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  • 1.
    Chaillou, Thomas
    et al.
    Örebro University, School of Health Sciences.
    Cheng, Arthur J.
    Faculty of Health, School of Kinesiology and Health Sciences, York University, Canada.
    Mechanisms of prolonged low-frequency force depression: in-vivo studies get us closer to the truth2019In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 316, no 5, p. R502-R503Article in journal (Refereed)
  • 2.
    Chaillou, Thomas
    et al.
    Örebro University, School of Health Sciences. Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Koulmann, N.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Simler, N.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Meunier, A.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Serrurier, B.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Chapot, R.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Peinnequin, A.
    Genomic Core Facility, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Beaudry, M.
    Laboratoire “Réponses cellulaires et fonctionnelles a` l’hypoxie”, Université Paris, Bobigny, France.
    Bigard, X.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Hypoxia transiently affects skeletal muscle hypertrophy in a functional overload model2012In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 302, p. R643-R654Article in journal (Refereed)
    Abstract [en]

    Hypoxia induces a loss of skeletal muscle mass, but the signaling pathways and molecular mechanisms involved remain poorly understood. We hypothesized that hypoxia could impair skeletal muscle hypertrophy induced by functional overload (Ov). To test this hypothesis, plantaris muscles were overloaded during 5, 12, and 56 days in female rats exposed to hypobaric hypoxia (5,500 m), and then, we examined the responses of specific signaling pathways involved in protein synthesis (Akt/mTOR) and breakdown (atrogenes). Hypoxia minimized the Ov-induced hypertrophy at days 5 and 12 but did not affect the hypertrophic response measured at day 56. Hypoxia early reduced the phosphorylation levels of mTOR and its downstream targets P70(S6K) and rpS6, but it did not affect the phosphorylation levels of Akt and 4E-BP1, in Ov muscles. The role played by specific inhibitors of mTOR, such as AMPK and hypoxia-induced factors (i.e., REDD1 and BNIP-3) was studied. REDD1 protein levels were reduced by overload and were not affected by hypoxia in Ov muscles, whereas AMPK was not activated by hypoxia. Although hypoxia significantly increased BNIP-3 mRNA levels at day 5, protein levels remained unaffected. The mRNA levels of the two atrogenes MURF1 and MAFbx were early increased by hypoxia in Ov muscles. In conclusion, hypoxia induced a transient alteration of muscle growth in this hypertrophic model, at least partly due to a specific impairment of the mTOR/P70(S6K) pathway, independently of Akt, by an undefined mechanism, and increased transcript levels for MURF1 and MAFbx that could contribute to stimulate the proteasomal proteolysis.

  • 3.
    Daussin, Frederic
    et al.
    University of Strasbourg, Faculty of Medicine, Physiology Department, Strasbourg, FRANCE.
    Zoll, Joffrey
    University of Strasbourg, Faculty of Medicine, Physiology Department, Strasbourg, FRANCE.
    Dufour, Stephane
    Faculty of Sport Sciences, University of Strasbourg, Strasbourg, FRANCE.
    Ponsot, Elodie
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Lonsdorfer-Wolf, Evelyne
    CHRU of Strasbourg, Physiology and Functional Explorations Department, New Civil Hospital, Strasbourg, FRANCE .
    Doutreleau, Stephane
    CHRU of Strasbourg, Physiology and Functional Explorations Department, New Civil Hospital, Strasbourg, FRANCE .
    Mettauer, Bertrand
    Piquard, Francois
    University of Strasbourg, Faculty of Medicine, Physiology Department, Strasbourg, FRANCE.
    Geny, Bernard
    University of Strasbourg, Faculty of Medicine, Physiology Department, Strasbourg, FRANCE.
    Richard, Ruddy
    Effect of interval versus continuous training on cardiorespiratory and mitochondrial functions: relationship to aerobic performance improvements in sedentary subjects2008In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 295, no 1, p. R264-272Article in journal (Refereed)
    Abstract [en]

