Laboratoire Mouvement Sport Santé

According to the demographic evolution in industrialized countries, more and more elderly people will experience falls at home and will require emergency services. The main problem comes from fall-prone elderly living alone at home. To resolve this lack of safety, we propose a new method to detect falls at home, based on a multiple-cameras network for reconstructing the 3-D shape of people. Fall events are detected by analyzing the volume distribution along the vertical axis, and an alarm is triggered when the major part of this distribution is abnormally near the floor during a predefined period of time, which implies that a person has fallen on the floor. This method was validated with videos of a healthy subject who performed 24 realistic scenarios showing 22 fall events and 24 cofounding events (11 crouching position, 9 sitting position, and 4 lying on a sofa position) under several camera configurations, and achieved 99.7% sensitivity and specificity or better with four cameras or more. A real-time implementation using a graphic processing unit (GPU) reached 10 frames per second (fps) with 8 cameras, and 16 fps with 3 cameras.

Evaluating potential musculoskeletal disorders risks in real workstations is challenging as the environment is cluttered, which makes it difficult to accurately assess workers' postures. Being marker-free and calibration-free, Microsoft Kinect is a promising device although it may be sensitive to occlusions. We propose and evaluate a RULA ergonomic assessment in real work conditions using recently published occlusion-resistant Kinect skeleton data correction. First, we compared postures estimated with this method to ground-truth data, in standardized laboratory conditions. Second, we compared RULA scores to those provided by two professional experts, in a non-laboratory cluttered workplace condition. The results show that the corrected Kinect data can provide more accurate RULA grand scores, even under sub-optimal conditions induced by the workplace environment. This study opens new perspectives in musculoskeletal risk assessment as it provides the ergonomists with 30 Hz continuous information that could be analyzed offline and in a real-time framework.

Gut microbiota is involved in the development of several chronic diseases, including diabetes, obesity, and cancer, through its interactions with the host organs. It has been suggested that the cross talk between gut microbiota and skeletal muscle plays a role in different pathological conditions, such as intestinal chronic inflammation and cachexia. However, it remains unclear whether gut microbiota directly influences skeletal muscle function. In this work, we studied the impact of gut microbiota modulation on mice skeletal muscle function and investigated the underlying mechanisms. We determined the consequences of gut microbiota depletion after treatment with a mixture of a broad spectrum of antibiotics for 21 days and after 10 days of natural reseeding. We found that, in gut microbiota-depleted mice, running endurance was decreased, as well as the extensor digitorum longus muscle fatigue index in an ex vivo contractile test. Importantly, the muscle endurance capacity was efficiently normalized by natural reseeding. These endurance changes were not related to variation in muscle mass, fiber typology, or mitochondrial function. However, several pertinent glucose metabolism markers, such as ileum gene expression of short fatty acid chain and glucose transporters G protein-coupled receptor 41 and sodium-glucose cotransporter 1 and muscle glycogen level, paralleled the muscle endurance changes observed after treatment with antibiotics for 21 days and reseeding. Because glycogen is a key energetic substrate for prolonged exercise, modulating its muscle availability via gut microbiota represents one potent mechanism that can contribute to the gut microbiota-skeletal muscle axis. Taken together, our results strongly support the hypothesis that gut bacteria are required for host optimal skeletal muscle function.

Improving performance in sports can be difficult because many biomechanical, physiological, and psychological factors come into play during competition. A better understanding of the perception-action loop employed by athletes is necessary. This requires isolating contributing factors to determine their role in player performance. Because of its inherent limitations, video playback doesn't permit such in-depth analysis. Interactive, immersive virtual reality (VR) can overcome these limitations and foster a better understanding of sports performance from a behavioral-neuroscience perspective. Two case studies using VR technology and a sophisticated animation engine demonstrate how to use information from visual displays to inform a player's future course of action.

