The objective of this study was to characterize the mechanics of maximal running sprint acceleration in high-level athletes. Four elite (100-m best time 9.95-10.29 s) and five sub-elite (10.40-10.60 s) sprinters performed seven sprints in overground conditions. A single virtual 40-m sprint was reconstructed and kinetics parameters were calculated for each step using a force platform system and video analyses. Anteroposterior force (FY), power (PY), and the ratio of the horizontal force component to the resultant (total) force (RF, which reflects the orientation of the resultant ground reaction force for each support phase) were computed as a function of velocity (V). FY-V, RF-V, and PY-V relationships were well described by significant linear (mean R(2) of 0.892 ± 0.049 and 0.950 ± 0.023) and quadratic (mean R(2) = 0.732 ± 0.114) models, respectively. The current study allows a better understanding of the mechanics of the sprint acceleration notably by modeling the relationships between the forward velocity and the main mechanical key variables of the sprint. As these findings partly concern world-class sprinters tested in overground conditions, they give new insights into some aspects of the biomechanical limits of human locomotion.

Hug F, Turpin NA, Couturier A, Dorel S. Consistency of muscle synergies during pedaling across different mechanical constraints. J Neurophysiol 106: 91-103, 2011. First published April 13, 2011 doi:10.1152/jn.01096.2010The purpose of the present study was to determine whether muscle synergies are constrained by changes in the mechanics of pedaling. The decomposition algorithm used to identify muscle synergies was based on two components: "muscle synergy vectors," which represent the relative weighting of each muscle within each synergy, and "synergy activation coefficients," which represent the relative contribution of muscle synergy to the overall muscle activity pattern. We hypothesized that muscle synergy vectors would remain fixed but that synergy activation coefficients could vary, resulting in observed variations in individual electromyographic (EMG) patterns. Eleven cyclists were tested during a submaximal pedaling exercise and five all-out sprints. The effects of torque, maximal torque-velocity combination, and posture were studied. First, muscle synergies were extracted from each pedaling exercise independently using non-negative matrix factorization. Then, to crossvalidate the results, muscle synergies were extracted from the entire data pooled across all conditions, and muscle synergy vectors extracted from the submaximal exercise were used to reconstruct EMG patterns of the five all-out sprints. Whatever the mechanical constraints, three muscle synergies accounted for the majority of variability [mean variance accounted for (VAF) ϭ 93.3 Ϯ 1.6%, VAF muscle Ͼ 82.5%] in the EMG signals of 11 lower limb muscles. In addition, there was a robust consistency in the muscle synergy vectors. This high similarity in the composition of the three extracted synergies was accompanied by slight adaptations in their activation coefficients in response to extreme changes in torque and posture. Thus, our results support the hypothesis that these muscle synergies reflect a neural control strategy, with only a few timing adjustments in their activation regarding the mechanical constraints.module; non-negative matrix factorization; motor control; cycling THE REDUNDANCY of the musculoskeletal system (Bernstein 1967) implies vast degrees of freedom. This provides great flexibility but makes the control of these degrees of freedom extremely complex. Consequently, the question of how the central nervous system coordinates activity among numerous muscles is central to understanding motor control. Low-dimensional modules formed by muscles activated in synchrony, named muscle synergies, have been proposed as building blocks that could simplify the construction of motor behaviors (2005) reported that combinations of a small number of synergies accounted for a large fraction of the variation in the EMG patterns observed during jumping, swimming, and walking in frogs. However, due to different muscle architectures and fiber type composition (and thus to different mechanical advantages) among muscles participating in the same mus...

Our results show homogeneous changes in muscle shear elastic modulus within and between elbow flexors. The greater increase in shear elastic modulus observed at long muscle lengths suggests the putative involvement of both cross-bridges number and titin in the modifications of muscle shear elastic modulus after damaging exercise.

