Publications by authors named "Regis Bonnefoy"

Purpose: Sleep deprivation (SD) is characterized by reduced cognitive capabilities and endurance exercise performance and increased perceived exertion (RPE) during exercise. The combined effects of SD and exercise-induced changes in neuromuscular function and cognition are unknown. This study aimed to determine whether central fatigue is greater with SD, and if so, whether this corresponds to diminished cognitive and physical responses.

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We investigated the physiological consequences of one of the most extreme exercises realized by humans in race conditions: a 166-km mountain ultra-marathon (MUM) with 9500 m of positive and negative elevation change. For this purpose, (i) the fatigue induced by the MUM and (ii) the recovery processes over two weeks were assessed. Evaluation of neuromuscular function (NMF) and blood markers of muscle damage and inflammation were performed before and immediately following (n = 22), and 2, 5, 9 and 16 days after the MUM (n = 11) in experienced ultra-marathon runners.

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Although it is well established that chronic hypoxia leads to an inexorable loss of skeletal muscle mass in healthy subjects, the underlying molecular mechanisms involved in this process are currently unknown. Skeletal muscle atrophy is also an important systemic consequence of chronic obstructive pulmonary disease (COPD), but the role of hypoxemia in this regulation is still debated. Our general aim was to determine the molecular mechanisms involved in the regulation of skeletal muscle mass after exposure to chronic hypoxia and to test the biological relevance of our findings into the clinical context of COPD.

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This experiment investigated the fatigue induced by a 24-h running exercise (24TR) and particularly aimed at testing the hypothesis that the central component would be the main mechanism responsible for neuromuscular fatigue. Neuromuscular function evaluation was performed before, every 4 h during, and at the end of the 24TR on 12 experienced ultramarathon runners. It consisted of a determination of the maximal voluntary contractions (MVC) of the knee extensors (KE) and plantar flexors (PF), the maximal voluntary activation (%VA) of the KE and PF, and the maximal compound muscle action potential amplitude (Mmax) on the soleus and vastus lateralis.

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Myostatin, a member of the TGF-beta family, has been identified as a master regulator of embryonic myogenesis and early postnatal skeletal muscle growth. However, cumulative evidence also suggests that alterations in skeletal muscle mass are associated with dysregulation in myostatin expression and that myostatin may contribute to muscle mass loss in adulthood. Two major branches of the Akt pathway are relevant for the regulation of skeletal muscle mass, the Akt/mammalian target of rapamycin (mTOR) pathway, which controls protein synthesis, and the Akt/forkhead box O (FOXO) pathway, which controls protein degradation.

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Article Synopsis
  • Myostatin is a key regulator of muscle growth, influencing both early development and adult muscle mass, particularly in the context of muscle wasting.
  • In a study involving adult rats, myostatin was overexpressed in specific muscles through gene electrotransfer, leading to significant reductions in muscle mass, fiber size, and protein content without affecting fiber count.
  • The overexpression of myostatin resulted in decreased levels of crucial muscle structural genes and transcription factors, indicating its role in promoting muscle atrophy by down-regulating muscle-specific gene expression.
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Article Synopsis
  • - The study explores how slow-twitch muscle fibers rely on mitochondrial activity, highlighting a connection between muscle-specific protein expression and mitochondrial development, particularly focusing on the role of PGC-1alpha.
  • - Researchers utilized gene electrotransfer to show that introducing PGC-1alpha into rat muscle significantly boosts the activity of the cytochrome c promoter and also affects the MyoD promoter, but not the fast troponin I promoter.
  • - The findings indicate that calcineurin A (CnA) and calcium/calmodulin kinase IV (CaMKIV) can activate the PGC-1alpha promoter, suggesting that CnA plays a key role in regulating the expression of certain muscle proteins linked to mitochondrial function.
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We determined over a 3-week period some of the factors that may influence the kinetic of gene expression following in vivo gene electrotransfer. Histochemical analysis of beta-galactosidase and biochemical analysis of luciferase expressions were used to determine reporter gene activity in the Tibialis anterior muscles of young Sprague-Dawley male rats. Transfection efficiency peaked 5 days after gene electrotransfer and then exponentially decreased to reach non-detectable levels at day 28.

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This report describes a new method allowing to measure the three-dimensional forces applied on right and left pedals during cycling. This method is based on a cycle ergometer mounted on a force platform. By recording the forces applied on the force platform and applying the fundamental mechanical equations, it was possible to calculate the instantaneous three-dimensional forces applied on pedals.

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Article Synopsis
  • This study explores the factors contributing to muscle damage during gene electrotransfer, aiming to enhance gene delivery strategies for medical applications.
  • Histochemical analyses in rats revealed that while muscle degeneration was evident five days post-treatment, recovery was largely observed by 21 days, with some signs persisting only in the form of central myonuclei.
  • The extent of muscle damage correlates more with plasmid DNA that supports gene expression rather than the electric pulses alone, highlighting that specific parameters of the electrotransfer process can significantly impact tissue integrity.
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Efficiency and reproducibility of gene electrotransfer depend on the electrical specifications provided by the pulse generator, such as pulse duration, pulse number, pulse frequency, pulse combination, and current intensity. Here, we describe the performances of GET42, a pulse generator specifically designed for gene electrotransfer into skeletal muscle. Expression of beta-galactosidase in the Tibialis anterior muscle of Sprague-Dawley male rats was increased 250-fold by GET42 compared to DNA injection alone.

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The aim of this study was to analyze the effect of an increase in training frequency on exercise-induced fatigue by using a systems model with parameters free to vary over time. Six previously untrained subjects undertook a 15-wk training experiment composed of 1) an 8-wk training period with three sessions per week (low-frequency training), 2) 1 wk without training, 3) a 4-wk training period with five sessions per week [high frequency training (HFT)], and 4) 2 wk without training. The systems input ascribed to training loads was computed from interval exercises and expressed in arbitrary units.

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