Skeletal muscle shows high plasticity in response to external demand. Moreover, adult skeletal muscle is capable of complete regeneration after injury, due to the properties of muscle stem cells (MuSCs), the satellite cells, which follow a tightly regulated myogenic program to generate both new myofibers and new MuSCs for further needs. Although reactive oxygen species (ROS) and reactive nitrogen species (RNS) have long been associated with skeletal muscle physiology, their implication in the cell and molecular processes at work during muscle regeneration is more recent. This review focuses on redox regulation during skeletal muscle regeneration. An overview of the basics of ROS/RNS and antioxidant chemistry and biology occurring in skeletal muscle is first provided. Then, the comprehensive knowledge on redox regulation of MuSCs and their surrounding cell partners (macrophages, endothelial cells) during skeletal muscle regeneration is presented in normal muscle and in specific physiological (exercise-induced muscle damage, aging) and pathological (muscular dystrophies) contexts. Recent advances in the comprehension of these processes has led to the development of therapeutic assays using antioxidant supplementation, which result in inconsistent efficiency, underlying the need for new tools that are aimed at precisely deciphering and targeting ROS networks. This review should provide an overall insight of the redox regulation of skeletal muscle regeneration while highlighting the limits of the use of nonspecific antioxidants to improve muscle function. Antioxid. Redox Signal. 27, 276-310.

The large doses of vitamins C and E and β-carotene used to reduce reactive oxygen species (ROS) production and oxidative damages in cancerous tissue have produced disappointing and contradictory results. This therapeutic conundrum was attributed to the double-faced role of ROS, notably, their ability to induce either proliferation or apoptosis of cancer cells. However, for a ROS-inhibitory approach to be effective, it must target ROS when they induce proliferation rather than apoptosis. On the basis of recent advances in redox biology, this review underlined a differential regulation of prooxidant and antioxidant system, respective to the stage of cancer. At early precancerous and neoplastic stages, antioxidant activity decreases and ROS appear to promote cancer initiation via inducing oxidative damage and base pair substitution mutations in prooncogenes and tumor suppressor genes, such as RAS and TP53, respectively. Whereas in late stages of cancer progression, tumor cells escape apoptosis by producing high levels of intracellular antioxidants, like NADPH and GSH, via the pentose phosphate pathway to buffer the excessive production of ROS and related intratumor oxidative injuries. Therefore, antioxidants should be prohibited in patients with advanced stages of cancer and/or undergoing anticancer therapies. Interestingly, the biochemical and biophysical properties of some polyphenols allow them to selectively recognize tumor cells. This characteristic was exploited to design and deliver nanoparticles coated with low doses of polyphenols and containing chemotherapeutic drugs into tumor-bearing animals. First results are encouraging, which may revolutionize the conventional use of antioxidants in cancer.

Although coordinated patterns of body movement can be used to communicate action intention, they can also be used to deceive. Often known as deceptive movements, these unpredictable patterns of body movement can give a competitive advantage to an attacker when trying to outwit a defender. In this particular study, we immersed novice and expert rugby players in an interactive virtual rugby environment to understand how the dynamics of deceptive body movement influence a defending player's decisions about how and when to act. When asked to judge final running direction, expert players who were found to tune into prospective tau-based information specified in the dynamics of 'honest' movement signals (Centre of Mass), performed significantly better than novices who tuned into the dynamics of 'deceptive' movement signals (upper trunk yaw and out-foot placement) (p<.001). These findings were further corroborated in a second experiment where players were able to move as if to intercept or 'tackle' the virtual attacker. An analysis of action responses showed that experts waited significantly longer before initiating movement (p<.001). By waiting longer and picking up more information that would inform about future running direction these experts made significantly fewer errors (p<.05). In this paper we not only present a mathematical model that describes how deception in body-based movement is detected, but we also show how perceptual expertise is manifested in action expertise. We conclude that being able to tune into the 'honest' information specifying true running action intention gives a strong competitive advantage.