Faced with mechanical inspiratory loading, awake animals and anaesthetized humans develop alveolar hypoventilation, whereas awake humans do defend ventilation. This points to a suprapontine compensatory mechanism instead of or in addition to the 'traditional' brainstem respiratory regulation. This study assesses the role of the cortical pre-motor representation of inspiratory muscles in this behaviour. Ten healthy subjects (age 19-34 years, three men) were studied during quiet breathing, CO 2 -stimulated breathing, inspiratory resistive loading, inspiratory threshold loading, and during self-paced voluntary sniffs. Pre-triggered ensemble averaging of Cz EEG epochs starting 2.5 s before the onset of inspiration was used to look for pre-motor activity. Pre-motor potentials were present during voluntary sniffs in all subjects (average latency (±S.D.): 1325 ± 521 ms), but also during inspiratory threshold loading (1427 ± 537 ms) and during inspiratory resistive loading (1109 ± 465 ms). Pre-motor potentials were systematically followed by motor potentials during inspiratory loading. Pre-motor potentials were lacking during quiet breathing (except in one case) and during CO 2 -stimulated breathing (except in two cases). The same pattern was observed during repeated experiments at an interval of several weeks in a subset of three subjects. The behavioural component of inspiratory loading compensation in awake humans could thus depend on higher cortical motor areas. Demonstrating a similar role of the cerebral cortex in the compensation of disease-related inspiratory loads (e.g. asthma attacks) would have important pathophysiological implications: it could for example contribute to explain why sleep is both altered and deleterious in such situations.

Recent studies of translational control suggest that translation termination may not be simply the end of synthesizing a protein but rather be involved in modulating both the translation efficiency and stability of a given transcript. Using recombinant eukaryotic release factor 3 (eRF3) and cellular extracts, we have shown for Saccharomyces cerevisiae that yeast eRF3 and Pab1p can interact. This interaction, mediated by the N؉M domain of eRF3 and amino acids 473 to 577 of Pab1p, was demonstrated to be direct by the two-hybrid approach. We confirmed that a genetic interaction exists between eRF3 and Pab1p and showed that Pab1p overexpression enhances the efficiency of termination in SUP35 ( In general, termination of protein synthesis occurs when the ribosome elongation machinery encounters an in-frame termination codon on the mRNA. In eukaryotes two release factors have been identified, eukaryotic release factor 1 (eRF1), which recognizes all three stop codons, and eRF3, a GTPase that binds to eRF1 and stimulates its release activity in vitro (35,109). The eRF1 protein has a structure mimicking that of a tRNA molecule. It recognizes the stop codon in the A site of the ribosome and catalyzes the hydrolysis of the peptidyltRNA bond (88).In Saccharomyces cerevisiae eRF1 and eRF3 termination factors are encoded by the essential genes SUP45 and SUP35, respectively (10,43,53,60,105). Mutations in either of these genes give the same pleiotropic phenotypes which were selected as omnipotent nonsense suppressors (for a review see reference 49). Moreover, overexpression of both eRF1 and eRF3 is required to enhance the efficiency of termination in yeast (90). In higher eukaryotes, overproduction of eRF1 alone is sufficient to compete with a suppressor tRNA (62). Either Xenopus laevis or human eRF1 alone was also shown previously to have an antisuppressor effect against a suppressor tRNA in the reticulocyte lysate translation system (28). In vitro the eRF1 of higher eukaryotes has a release activity and does not need any other factor (28, 35), and eRF3 by itself binds GTP, but GTPase activity requires the presence of both eRF1 and ribosomes (36). It has been shown previously that eRF1 and eRF3 interact, suggesting that they form a functional complex (70,90,99,109 . Yeast eRF3 consists of an N-terminal prionforming domain (PrD), a charged M (middle) domain of unknown function, and a C-terminal domain that provides the essential translation termination activity (96,97,105). Recently, the minimum length of PrD was defined as amino acids (aa) 1 to 97 (76). It was shown previously that Hsp104 protein is required for formation and maintenance of [PSI ϩ ] aggregates of eRF3: its overproduction or inactivation cures cells of [PSI ϩ ] (14). The eRF3 family includes proteins from yeasts, humans, X. laevis, and other species that are strongly conserved in the C-terminal region, which has a significant homology with the translation elongation factor eEF1A (47,60,109). In contrast to the C-terminal part, the N-terminal region of eRF3 is ...