. Median (25th-75th percentile) PP duration was 9 h (6-11 h) in obese patients and 8 h (7-12 h) in nonobese patients ( P = .28). We collected 51 complications: 25 in obese and 26 in nonobese patients. The number of patients with at least one complication was similar across groups (n = 10, 30%). Pao 2 /Fio 2 ratio increased significantly more in obese patients (from 118 ± 43 mm Hg to 222 ± 84 mm Hg) than in nonobese patients (from 113 ± 43 mm Hg to 174 ± 80 mm Hg; P = .03). Length of mechanical ventilation, ICU stay, and nosocomial infections did not differ significantly, but mortality at 90 days was significantly lower in obese patients (27% vs 48%, P Conclusions PP seems safe in obese patients and may improve oxygenation more than in nonobese patients. Obese patients could be a subgroup of patients with ARDS who may benefit the most of PP.

Objective: To characterize pulmonary hemodynamic changes in relation to lung injury at 2 time points [48 h (H48) and 168 h (H168)] after pneumonectomy under intraoperative protective ventilation in order to improve postpneumonectomy pulmonary edema (PPE) prevention. Method: Fifteen pigs (25 ± 1.9 kg) were randomly allocated to nonsurgical (control, n = 5) and surgical (H48 and H168) groups. A left pneumonectomy under volume-controlled one-lung ventilation (OLV) (low tidal volume, positive end-expiratory pressure = 4 cm H2O, inspired oxygen fraction = 50%) was performed in surgical animals. Mean pulmonary artery pressure (MPAP) and pulmonary artery occlusion pressure were recorded. Pulmonary vascular resistance (PVR) was calculated. Pulmonary damage score (PDS) and bronchoalveolar albumin level were evaluated. Data were collected after induction (T0), after OLV (T1), after left pneumonectomy (T2), and at H48 or H168 (T3). Results: Pneumonectomy caused precapillary pulmonary arterial hypertension (PAH) measured at T3 H48 (36.2 ± 3.67 mm Hg). PAH was delayed temporarily (both after OLV and after pneumonectomy) (p < 0.001), and linked with PVR (r = 0.93; p < 0.05). PDS and bronchoalveolar albumin level varied with MPAP (r = 0.76; p < 0.001 and r = 0.55; p < 0.05). Conclusion: Given that PAH is delayed and related to PVR increase, indicating secondary pulmonary vascular bed adaptation limits, pharmacological treatment should focus on a delayed failure in pulmonary capacitance in patients at risk of PPE.

Facioscapulohumeral muscular dystrophy (FSHD) is one of the most frequent hereditary muscle disorders. It is linked to contractions of the D4Z4 repeat array in 4q35. We have characterized the double homeobox 4 (DUX4) gene in D4Z4 and its mRNA transcribed from the distal D4Z4 unit to a polyadenylation signal in the flanking pLAM region. It encodes a transcription factor expressed in FSHD but not healthy muscle cells which initiates a gene deregulation cascade causing differentiation defects, muscle atrophy and oxidative stress. PITX1 was the first identified DUX4 target and encodes a transcription factor involved in muscle atrophy. DUX4 was found expressed in only 1/1000 FSHD myoblasts. We have now shown it was induced upon differentiation and detected in about 1/200 myotube nuclei. The DUX4 and PITX1 proteins presented staining gradients in consecutive myonuclei which suggested a diffusion as known for other muscle nuclear proteins. Both protein half-lifes were regulated by the ubiquitin-proteasome pathway. In addition, we could immunodetect the DUX4 protein in FSHD muscle extracts. As a model, we propose the DUX4 gene is stochastically activated in a small number of FSHD myonuclei. The resulting mRNAs are translated in the cytoplasm around an activated nucleus and the DUX4 proteins diffuse to adjacent nuclei where they activate target genes such as PITX1. The PITX1 protein can further diffuse to additional myonuclei and expand the transcriptional deregulation cascade initiated by DUX4. Together the diffusion and the deregulation cascade would explain how a rare protein could cause the muscle defects observed in FSHD.