The aim of this study was to compare the effects of 12 weeks of high-intensity interval training (HIIT) with the effects of 12 weeks of plyometric exercise combined with HIIT (P+HIIT) on anthropometric, biochemical, and physical fitness data in young obese females. Sixty-eight participants (age, 16.6 ± 1.3 y; body mass, 82.8 ± 5.0 kg; body fat, 39.4% ± 3.3%; body mass index z score, 2.9 ± 0.4) were assigned to 1 of 3 groups: HIIT (2 blocks per session of 6-8 bouts of 30-s runs at 100% velocity at peak oxygen uptake, with 30-s active recovery between bouts at 50%velocity at peak oxygen uptake (n = 23)); P+HIIT (2 blocks per session of 3 different 15-s plyometric exercises with 15-s passive recoveries, totaling 2 min for each plyometric exercise + the same HIIT program (n = 26)); or control (no exercise (n = 19)). Anthropometric (body mass, body mass index z score, body fat, lean body mass, and waist circumference), biochemical (plasma glucose, insulin, leptin and adiponectin concentrations, leptin/adiponectin ratio, and homeostasis model assessment of insulin resistance (HOMA-IR)), physical fitness (peak oxygen uptake, velocity at peak oxygen uptake, squat jump, and countermovement jump performances), and energy intake data were collected. Both training programs improved the anthropometric, biochemical, and physical fitness variables. However, the P+HIIT program induced greater improvements than did the HIIT program in lean body mass (+3.0% ± 1.7%), plasma glucose and leptin concentrations (-11.0% ± 4.7% and -23.8% ± 5.8%, respectively), plasma leptin/adiponectin ratio (-40.9% ± 10.9%), HOMA-IR (-37.3% ± 6.2%), and squat jump performance (22.2% ± 7.5%). Taken together, these findings suggest that adding plyometric exercises to a HIIT program may be more beneficial than HIIT alone in obese female adolescents.

Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in rats, and its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinase, and the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, the Muscle atrophy F-Box (MAFbx; also known as atrogin-1) and Muscle RING (Really Interesting New Gene) Finger-1 (MuRF-1). We found that hindlimb unloading induced a significant increase in XO activity and in the protein expression of the antioxidant enzymes CuZnSOD and Catalase in skeletal muscle. The most relevant new fact reported in this paper is that inhibition of XO with allopurinol, a drug widely used in clinical practice, prevents soleus muscle atrophy by ~20% after hindlimb unloading. This was associated with the inhibition of the p38 MAPK-MAFbx pathway. Our data suggest that XO was involved in the loss of muscle mass via the activation of the p38MAPK-MAFbx pathway in unloaded muscle atrophy. Thus, allopurinol may have clinical benefits to combat skeletal muscle atrophy in bedridden, astronauts, sarcopenic, and cachexic patients.

OBJECTIVE: The purpose of this study was to determine the relationship between athletic performance and the change in body weight (BW) during a 42 km marathon in a large cohort of runners. METHODS: The study took place during the 2009 Mont Saint-Michel Marathon (France). 643 marathon finishers (560 males and 83 females) were studied. The change in BW during the race was calculated from measurements of each runner's BW immediately before and after the race. RESULTS: BW loss was 2.3 ± 2.2% (mean±SEM) (p<0.01). BW loss was -3.1 ± 1.9% for runners finishing the marathon in less than 3 h; -2.5 ± 2.1% for runners finishing between 3 and 4 h; and -1.8 ± 2.4% for runners who required more than 4 h to complete the marathon. The degree of BW loss was linearly related to 42 km race finishing time (p<0.0000001). Neither age nor gender influenced BW loss during the race. CONCLUSIONS: BW loss during the marathon was inversely related to race finishing time in 643 marathon runners and was >3% in runners completing the race in less than 3 h. These data are not compatible with laboratory-derived data suggesting that BW loss greater than 2% during exercise impairs athletic performance. They match an extensive body of evidence showing that the most successful athletes in marathon and ultra-marathon running and triathlon events are frequently those who lose substantially more than 3-4% BW during competition.

