Publications by authors named "Daussin F"

This study aimed to assess the physiological responses to repeated running exercise performed at supramaximal intensity and with end-expiratory breath holding (EEBH) up to the breaking point. Eight male runners participated in two running testing sessions on a motorized treadmill. In the first session, participants performed two sets of 8 repetitions at 125% of maximal aerobic velocity and with maximum EEBH.

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Hingrand, C, Olivier, N, Combes, A, Bensaid, S, and Daussin, FN. Power is more relevant than ascensional speed to determine metabolic demand at different gradient slopes during running. J Strength Cond Res 37(11): 2298-2301, 2023-Trail running is characterized by successive uphill and downhill running sessions.

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Article Synopsis
  • - Sepsis-induced myopathy leads to muscle fiber atrophy and mitochondrial issues, impacting recovery outcomes, but the role of overall energy deficit in this process was not previously studied.
  • - In the experiment, three mouse groups were analyzed: sepsis mice with reduced caloric intake, sham-fed mice, and sham mice fed in line with the sepsis group's intake, to determine energy balance and muscle characteristics.
  • - Results indicated that while sepsis caused a 17% reduction in muscle size and decreased mitochondrial function, the energy deficit alone did not fully explain the observed muscle issues, suggesting different metabolic adaptations in the sham pair-fed mice compared to the sepsis group.
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Introduction: The study aimed to interpret the evolution of the physical performance of rugby sevens and rugby union French international players from 2009 to 2020.

Methods: 631 players from the French national teams were divided into three groups: forwards, backs and sevens. The performances evaluated were anthropometric characteristics, strength tests (1 RM bench press and 1 RM pull-up), aerobic capacity (YoYo IR1 test) and speed tests (10 m, 20 m and 50 m).

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Protein O-GlcNAcylation is increasingly recognized as an important cellular regulatory mechanism, in multiple organs including the heart. However, the mechanisms leading to O-GlcNAcylation in mitochondria and the consequences on their function remain poorly understood. In this study, we use an in vitro reconstitution assay to characterize the intra-mitochondrial O-GlcNAc system without potential cytoplasmic confounding effects.

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In healthy subjects, at low minute ventilation (V̇e) during physical exercise, the water content and temperature of the airways are well regulated. However, with the increase in V̇e, the bronchial mucosa becomes dehydrated and epithelial damage occurs. Our goal was to demonstrate the correspondence between the ventilatory threshold inducing epithelial damage, measured experimentally, and the dehydration threshold, estimated numerically.

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Several brands of water enriched with O (O-waters) are commercially available and are advertised as wellness and fitness waters with claims of physiological and psychological benefits, including improvement in exercise performance. However, these claims are based, at best, on anecdotal evidence or on a limited number of unreliable studies. The purpose of this double-blind randomized study was to compare the effect of two O-waters (~110 mg O·L) and a placebo (10 mg O·L, i.

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Article Synopsis
  • - Cocoa flavanols (CF) supplementation was found to enhance mitochondrial function and overall metabolism, particularly promoting carbohydrate use and improving glucose tolerance in wild type mice over 15 days of treatment.
  • - The study measured several metabolic parameters, including mitochondrial respiratory function and levels of pyridine nucleotides (NAD and NADH), showing that CF supplementation led to an increase in mitochondrial mass and enhanced NAD metabolism.
  • - The positive effects of CF supplementation were significantly diminished in Sirt3 mice, suggesting that the mitochondrial deacetylase Sirt3 plays a crucial role in mediating the metabolic benefits derived from cocoa flavanols.
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Sarcopenia is characterized by a loss of muscle mass and function that reduces mobility, diminishes quality of life, and can lead to fall-related injuries. At the intracellular level, mitochondrial population alterations are considered as key contributors to the complex etiology of sarcopenia. Mitochondrial dysfunctions lead to reactive oxygen species production, altered cellular proteostasis, and promotes inflammation.

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Mitochondrial dysfunction is observed in a broad range of human diseases, including rare genetic disorders and complex acquired pathologies. For this reason, there is increasing interest in identifying safe and effective strategies to mitigate mitochondrial impairments. Natural compounds are widely used for multiple indications, and their broad healing properties suggest that several may improve mitochondrial function.

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Objective: Long before clinical complications of type 1 diabetes (T1D) develop, oxygen supply and use can be altered during activities of daily life. We examined in patients with uncomplicated T1D all steps of the oxygen pathway, from the lungs to the mitochondria, using an integrative ex vivo (muscle biopsies) and in vivo (during exercise) approach.

Research Design And Methods: We compared 16 adults with T1D with 16 strictly matched healthy control subjects.

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Article Synopsis
  • Continuous exercise (CE) leads to greater ventilation compared to intermittent exercise (IE), which could impact airway health.
  • A study with 16 young adults showed that CE at 70% of maximum work rate resulted in mild airway damage, as indicated by changes in serum markers like CC16 and SP-D.
  • In contrast, IE did not cause significant airway damage, suggesting that the intensity and sustained ventilation during CE are key factors in airway epithelial cell damage.
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Swimming and throwing are involved in water-polo player performance. These movements have a common biomechanical basis in the use of the internal shoulder rotation and adductor muscles. The aim of the study was to evaluate the relationship between shoulder isokinetic evaluation and throwing velocity as well as swimming performance in female water-polo players.