International audience; Background: Although the benefits of comprehensive pulmonary rehabilitation have been demonstrated in patients with COPD, the effects of exercise sessions within self-management programs remain unclear. We hypothesized that 8 supervised exercise sessions incorporated in a 1-month self-management education program in COPD patients would be effective to improve health outcomes and to reduce direct medical costs after one year, compared to usual care. Methods: In this randomized controlled trial, 38 moderate-to-severe COPD patients were assigned either to an intervention group or to a usual care group. The hospital-based intervention program provided a combination of 8 sessions of supervised exercise with 8 self-management education sessions over a 1-month period. The primary end-point was the 6-min walking distance (6MWD), with secondary outcomes being health-related quality of life (HRQoL) e using the St. George’s Respiratory Questionnaire (SGRQ) and Nottingham Health Profile (NHP), maximal exercise capacity and healthcare utilization. Data were collected before and one year after the program.Results: After 12 months, we found statistically significant between-group differences in favor of the intervention group in 6MWD (þ50.5 m (95%CI, 2 to 99), in two domains of NHP (energy, 19.8 ( 38 to 1); emotional reaction, e10.4 ( 20 to 0)); in SGRQ-symptoms ( 14.0 ( 23 to 5)), and in cost of COPD medication ( 480.7 V (CI, 891 to 70) per patient per year).Conclusion: The present hospital-based intervention combining supervised exercise with self- management education provides significant improvements in patient’s exercise tolerance and HRQoL, and significant decrease of COPD medication costs, compared to usual care.

Background Neurally adjusted ventilatory assist (NAVA) is a new mode of mechanical ventilation that delivers ventilatory assist in proportion to the electrical activity of the diaphragm. This study aimed to compare the ventilatory and gas exchange effects between NAVA and pressure support ventilation (PSV) during the weaning phase of critically ill patients who required mechanical ventilation subsequent to surgery. Methods Fifteen patients, the majority of whom underwent abdominal surgery, were enrolled. They were ventilated with PSV and NAVA for 24 h each in a randomized crossover order. The ventilatory parameters and gas exchange effects produced by the two ventilation modes were compared. The variability of the ventilatory parameters was also evaluated by the coefficient of variation (SD to mean ratio). Results Two patients failed to shift to NAVA because of postoperative bilateral diaphragmatic paralysis, and one patient interrupted the study because of worsening of his sickness. In the other 12 cases, the 48 h of the study protocol were completed, using both ventilation modes, with no signs of intolerance or complications. The Pao2/Fio2 (mean ± SD) ratio in NAVA was significantly higher than with PSV (264 ± 71 vs. 230 ± 75 mmHg, P < 0.05). Paco2 did not differ significantly between the two modes. The tidal volume (median [interquartile range]) with NAVA was significantly lower than with PSV (7.0 [6.4-8.6] vs. 6.5 [6.3-7.4] ml/kg predicted body weight, P < 0.05).Variability of insufflation airway pressure, tidal volume, and minute ventilation were significantly higher with NAVA than with PSV. Electrical activity of the diaphragm variability was significantly lower with NAVA than with PSV. Conclusions Compared with PSV, respiratory parameter variability was greater with NAVA, probably leading in part to the significant improvement in patient oxygenation.

