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  • 1.
    Adolfsson, Peter
    et al.
    Institute of Clinical Sciences, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden; Endocrine and Diabetes Center, The hospital of Halland Kungsbacka, Kungsbacka, Sweden.
    Mattsson, Stig
    Faculty of Health Sciences and Medicine, Örebro University Hospital, Örebro, Sweden; Endocrine and Diabetes Center, Falun Hospital, Falun, Sweden.
    Jendle, Johan
    Faculty of Health Sciences and Medicine, Örebro University Hospital, Örebro, Sweden; Endocrine and Diabetes Center, Karlstad Hospital, Karlstad, Sweden.
    Evaluation of glucose control when a new strategy of increased carbohydrate supply is implemented during prolonged physical exercise in type 1 diabetes2015Inngår i: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 115, nr 12, s. 2599-2607Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Purpose: In healthy individuals, high carbohydrate intake is recommended during prolonged exercise for maximum performance. In type 1 diabetes (T1D), this would alter the insulin requirements. The aim of the study was to evaluate the safety of high glucose supplementation during prolonged exercise and the glucose control when a novel strategy of increased carbohydrate supply was implemented during prolonged exercise in T1D.

    Methods: Eight subjects with T1D participated in a sports camp including sessions of prolonged exercise and individualized feedback during three consecutive days. This was later followed by a 90 km cross-country skiing race. Large amounts of carbohydrates, 75 g/h, were supplied during exercise and the insulin requirements were registered. Glucose was measured before, during and after exercise aiming at euglycaemia, 4-8 mmol/L (72-144 mg/dL). During the race, continuous glucose monitoring (CGM) was used as an aspect of safety and to allow direct and individual adjustments.

    Results: Compared to ordinary carbohydrate supply during exercise, the high carbohydrate supplementation resulted in significantly increased insulin doses to maintain euglycaemia. During the cross-country skiing race, the participants succeeded to reach mean target glucose levels; 6.5 ± 1.9 mmol/L (117 ± 34 mg/dL) and 5.7 ± 1.5 mmol/L (103 ± 27 mg/dL) at the start and finish of the race, respectively. Episodes of documented hypoglycemia (<4 mmol/L/72 mg/dL) were rare. CGM was used for adjustments.

    Conclusion: In this study, large carbohydrate supplementation in T1D individuals during prolonged aerobic exercise is safe and allows the subjects to maintain glycaemic control and indicates the feasibility of CGM under these conditions.

  • 2.
    Aghanavesi, Somayeh
    et al.
    Computer Engineering, School of Technology and Business Studies, Borlänge, Dalarna University, Sweden.
    Bergquist, Filip
    Dept. of Pharmacology, University of Gothenburg, Gothenburg, Sweden.
    Nyholm, Dag
    Dept. of Neuroscience, Neurology, Uppsala University, Uppsala, Sweden.
    Senek, Marina
    Dept. of Neuroscience, Neurology, Uppsala University, Uppsala, Sweden.
    Memedi, Mevludin
    Örebro universitet, Handelshögskolan vid Örebro Universitet.
    Objective assessment of Parkinson’s disease motor symptoms during leg agility test using motion sensors2018Konferansepaper (Fagfellevurdert)
    Abstract [en]

    Title: Objective assessment of Parkinson’s disease motor symptoms during leg agility test using motion sensors

    Objective: To develop and evaluate machine learning methods for assessment of Parkinson’s disease (PD) motor symptoms using leg agility (LA) data collected with motion sensors during a single dose experiment.

    Background: Nineteen advanced PD patients (Gender: 14 males and 5 females, mean age: 71.4, mean years with PD: 9.7, mean years with levodopa: 9.5) were recruited in a single center, open label, single dose clinical trial in Sweden [1].

    Methods: The patients performed up to 15 LA tasks while wearing motions sensors on their foot ankle. They performed tests at pre-defined time points starting from baseline, at the time they received a morning dose (150% of their levodopa equivalent morning dose), and at follow-up time points until the medication wore off. The patients were video recorded while performing the motor tasks. and three movement disorder experts rated the observed motor symptoms using 4 items from the Unified PD Rating Scale (UPDRS) motor section including UPDRS #26 (leg agility), UPDRS #27 (Arising from chair), UPDRS #29 (Gait), UPDRS #31 (Body Bradykinesia and Hypokinesia), and dyskinesia scale. In addition, they rated the overall mobility of the patients using Treatment Response Scale (TRS), ranging from -3 (very off) to 3 (very dyskinetic). Sensors data were processed and their quantitative measures were used to develop machine learning methods, which mapped them to the mean ratings of the three raters. The quality of measurements of the machine learning methods was assessed by convergence validity, test-retest reliability and sensitivity to treatment.