    The goal of the study was to determine the effects of continuous (CT) vs. intermittent (IT) training yielding identical mechanical work and training duration on skeletal muscle and cardiorespiratory adaptations in sedentary subjects. Eleven subjects (6 men and 5 women, 45 +/- 3 years) were randomly assigned to either of the two 8-wk training programs in a cross-over design, separated by 12 wk of detraining. Maximal oxygen uptake (Vo2max) increased after both trainings (9% with CT vs. 15% with IT), whereas only IT was associated with faster Vo2 kinetics (tau: 68.0 +/- 1.6 vs. 54.9 +/- 0.7 s, P < 0.05) measured during a test to exhaustion (TTE) and with improvements in maximal cardiac output (Qmax, from 18.1 +/- 1.1 to 20.1 +/- 1.2 l/min; P < 0.01). Skeletal muscle mitochondrial oxidative capacities (Vmax) were only increased after IT (3.3 +/- 0.4 before and 4.5 +/- 0.6 micromol O2 x min(-1) x g dw(-1) after training; P < 0.05), whereas capillary density increased after both trainings, with a two-fold higher enhancement after CT (+21 +/- 1% for IT and +40 +/- 3% after CT, P < 0.05). The gain of Vmax was correlated with the gain of TTE and the gain of Vo2max with IT. The gain of Qmax was also correlated with the gain of VO2max. These results suggest that fluctuations of workload and oxygen uptake during training sessions, rather than exercise duration or global energy expenditure, are key factors in improving muscle oxidative capacities. In an integrative view, IT seems optimal in maximizing both peripheral muscle and central cardiorespiratory adaptations, permitting significant functional improvement. These data support the symmorphosis concept in sedentary subjects.

  • 4. Paulsen, Gøran
    et al.
    Vissing, Kristian
    Kalhovde, John Magne
    Ugelstad, Ingrid
    Bayer, Monika Lucia
    Kadi, Fawzi
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Schjerling, Peter
    Hallén, Jostein
    Raastad, Truls
    Maximal eccentric exercise induces a rapid accumulation of small heat shock proteins on myofibrils and a delayed HSP70 response in humans2007In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 293, no 2, p. R844-R853Article in journal (Refereed)
    Abstract [en]

    In this study the stress protein response to unaccustomed maximal eccentric exercise in humans was investigated. Eleven healthy males performed 300 maximal eccentric actions with the quadriceps muscle. Biopsies from vastus lateralis were collected at 30 min and 4, 8, 24, 96, and 168 h after exercise. Cellular regulation and localization of heat shock protein (HSP) 27, alpha B-crystallin, and HSP70 were analyzed by immunohistochemistry, ELISA technique, and Western blotting. Additionally, mRNA levels of HSP27, alpha B-crystallin, and HSP70 were quantified by Northern blotting. After exercise (30 min), 81 +/- 8% of the myofibers showed strong HSP27 staining (P < 0.01) that gradually decreased during the following week. alpha B-Crystallin mimicked the changes observed in HSP27. After exercise (30 min), the ELISA analysis showed a 49 +/- 13% reduction of the HSP27 level in the cytosolic fraction (P < 0.01), whereas Western blotting revealed a 15-fold increase of the HSP27 level in the myofibrillar fraction (P < 0.01). The cytosolic HSP70 level increased to 203 +/- 37% of the control level 24 h after exercise (P < 0.05). After 4 days, myofibrillar-bound HSP70 had increased approximately 10-fold (P < 0.01) and was accompanied by strong staining on cross sections. mRNA levels of HSP27, alpha B-crystallin, and HSP70 were all elevated the first day after exercise (P < 0.01); HSP70 mRNA showed the largest increase (20-fold at 8 h). HSP27 and alpha B-crystallin seemed to respond immediately to maximal eccentric exercise by binding to cytoskeletal/myofibrillar proteins, probably to function as stabilizers of disrupted myofibrillar structures. Later, mRNA and total HSP protein levels, especially HSP70, increased, indicating that HSPs play a role in skeletal muscle recovery and remodeling/adaptation processes to high-force exercise

  • 5.
    Ponsot, Elodie
    et al.
    Örebro University, School of Health and Medical Sciences. Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Dufour, Stephane P.
    UFR STAPS, Univ Strasbourg, Strasbourg, France; Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Doutreleau, Stephane
    Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Lonsdorfer-Wolf, Evelyne
    Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Lampert, Eliane
    Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Piquard, Francois
    Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Geny, Bernard
    Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Mettauer, Bertrand
    Serv Cardiol, Hop Civils Colmar, Colmar, France.
    Ventura-Clapier, Renee
    Fac Pharm, INSERM, U769, Univ Paris 11, Chatenay Malabry, France.
    Richard, Ruddy
    Serv Physiol & Explorat Fonct, Hop Civil, Strasbourg, France; Fac Med, Dept Physiol, UPRES EA3072, Strasbourg, France.
    Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?2010In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 298, no 3, p. R558-R566Article in journal (Refereed)
    Abstract [en]