Patients with Duchenne muscular dystrophy (DMD) and mdx mice, devoid of dystrophin proteins, show altered ionic homeostasis. To clarify dystrophin's involvement in the central control of osmotic stimuli, we investigated the effect of the disruption of Dp71, the major form of dystrophin in the brain, on the hypothalamoneurohypophysis system (HNHS) osmoregulatory response. Dp71 and Dp140 are the principal DMD gene products in the supraoptic nucleus (SON) and neurohypophysis (NH). They are present in astrocyte and pituicyte end-feet, suggesting involvement in both intrinsic osmosensitivity of the SON and vasopressin (AVP) release from the NH. In Dp71-null mice, the cellular distribution of Dp140 was modified, this protein being detected on the membrane of magnocellular soma. The plasma osmolality of Dp71-null mice was lower than that of wild-type mice under normal conditions, and this difference was maintained after salt loading, indicating a change in the set point for osmoregulation in the absence of Dp71. The increase in AVP levels detected in the SON and NH of the wild-type was not observed in Dp71-null mice following salt loading, and the increase in AVP mRNA levels in the SON was smaller in Dp71-null than in wild-type mice. This suggests that Dp71 may be involved in the functional activity of the HNHS. Its astrocyte end-feet localization emphasizes the importance of neuronal–vascular–glial interactions for the central detection of osmolality. In the SON, Dp71 may be involved in osmosensitivity and definition of the “osmostat,” whereas, in the neurohypopohysis, it may be involved in fine-tuning AVP release. © 2009 Wiley-Liss, Inc.

International audience; Objective: To determined whether the implementation of an intubation management protocol leads to the reduction of intubation-related complications in the intensive care unit (ICU). Design: Two-phase, prospective, multicenter controlled study. Setting: Three medical-surgical ICUs in two university hospitals. Patients: Two hundred three consecutive ICU patients required 244 intubations. Interventions: All intubations performed during two consecutive phases (a 6-month quality control phase followed by a 6-month intervention phase based on the implementation of an ICU intubation bundle management protocol) were evaluated. The ten bundle components were: preoxygenation with noninvasive positive pressure ventilation , presence of two operators, rapid sequence induction, cricoid pressure, capnography, protective ventilation, fluid loading, preparation and early administration of sedation and vasopressor use if needed. Measurements and main results: The primary end points were the incidence of life-threatening complications occurring within 60 min after intubation (cardiac arrest or death, severe cardiovascular collapse and hypoxemia). Other complications (mild to moderate) were also evaluated. Baseline characteristics, including demographic data and reason for intubation (mainly acute respiratory failure), were similar in the two phases. The intubation procedure in the intervention phase (n = 121) was associated with significant decreases in both life-threatening complications (21 vs. 34%, p = 0.03) and other complications (9 vs. 21%, p = 0.01) compared to the control phase (n = 123). Conclusions: The implementation of an intubation management protocol can reduce immediate severe life-threatening complications associated with intubation of ICU patients.

Cross-sectional studies have demonstrated that physical activity can improve bone mass acquisition. However, this design is not adequate to describe the specific kinetics of bone mass gain during pubertal development.To compare the kinetics of bone mass acquisition in female adolescent athletes of sports that impose different mechanical loads and untrained controls throughout puberty.A total of 72 girls with ages ranging from 10.8 to 18.0 years were recruited: 24 rhythmic gymnasts (RG, impact activity group), 24 swimmers (SW, no-impact activity), and 24 age-matched controls (CON).Areal bone mineral density (aBMD) was determined using dual-energy x-ray absorptiometry and bone turnover markers were analyzed. All the investigations were performed at baseline and after 1 year.At baseline and after 1 year of follow-up, RG presented significantly greater aBMD adjusted for age, fat-free soft tissue, and fat mass compared with CON and SW, only at the femoral region. When aBMD variation throughout the pubertal period was modeled for each group from individual values, the aBMD at the femoral region was significantly higher in RG compared with the other 2 groups from 12.5 to 14 years, and this difference lasted up to 18 years. Moreover, the mean annual aBMD gain tended to be higher in RG compared with SW and CON only at the femoral region and this gain lasted longer in RG. Bone remodeling markers decreased similarly with age in the 3 groups.This study, which was based on linear mixed models for longitudinal data, demonstrated that the osteogenic effect of gymnastics is characterized by greater bone mass gain localized at mechanically loaded bone (ie, the proximal femur) principally around the menarcheal period. Moreover, the bone mass gain lasts longer in gymnasts, which may be explained by the delay in sexual maturation.