    Results: Results from the 10-fold cross validation showed good convergent validity of the machine learning methods (Support Vector Machines, SVM) with correlation coefficients of 0.81 for TRS, 0.78 for UPDRS #26, 0.69 for UPDRS #27, 0.78 for UPDRS #29, 0.83 for UPDRS #31, and 0.67 for dyskinesia scale (P<0.001). There were good correlations between scores produced by the methods during the first (baseline) and second tests with coefficients ranging from 0.58 to 0.96, indicating good test-retest reliability. The machine learning methods had lower sensitivity than mean clinical ratings (Figure. 1).

    Conclusions: The presented methodology was able to assess motor symptoms in PD well, comparable to movement disorder experts. The leg agility test did not reflect treatment related changes.

    Fulltekst (pdf)
    Objective assessment of Parkinson’s disease motor symptoms during leg agility test using motion sensors
  • 3.
    Aghanavesi, Somayeh
    et al.
    Computer Engineering, School of Technology and Business Studies, Dalarna University, Borlänge, Sweden.
    Filip, Bergquist
    Dept. of Pharmacology, University of Gothenburg, Gothenbrug, Sweden.
    Nyholm, Dag
    Dept. of Neuroscience, Neurology, Uppsala University, Uppsala, Sweden.
    Senek, Marina
    Dept. of Neuroscience, Neurology, Uppsala University, Uppsala, Sweden.
    Memedi, Mevludin
    Örebro universitet, Handelshögskolan vid Örebro Universitet.
    Feasibility of a multi-sensor data fusion method for assessment of Parkinson’s disease motor symptoms2018Konferansepaper (Annet vitenskapelig)
    Abstract [en]

    Title: Feasibility of a multi-sensor data fusion method for assessment of Parkinson’s disease motor symptoms

    Objective: To assess the feasibility of measuring Parkinson’s disease (PD) motor symptoms with a multi-sensor data fusion method. More specifically, the aim is to assess validity, reliability and sensitivity to treatment of the methods.

    Background: Data from 19 advanced PD patients (Gender: 14 males and 5 females, mean age: 71.4, mean years with PD: 9.7, mean years with levodopa: 9.5) were collected in a single center, open label, single dose clinical trial in Sweden [1].

    Methods: The patients performed leg agility and 2-5 meter straight walking tests while wearing motion sensors on their limbs. They performed the tests at baseline, at the time they received the morning dose, and at pre-specified time points until the medication wore off. While performing the tests the patients were video recorded. The videos were observed by three movement disorder specialists who rated the symptoms using a treatment response scale (TRS), ranging from -3 (very off) to 3 (very dyskinetic). The sensor data consisted of lower limb data during leg agility, upper limb data during walking, and lower limb data during walking. Time series analysis was performed on the raw sensor data extracted from 17 patients to derive a set of quantitative measures, which were then used during machine learning to be mapped to mean ratings of the three raters on the TRS scale. Combinations of data were tested during the machine learning procedure.

    Results: Using data from both tests, the Support Vector Machines (SVM) could predict the motor states of the patients on the TRS scale with a good agreement in relation to the mean ratings of the three raters (correlation coefficient = 0.92, root mean square error = 0.42, p<0.001). Additionally, there was good test-retest reliability of the SVM scores during baseline and second tests with intraclass-correlation coefficient of 0.84. Sensitivity to treatment for SVM was good (Figure 1), indicating its ability to detect changes in motor symptoms. The upper limb data during walking was more informative than lower limb data during walking since SVMs had higher correlation coefficient to mean ratings.  

    Conclusions: The methodology demonstrates good validity, reliability, and sensitivity to treatment. This indicates that it could be useful for individualized optimization of treatments among PD patients, leading to an improvement in health-related quality of life.

    Fulltekst (pdf)
    Feasibility of a multi-sensor data fusion method for assessment of Parkinson’s disease motor symptoms
  • 4.
    Agvald, Per
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Adding, L. Christofer
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Nilsson, Kristofer F.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Gustafsson, Lars E.
    Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden.
    Linnarsson, Dag
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Increased expired NO and roles of CO2 and endogenous NO after venous gas embolism in rabbits2006Inngår i: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 97, nr 2, s. 210-215Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Venous gas embolism (VGE) is a feared complication in diving, aviation, surgery and trauma. We hypothesized that air emboli in the lung circulation might change expired nitric oxide (FeNO). A single intravenous infusion of air was given (100 mul kg(-1)) to three groups of anaesthetized mechanically ventilated rabbits: (A) one with intact NO production, (B) one with intact NO production and where end-tidal CO(2) was controlled, and (C) one with endogenous NO synthesis blockade (L: -NAME, 30 mg kg(-1)). Air infusions resulted in increased FeNO of the control group from 20 (4) [mean (SD)] ppb to a peak value of 39 (4) ppb within 5 min (P < 0.05), and FeNO was still significantly elevated [27 (2) ppb] after 20 min (P < 0.05). Parallel to the NO increase there were significant decreases in end-tidal CO(2 )(ETCO(2)) and mean arterial pressure and an increase in insufflation pressure. In group B, when CO(2) was supplemented after air infusion, NO was suppressed (P = 0.033), but was still significantly elevated compared with pre-infusion control (P < 0.05). In group C, all animals died within 40 min of air infusion whereas all animals in the other groups were still alive at this time point. We conclude that venous air embolization increases FeNO, and that a part of this effect is due to the concomitant decrease in ETCO(2). Furthermore, an intact NO production may be critical for the tolerance to VGE. Finally, FeNO might have a potential in the diagnosis and monitoring of pulmonary gas embolism.