Epidemiological data indicate that physical inactivity, a main factor of global energetic imbalance, is involved in the worldwide epidemic of obesity and metabolic disorders such as insulin resistance. Although the complex pathogenesis of insulin resistance is not fully understood, literature data accumulated during the past decades clearly indicate that the activation of the oxidative-inflammatory loop plays a major role. By activating the oxidative-inflammatory loop in insulin-sensitive tissues, fat gain and adipose tissue dysfunction likely contribute to induce insulin resistance during chronic and prolonged physical inactivity. However, in the past years, evidence has emerged showing that early insulin resistance also occurs after very short-term exposure to physical inactivity (1-7 days) without any fat gain or energetic imbalance. The possible role of liver disturbances or endothelial dysfunction is suggested, but further studies are necessary to really conclude. Inactive skeletal muscle probably constitutes the primary triggering tissue for the development of early insulin resistance. In the present review, we discuss on the current knowledge about the effect of physical inactivity on whole-body and peripheral insulin sensitivity, and how local inflammation and oxidative stress arising with physical inactivity could potentially induce insulin resistance. We assume that early muscle insulin resistance allows the excess nutrients to shift in the storage tissues to withstand starvation through energy storage. We also consider when chronic and prolonged, physical inactivity over an extended period of time is an underestimated contributor to pathological insulin resistance and hence indirectly to numerous chronic diseases.

Analyzing human poses with a Kinect is a promising method to evaluate potentials risks of musculoskeletal disorders at workstations. In ecological situations, complex 3D poses and constraints imposed by the environment make it difficult to obtain reliable kinematic information. Thus, being able to predict the potential accuracy of the measurement for such complex 3D poses and sensor placements is challenging in classical experimental setups. To tackle this problem, we propose a new evaluation method based on a virtual mannequin. In this study, we apply this method to the evaluation of joint positions (shoulder, elbow, and wrist), joint angles (shoulder and elbow), and the corresponding RULA (a popular ergonomics assessment grid) upper-limb score for a large set of poses and sensor placements. Thanks to this evaluation method, more than 500,000 configurations have been automatically tested, which would be almost impossible to evaluate with classical protocols. The results show that the kinematic information obtained by the Kinect software is generally accurate enough to fill in ergonomic assessment grids. However inaccuracy strongly increases for some specific poses and sensor positions. Using this evaluation method enabled us to report configurations that could lead to these high inaccuracies. As a supplementary material, we provide a software tool to help designers to evaluate the expected accuracy of this sensor for a set of upper-limb configurations. Results obtained with the virtual mannequin are in accordance with those obtained from a real subject for a limited set of poses and sensor placements.

BACKGROUND: Energy flow has been hypothesized to be one of the most critical biomechanical concepts related to tennis performance and overuse injuries. However, the relationships among energy flow during the tennis serve, ball velocity, and overuse injuries have not been assessed. PURPOSE: To investigate the relationships among the quality and magnitude of energy flow, the ball velocity, and the peaks of upper limb joint kinetics and to compare the energy flow during the serve between injured and noninjured tennis players. STUDY DESIGN: Case-control study; Level of evidence, 3. METHODS: The serves of expert tennis players were recorded with an optoelectronic motion capture system. The forces and torques of the upper limb joints were calculated from the motion captures by use of inverse dynamics. The amount of mechanical energy generated, absorbed, and transferred was determined by use of a joint power analysis. Then the players were followed during 2 seasons to identify upper limb overuse injuries with a questionnaire. Finally, players were classified into 2 groups according to the questionnaire results: injured or noninjured. RESULTS: Ball velocity increased and upper limb joint kinetics decreased with the quality of energy flow from the trunk to the hand + racket segment. Injured players showed a lower quality of energy flow through the upper limb kinetic chain, a lower ball velocity, and higher rates of energy absorbed by the shoulder and elbow compared with noninjured players. CONCLUSION: The findings of this study imply that improper energy flow during the tennis serve can decrease ball velocity, increase upper limb joint kinetics, and thus increase overuse injuries of the upper limb joints.

Most current anticancer therapies induce tumor cell death through apoptosis where its specific involved pathways are poorly understood. For example, for many DNA-damaging agents, the specific biochemical lesions (DNA adducts) are associated with the induction of apoptosis via the mitochondria death pathway. However, several of these DNA-damaging agents like cisplatin induce apoptosis through plasma membrane disruption, triggering the Fas death receptor pathway. In this review, we focus on the role of early plasma membrane events in cisplatin-induced apoptosis. Special attention is given to changes in plasma membrane fluidity, inhibition of NHE1 exchanger, activation of acid sphingomyelinase and their consequences on the Fas death pathway in response to cisplatin.