Background: Facioscapulohumeral muscular dystrophy (FSHD) is linked to deletions in 4q35 within the D4Z4 repeat array in which we identified the double homeobo x4( DUX4) gene. We found stable DUX4 mRNAs only derived from the most distal D4Z4 unit and unexpectedly extended to the flanking pLAM region that provided an intron and a polyadenylation signal. DUX4 encodes a transcription factor expressed in FSHD but not control primary myoblasts or muscle biopsies. The DUX4 protein initiates a large transcription deregulation cascade leading to muscle atrophy and oxidative stress, which are FSHD key features. Methodology/Principal Findings: We now show that transfection of myoblasts with a DUX4 expression vector leads to atrophic myotube formation associated with the induction of E3 ubiquitin ligases (MuRF1 and Atrogin1/MAFbx) typical of muscle atrophy. DUX4 induces expression of downstream targets deregulated in FSHD such as mu-crystallin and TP53. We developed specific siRNAs and antisense oligonucleotides (AOs) targeting the DUX4 mRNA. Addition of these antisense agents to primary FSHD myoblast cultures suppressed DUX4 protein expression and affected expression of the abovementioned markers. Conclusions/Significance: These results constitute a proof of concept for the development of therapeutic approaches for FSHD targeting DUX4 expression.

Background & Aims Beyond 5years, poorer survival, related to alcohol relapse, is observed in patients with liver transplant for alcohol-related liver disease (ALD). However, alcohol consumption has been significantly understudied in non-ALD transplant recipients. We aimed at analyzing the impact of alcohol consumption on long-term survival irrespective of the indication for transplantation. Methods This observational study included consecutive adult recipients of a primary liver graft between 1991 and 2007 in our hospital, who survived >6months. Patients without ALD as primary indication, but with a history of excessive alcohol consumption before transplantation, were classified as secondary indication ALD. We studied the impact on survival of excessive consumption of alcohol after transplantation and several other variables. Results The 441 patients had mean follow-up of 81.7months. Among the 281 patients with excessive alcohol consumption before transplantation, 206 had ALD as primary indication. After transplantation, alcohol consumption was reported by 32.3% of the study population, 43.7% in primary indication ALD, and 24.3% in non-ALD patients. Survival was 82% at 5years and 49% at 10years for patients with excessive alcohol relapse, compared with 86% and 75%, respectively, for patients without persistent excessive alcohol relapse. By multivariable analysis, the independent risk factors of death were: excessive alcohol relapse, age >51years, post-transplantation diabetes mellitus, cyclosporine-based immunosuppression, and non-hepatic cancer. Conclusions Excessive alcohol consumption has a negative impact on long-term survival after liver transplant, irrespective of the primary indication. Death is mainly due to recurrence of liver disease and non-hepatic cancer.

Background & Aims Gastrointestinal development requires regulated differentiation of visceral smooth muscle cells (SMCs) and their contractile activities; alterations in these processes might lead to gastrointestinal neuromuscular disorders. Gastrointestinal SMC development and remodeling involves post-transcriptional modification of messenger RNA. We investigated the function of the RNA-binding protein for multiple splicing 2 (RBPMS2) during normal development of visceral smooth muscle in chicken and expression of its transcript in human pathophysiological conditions. Methods We used avian replication-competent retroviral misexpression approaches to analyze the function of RBPMS2 in vivo and in primary cultures of chicken SMCs. We analyzed levels of RBPMS2 transcripts in colon samples from pediatric patients with Hirschsprung's disease and patients with chronic pseudo obstruction syndrome (CIPO) with megacystis. Results RBPMS2 was expressed strongly during the early stage of visceral SMC development and quickly down-regulated in differentiated and mature SMCs. Misexpression of RBPMS2 in differentiated visceral SMCs induced their dedifferentiation and reduced their contractility by up-regulating expression of Noggin , which reduced activity of bone morphogenetic protein. Visceral smooth muscles from pediatric patients with CIPO expressed high levels of RBPMS2 transcripts, compared with smooth muscle from patients without this disorder. Conclusions Expression of RBPMS2 is present in visceral SMC precursors. Sustained expression of RBPMS2 inhibits the expression of markers of SMC differentiation by inhibiting bone morphogenetic protein activity, and stimulates SMC proliferation. RBPMS2 transcripts are up-regulated in patients with CIPO; alterations in RBPMS2 function might be involved in digestive motility disorders, particularly those characterized by the presence of muscular lesions (visceral myopathies).