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VO2 fluctuations are argued to be an important mechanism underpinning chronic adaptations following interval training. We compared the effect of exercise modality, continuous vs. intermittent realized at a same intensity, on electrical muscular activity, muscular oxygenation and on whole body oxygen uptake.

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The succession of on-transient phases that induce a repetition of metabolic changes is a possible mechanism responsible for the greater response to intermittent training (IT). The objective of this study was to quantify [Formula: see text] fluctuations during intermittent exercise characterised by the same work:rest ratio, but different durations and identify which duration leads to the greatest fluctuations. Ten participants (24 ± 5 years; [Formula: see text]: 42 ± 7 mL·min·kg) performed (1) an incremental test to exhaustion to determine peak work rate (WR) and oxygen uptake ([Formula: see text]), (2), and three 1 h intermittent exercises alternating work period at 70% WR with passive recovery period of different 1:1 work:recovery duty cycles (30 s:30 s, 60 s:60 s, 120 s:120 s).

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Unlabelled: The purpose of the study was to determine muscle metabolism adaptation to exercise in facioscapulohumeral muscular dystrophy patients (FSHD) and to study the correlation with clinical functional status (6-min walk test). 8 FSHD patients and 15 age-matched healthy controls (Controls) performed two isokinetic constant-load knee extension exercises: (1) at 20% of their maximal extensors' peak torque (i.e.

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During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α).

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Introduction: The effect of eccentric (ECC) versus concentric (CON) training on metabolic properties in skeletal muscle is understood poorly. We determined the responses in oxidative capacity and mitochondrial H2 O2 production after eccentric (ECC) versus concentric (CON) training performed at similar mechanical power.

Methods: Forty-eight rats performed 5- or 20-day eccentric (ECC) or concentric (CON) training programs.

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Introduction: Microbiopsies are increasingly used as an alternative to the standard Bergström technique for skeletal muscle sampling. The potential impact of these two different procedures on mitochondrial respiration rate is unknown. The objective of this work was to compare microbiopsies versus Bergström procedure on mitochondrial respiration in skeletal muscle.

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Introduction: Statins are associated with adverse skeletal muscle effects. Our objective was to determine if muscular adaptations following exercise training prevented deleterious effects of atorvastatin in glycolytic skeletal muscle.

Methods: Twenty rats were divided into 2 groups: a control group (n = 10; Cont) and a 10 days of training group (n = 10; Training).

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Alterations of mitochondrial function have been implicated in the pathogenesis of Duchenne muscular dystrophy. In the present study, mitochondrial respiratory function, reactive oxygen species (ROS) dynamics and susceptibility to Ca(2+)-induced permeability transition pore (PTP) opening were investigated in permeabilized skeletal muscle fibres of 6-week-old mdx mice, in order to characterize the magnitude and nature of mitochondrial dysfunction at an early post-necrotic stage of the disease. Short-term overexpression of the transcriptional co-activator PGC1α, achieved by in vivo plasmid transfection, was then performed to determine whether this intervention could prevent mitochondrial impairment and mitigate associated biochemical abnormalities.

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Duchenne muscular dystrophy (DMD) is characterized by myofiber death from apoptosis or necrosis, leading in many patients to fatal respiratory muscle weakness. Among other pathological features, DMD muscles show severely deranged metabolic gene regulation and mitochondrial dysfunction. Defective mitochondria not only cause energetic deficiency, but also play roles in promoting myofiber atrophy and injury via opening of the mitochondrial permeability transition pore.

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Aims: Statins protect against cardiovascular-related mortality but induce skeletal muscle toxicity. To investigate mechanisms of statins, we tested the hypothesis that statins optimized cardiac mitochondrial function but impaired vulnerable skeletal muscle by inducing different level of reactive oxygen species (ROS).

Methods And Results: In atrium of patients treated with statins, ROS production was decreased and oxidative capacities were enhanced together with an extensive augmentation of mRNAs expression of peroxisome proliferator-activated receptor gamma co-activator (PGC-1) family.

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Purpose: The objective of this study was to investigate the time course of the endurance training-induced adaptations in two major mitochondrial functions.

Methods: Forty rats were divided into four groups: a control group and three training groups--a 1-d training group, a 5-d training group, and a 10-d training group. The training protocol consisted of 30 min of running on a motorized treadmill (26 m·min(-1), 15% grade).

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In the present study, we specifically determined whether the regulatory protein cyclophilin-D (CypD), and by extension opening of the permeability transition pore (PTP), is involved in the activation of mitochondria-derived apoptotic signalling previously described in skeletal muscle following loss of innervation. For this purpose, CypD-defficient (CypD-KO) mice and their littermate controls were submitted to unilateral sciatic nerve transection, and mitochondrial resistance to Ca2+-induced opening of the PTP, and muscle apoptotic signalling were investigated 14 days post-surgery. Denervation caused atrophy, facilitated Ca2+-induced opening of the PTP in vitro in permeabilized muscle fibres, and activation of the apoptotic proteolytic cascade in the whole muscle of both mouse strains.

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