The aim of the present study was to show if the use of continuous-running training vs. intermittent-running training has comparable or distinct impact on aerobic fitness in children. At first, children were matched according to their chronological age, their biological age (secondary sexual stages), and their physical activity or training status. Then, after randomization 3 groups were composed. Sixty-three children (X 9.6 +/- 1.0 years) were divided into an intermittent-running training group (ITG, 11 girls and 11 boys), a continuous-running training group (CTG, 10 girls and 12 boys), and a control group (CG, 10 girls and 9 boys). Over 7 weeks, ITG and CTG participated in 3 running sessions per week. Before and after the training period, they underwent a maximal graded test to determine peak oxygen uptake (peak VO2) and maximal aerobic velocity (MAV). Intermittent training consisted of short intermittent runs with repeated exercise and recovery sequences lasting from 5/15 to 30/30 seconds. With respect to continuous training sessions, repeated exercise sequences lasted from 6' to 20'. Training-effect threshold for statistical significance was set at p < 0.05. After training, peak VO2 was significantly improved in CTG (+7%, p < 0.001) and ITG (+4.8%, p < 0.001), whereas no difference occurred for the CG (-1.5%). Similarly, MAV increased significantly (p < 0.001) in both CTG (+8.7%) and ITG (+6.4%) with no significant change for CG. Our results demonstrated that both continuous and intermittent-running sessions induced significant increase in peak VO2 and MAV. Therefore, when adequate combinations of intensity/duration exercises are offered to prepubertal children, many modalities of exercises can successfully be used to increase their aerobic fitness. Aerobic running training is often made up of regular and long-distance running exercises at moderate velocity, which causes sometimes boredom in young children. During the developmental years, it seems therefore worthwhile to use various training modalities, to make this activity more attractive and thus create conditions for progress and enhanced motivation.

Sarcopenia could be currently defined as a geriatric syndrome initially characterized by a decrease in muscle mass that will get worse causing deterioration in strength and physical performance. A negative protein turnover, impaired mitochondrial dynamics and functions, a decreased muscle regeneration capacity, as well as an exacerbation of apoptosis are usually considered to be cellular mechanisms involved in muscle atrophy leading to sarcopenia. In this review, we first present that muscle overproduction of reactive oxygen and nitrogen species (RONS) and oxidative stress observed during aging are associated with sarcopenia, and then discuss how RONS are involved in redox-sensitive signaling pathways leading to sarcopenia. The identification of cost-effectiveness interventions to maintain muscle mass and physical functions in the elderly is one of the most important public health challenges. Here, we also discuss about the efficiency of different kind of antioxidant strategies against sarcopenia. Since exercise is the best strategy to prevent and reverse sarcopenia, we also highlight that exercise acts as an antioxidant.

Ageing causes a progressive decline in skeletal muscle mass that may lead to decreased strength and functionality. The term sarcopenia is especially used to characterise this geriatric syndrome. Numerous conditions and behaviours are considered to accelerate the progression of sarcopenia such as chronic diseases, malnutrition and physical inactivity. As people in modern countries are more and more sedentary, the impact of physical inactivity on the prevalence of sarcopenia might be more and more important in the future. In this review, we discuss how reactive oxygen species (ROS) could mediate the effects of lifelong inactivity in the onset and progression of age-related sarcopenia. Although the cellular mechanisms responsible for muscle ROS production are not necessarily the same, both inactivity and ageing are indeed known to increase basal ROS concentrations in skeletal muscle. New data and literature review are provided showing that chronic ROS overproduction induced by physical inactivity may exacerbate the activation of some redox-sensitive signalling pathways involved in age-related sarcopenia. We also address the scientific evidences implicating the role of ROS overproduction in the precocious failure of aged muscles to activate intracellular signalling responses to contractions.