Objectives To study the ventilatory response during exercise in 8- to 10-year-old children born in 1998 to 2000 with a birthweight Study design We studied 19 VLBW children and 20 full-term children paired for age and sex. A physical activity questionnaire was administered. Lean body mass, spirometry, and maximal inspiratory pressure were assessed at rest. Gas exchange, breathing pattern, and the tension-time index of the inspiratory muscles, a noninvasive indicator of inspiratory muscle effort, were evaluated during a continuous incremental cycling protocol. Results VLBW children had lower weight, height, lean body mass, and maximal inspiratory pressure than control subjects. Their physical activity level was not different. During exercise, they had a higher respiratory rate and minute ventilation for the same metabolic level (VCO 2 /kg) and a higher tension-time index of the inspiratory muscles for the same exercise level (percentage of maximal oxygen consumption). Conclusions The lower inspiratory muscle strength observed in school-age VLBW children resulted in a higher inspiratory effort during incremental exercise. The rapid but not shallow breathing pattern adopted by this population during exercise may have been in response to their lower inspiratory muscle resistance to fatigue. VLBW children complaining of dyspnea should be investigated with exercise testing.

International audience; Rationale: Controlled mechanical ventilation (CMV) results in atrophy of the human diaphragm. The autophagy-lysosome pathway (ALP) contributes to skeletal muscle proteolysis, but its contribution to diaphragmatic protein degradation in mechanically ventilated patients is unknown.Objectives: To evaluate the autophagy pathway responses to CMV in the diaphragm and limb muscles of humans and to identify the roles of FOXO transcription factors in these responses.Methods: Muscle biopsies were obtained from nine control subjects and nine brain-dead organ donors. Subjects were mechanically ventilated for 2 to 4 hours and 15 to 276 hours, respectively. Activation of the ubiquitin-proteasome system was detected by measuring mRNA expressions of Atrogin-1, MURF1, and protein expressions of UBC2, UBC4, and the α subunits of the 20S proteasome (MCP231). Activation of the ALP was detected by electron microscopy and by measuring the expressions of several autophagy-related genes. Total carbonyl content and HNE-protein adduct formation were measured to assess oxidative stress. Total AKT, phosphorylated and total FOXO1, and FOXO3A protein levels were also measured.Measurements and Main Results: Prolonged CMV triggered activation of the ALP as measured by the appearance of autophagosomes in the diaphragm and increased expressions of autophagy-related genes, as compared with controls. Induction of autophagy was associated with increased protein oxidation and enhanced expression of the FOXO1 gene, but not the FOXO3A gene. CMV also triggered the inhibition of both AKT expression and FOXO1 phosphorylation.Conclusions: We propose that prolonged CMV causes diaphragm disuse, which, in turn, leads to activation of the ALP through oxidative stress and the induction of the FOXO1 transcription factor.

International audience; Background and Aims. Increasing environmental pollution may participate in the growing incidence of metabolic disorders. Static magnetic fields (SMFs) are an emerging environmental health issue due to increased exposure in residential and commercial areas; however, their metabolic effects in serum and skeletal muscle are largely unknown. The aim of this study was to investigate the effect of SMF exposure on glucose and lipid metabolism in serum and skeletal muscles of rats.Methods. Twelve 6-to 7-week-old male Wistar rats were randomly divided into two groups: rats exposed to 128 mT SMF and sham-exposed rats. This moderate-intensity exposure was performed for 1 h/day for 15 consecutive days.Results. Animals exposed to 128 mT SMF displayed significant changes in both glucose (i.e., increases in plasma glucose and lactate and decrease in plasma insulin levels) and lipid (i.e., increases in plasma glycerol, cholesterol and phospholipids but not triglyceride levels) metabolism. During intraperitoneal glucose tolerance tests, SMF-exposed rats displayed significantly higher hyperglycemia compared to sham-exposed rats despite similar insulin levels in both groups. In tissues, SMF exposure induced significant alterations in enzyme activities only in glycolytic muscles and caused a significant decrease in quadriceps and liver glycogen content together with increased phospholipid levels. Conclusions. This study provides evidence that subacute SMF exposure of moderate intensity induces important alterations of glucose and lipid metabolisms, which deserve further investigations to evaluate long-term consequences. Ó