    This study investigates the role of central vs. peripheral factors in the limitation of maximal oxygen uptake ((V) over dot O-2max) with moderate hypoxia [inspired fraction (FIO2) = 14.5%]. Fifteen endurance-trained athletes performed maximal cycle incremental tests to assess (V) over dotO(2max), maximal cardiac output ((Q) over dot(max)), and maximal arteriovenous oxygen (a-vO(2)) difference in normoxia and hypoxia. Muscle biopsies of vastus lateralis were taken 1 wk before the cycling tests to evaluate maximal muscle oxidative capacity ((V) over dot(max)) and sensitivity of mitochondrial respiration to ADP (K-m) on permeabilized muscle fibers in situ. Those athletes exhibiting the largest reduction of (V) over dotO(2max) in moderate hypoxia (Severe Loss group: -18 +/- 2%) suffered from significant reductions in Q(max) (-4 +/- 1%) and maximal a-vO(2) difference (-14 +/- 2%). Athletes who well tolerated hypoxia, as attested by a significantly smaller drop of (V) over dotO(2max) with hypoxia (Moderate Loss group: -7 +/- 1%), also display a blunted (Q) over dot(max) (-9 +/- 2%) but, conversely, were able to maintain maximal a-vO(2) difference (+1 +/- 2%). Though (V) over dot(max) was similar in the two experimental groups, the smallest reduction of (V) over dotO(2max) with moderate hypoxia was observed in those athletes presenting the lowest apparent Km for ADP in the presence of creatine (K-m (+) (Cr)). In already-trained athletes with high muscular oxidative capacities, the qualitative, rather than quantitative, aspects of the mitochondrial function may constitute a limiting factor to aerobic ATP turnover when exercising at low FIO2, presumably through the functional coupling between the mitochondrial creatine kinase and ATP production. This study suggests a potential role for peripheral factors, including the alteration of cellular homeostasis in active muscles, in determining the tolerance to hypoxia in maximally exercising endurance-trained athletes.

  • 6.
    Revsbech, Inge G.
    et al.
    Dept Biosci, Aarhus Univ, Aarhus, Denmark.
    Malte, Hans
    Dept Biosci, Aarhus Univ, Aarhus, Denmark.
    Fröbert, Ole
    Örebro University Hospital. Dept Cardiol.
    Evans, Alina
    Dept Forestry & Wildlife Management, Hedmark Univ Coll, Elverum, Norway.
    Blanc, Stephane
    Inst Pluridisciplinaire Hubert Curien, Dept Ecol Physiol & Ethol, Centre national de la recherche scientifique (CNRS), Strasbourg, France.
    Josefsson, Johan
    Dept Cardiol, Örebro University Hospital, Örebro, Sweden.
    Fago, Angela
    Dept Biosci, Aarhus Univ, Aarhus, Denmark.
    Decrease in the red cell cofactor 2,3-diphosphoglycerate increases hemoglobin oxygen affinity in the hibernating brown bear Ursus arctos2013In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 304, no 1, p. R43-R49Article in journal (Refereed)
    Abstract [en]

    Revsbech IG, Malte H, Frobert O, Evans A, Blanc S, Josefsson J, Fago A. Decrease in the red cell cofactor 2,3-diphosphoglycerate increases hemoglobin oxygen affinity in the hibernating brown bear Ursus arctos. Am J Physiol Regul Integr Comp Physiol 304: R43-R49, 2013. First published November 21, 2012; doi:10.1152/ajpregu.00440.2012.-During winter hibernation, brown bears (Ursus arctos) reduce basal O-2 consumption rate to similar to 25% compared with the active state, while body temperature decreases moderately (to similar to 30 degrees C), suggesting a temperature-independent component in their metabolic depression. To establish whether changes in O-2 consumption during hibernation correlate with changes in blood O-2 affinity, we took blood samples from the same six individuals of hibernating and nonhibernating free-ranging brown bears during winter and summer, respectively. A single hemoglobin (Hb) component was detected in all samples, indicating no switch in Hb synthesis. O-2 binding curves measured on red blood cell lysates at 30 degrees C and 37 degrees C showed a less temperature-sensitive O-2 affinity than in other vertebrates. Furthermore, hemolysates from hibernating bears consistently showed lower cooperativity and higher O-2 affinity than their summer counterparts, regardless of the temperature. We found that this increase in O-2 affinity was associated with a significant decrease in the red cell Hb-cofactor 2,3-diphosphoglycerate (DPG) during hibernation to approximately half of the summer value. Experiments performed on purified Hb, to which DPG had been added to match summer and winter levels, confirmed that the low DPG content was the cause of the left shift in the Hb-O-2 equilibrium curve during hibernation. Levels of plasma lactate indicated that glycolysis is not upregulated during hibernation and that metabolism is essentially aerobic. Calculations show that the increase in Hb-O-2 affinity and decrease in cooperativity resulting from decreased red cell DPG may be crucial in maintaining a fairly constant tissue oxygen tension during hibernation in vivo.

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