AIMS: Green tea extract (GTE) can exert antiobesity and anti-inflammatory effects. Our study determined whether the benefits of GTE are summative with exercise-induced changes in anthropometric indices, and the levels of inflammatory cytokines, adiponectin and irisin in inactive overweight women. METHODS: Thirty overweight female participants were randomized to 3 groups: endurance training + placebo (ET + P); endurance training + GTE (ET + GTE); and Control (no exercise) + placebo (Control, n = 10). The exercise intervention consisted of an 8-week endurance-training programme of 3 sessions per week (aerobics, aerobic circuit training, and fast walking or jogging at a moderate intensity of 40-59% of the heart rate reserve). The dose of GTE used was 500 mg/day in the form of a green tea capsule. RESULTS: Body weight, body mass index, waist to hip ratio and body fat percentage were decreased in both ET + P and ET + GTE interventions (P < .001 for both interventions). The reduction of anthropometric values in the ET + GTE group was significantly higher than ET + P interventions (P < .001). Both exercise interventions also significantly (P < .001) increased adiponectin (ET + GTE = 5.28 mg/mL [95% confidence interval {CI}, 4.48 to 6.08] and ET + P = 3.34 mg/mL [95% CI, 2.76 to 3.92]) and decreased high-sensitivity C-reactive protein (hs-CRP; ET + GTE = -0.95 mg/L [95% CI, -1.15 to -0.75] and ET + P = -0.35 mg/L [95% CI, -0.46 to -0.24]). Changes in adiponectin and hs-CRP were greater (P < .05) in ET + GTE compared to ET + P. There were no significant differences in irisin, interleukin-6 or tumour necrosis factor-α between the 3 groups (P > .05). CONCLUSIONS: GTE improves exercise-induced body composition by further decreasing exercise-induced changes in weight, body mass index, waist to hip ratio and body fat percentage. The combination of GTE and exercise also produced greater changes in anti-inflammatory (increases in adiponectin) and metabolic (decreases in hs-CRP) markers than exercise alone.

Fasting is defined as the abstinence from consuming food and/or beverages for different periods of time. Both traditional and modern healthcare systems recommend fasting as a therapeutic intervention for the management of several chronic, non-infectious diseases. Exercising during a fasting state increases lipolysis in adipose tissue while also stimulating peripheral fat oxidation, resulting in increased fat utilization and weight loss. A key focus of this review is to assess whether endurance training performed while fasting induces specific training adaptations, where increased fat oxidation improves long-term endurance levels. Fasting decreases body weight, lean body and fat content in both trained and untrained individuals. Several studies indicate a broader impact of fasting on metabolism, with effects on protein and glucose metabolism in sedentary and untrained subjects. However, there are conflicting data regarding the effects of fasting on glucose metabolism in highly trained athletes. The effects of fasting on physical performance indicators also remain unclear, with some reporting a decreased performance, while others found no significant effects. Differences in experimental design, severity of calorie restriction, duration, and participant characteristics could, at least in part, explain such discordant findings. Our review of the literature suggests that there is little evidence to support the notion of endurance training and fasting-mediated increases in fat oxidation, and we recommend that endurance athletes should avoid high intensity training while fasting.

The aim of our study was to elucidate the role of growth hormone (GH) replacement therapy in three of the main mechanisms involved in sarcopenia: alterations in mitochondrial biogenesis, increase in oxidative stress, and alterations in protein balance. We used young and old Wistar rats that received either placebo or low doses of GH to reach normal insulin-like growth factor-1 values observed in the young group. We found an increase in lean body mass and plasma and hepatic insulin-like growth factor-1 levels in the old animals treated with GH. We also found a lowering of age-associated oxidative damage and an induction of antioxidant enzymes in the skeletal muscle of the treated animals. GH replacement therapy resulted in an increase in the skeletal muscle protein synthesis and mitochondrial biogenesis pathways. This was paralleled by a lowering of inhibitory factors in skeletal muscle regeneration and in protein degradation. GH replacement therapy prevents sarcopenia by acting as a double-edged sword, antioxidant and hypertrophic.