Early and adequate treatment of ventilator-associated pneumonia (VAP) is mandatory to improve the outcome. The aim of this study was to evaluate, in medical ICU patients, the respective and combined impact of the Clinical Pulmonary Infection Score (CPIS), broncho-alveolar lavage (BAL) gram staining, endotracheal aspirate and a biomarker (procalcitonin) for the early diagnosis of VAP.Prospective, observational studyA medical intensive care unit in a teaching hospital.Over an 8-month period, we prospectively included 57 patients suspected of having 86 episodes of VAP.The day of suspicion, a BAL as well as alveolar and serum procalcitonin determinations and evaluation of CPIS were performed.Of 86 BAL performed, 48 were considered positive (cutoff of 10(4) cfu ml(-1)). We found no differences in alveolar or serum procalcitonin between VAP and non-VAP patients. Including procalcitonin in the CPIS score did not increase its accuracy (55%) for the diagnosis of VAP. The best tests to predict VAP were modified CPIS (threshold at 6) combined with microbiological data. Indeed, both routinely twice weekly performed endotracheal aspiration at a threshold of 10(5) cfu ml(-1) and BAL gram staining improved pre-test diagnostic accuracy of VAP (77 and 66%, respectively).This study showed that alveolar procalcitonin performed by BAL does not help the clinician to identify VAP. It confirmed that serum procalcitonin is not an accurate marker of VAP. In contrast, microbiological resources available at the time of VAP suspicion (BAL gram staining, last available endotracheal aspirate) combined or not with CPIS are helpful in distinguishing VAP diagnosed by BAL from patients with a negative BAL.

Airway management is a commonly performed procedure in the intensive care unit (ICU). Hypoxemia and cardiovascular collapse represent the initial and most serious life-threatening complications associated with difficult airway access, both in emergency intubation in the critically ill [1–4] and in planned intubations (e. g., scheduled surgery or invasive procedures) [5]. To prevent and limit the incidence of life-threatening complications following intubation, several pre-oxygenation techniques and intubation algorithms have been entertained.

The biological mechanisms responsible for the decline in skeletal muscle mass during aging remain unknown. It is hypothesized that elevations in the level of the acute phase C-reactive protein (CRP) negatively affect skeletal muscle mass in elderly. We examined the relationship between serum CRP and muscle mass in a population of active elderly women (65–70 years; n =23). Though all subjects were physically active, serum CRP levels were negatively associated to the amount of time spent in moderate-to-vigorous physical activity (R 2 = 0.20, P = 0.032) and to skeletal muscle mass (R 2 = 0.28, P = 0.009). We further aimed to determine the potential mechanisms behind the action of systemic inflammation on skeletal muscle by exposing myoblasts isolated from vastus lateralis to the different sera from each elderly woman. The doubling time (DT) of myoblasts increased when cells were exposed to sera with high CRP levels (R 2 = 0.27, P = 0.011), indicating that CRP contributes to the impairment of the proliferative rate of myoblasts in elderly. In order to further confirm our findings, we incubated human myoblasts in exogenous CRP. Exposition to exogenous CRP induced an increase in myoblast DT by 1.21-fold (P = 0.007) and a reduction in the expression of the proliferation marker ki-67 confirming the negative influence of CRP on myoblast proliferative rate. Collectively, these findings highlight the contribution of the systemic inflammatory status in the age-related decline in skeletal muscle function.