  • 5.
    Almon, Ricardo
    et al.
    Örebro universitet, Institutionen för klinisk medicin.
    Alvarez-Leon, Eva E.
    Engfeldt, Peter
    Örebro universitet, Institutionen för klinisk medicin.
    Serra-Majem, Lluis
    Magnuson, Anders
    Nilsson, Torbjörn K.
    Associations between lactase persistence and the metabolic syndrome: a Mendelian randomization study in the Canary Islands2009Konferansepaper (Fagfellevurdert)
  • 6.
    Almon, Ricardo
    et al.
    Örebro universitet, Institutionen för klinisk medicin.
    Alvarez-Leon, Eva E.
    Univ Las Palmas Gran Canaria, Fac Hlth Sci, Dept Clin Sci, Canary Isl, Spain; Hosp Insular Gran Canaria, Canarian Hlth Serv, Serv Prevent Med, Canary Isl, Spain.
    Engfeldt, Peter
    Örebro universitet, Institutionen för klinisk medicin.
    Serra-Majem, Lluis
    Univ Las Palmas Gran Canaria, Fac Hlth Sci, Dept Clin Sci, Canary Isl, Spain; Hosp Insular Gran Canaria, Canarian Hlth Serv, Serv Prevent Med, Canary Isl, Spain.
    Magnuson, Anders
    Örebro University hospital, Örebro, Sweden.
    Nilsson, Torbjörn K.
    Örebro University hospital, Örebro, Sweden.
    Associations between lactase persistence and the metabolic syndrome in a cross-sectional study in the Canary Islands2009Inngår i: European Journal of Nutrition, ISSN 1436-6207, E-ISSN 1436-6215, Vol. 49, nr 3, s. 141-146Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The single nucleotide polymorphism (SNP) LCT -13910 C>T, associated with genetically determined phenotypes of lactase persistence (LP) or non-persistence (LNP), was studied in relation to the metabolic syndrome (MS).

    AIim of the study: The aim was to determine if milk intake and MS are associated. We applied Mendelian randomization (MR). The SNP, LCT -13910 C>T, with the genotypes LP (TT/CT) and LNP (CC), was taken as a proxy for milk consumption.

    Methods: A representative sample of adults belonging to the Canary Islands Nutrition Survey (ENCA) in Spain aged 18-75 years (n = 551) was genotyped for the LCT -13910 C>T polymorphism. We used the International Diabetes Federation (IDF) criteria to define MS. RESULTS: 60% of the population was LP and 40% LNP. One hundred seven LP subjects (35.0%) and 53 LNP subjects (25.6%) showed MS (chi (2) = 5.04, p = 0.025). LP subjects showed a significantly higher odds ratio (OR) for MS than LNP subjects computed for the whole population: both the crude OR (1.56; 95% CI 1.06-2.31) and adjusted OR for sex, age, daily energy intake, physical activity and educational level (1.57; 95% CI 1.02-2.43). Adjusted OR for women with LP was 1.93; 95% CI 1.06-3.52.

    Conclusions: The T allele of the SNP might constitute a nutrigenetic factor increasing the susceptibility of LP subjects, especially women, to develop MS in the Canary Islands.

  • 7. Ambrosio, Fabrisia
    et al.
    Kadi, Fawzi
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Lexell, Jan
    Fitzgerald, G. Kelley
    Boninger, Michael L.
    Huard, Johnny
    The effect of muscle loading on skeletal muscle regenerative potential: an update of current research findings relating to aging and neuromuscular pathology2009Inngår i: American Journal of Physical Medicine & Rehabilitation, ISSN 0894-9115, E-ISSN 1537-7385, Vol. 88, nr 2, s. 145-155Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Skeletal muscle is a dynamic tissue with a remarkable ability to continuously respond to environmental stimuli. Among its adaptive responses is the widely investigated ability of skeletal muscle to regenerate after loading or injury or both. Although significant basic science efforts have been dedicated to better understand the underlying mechanism controlling skeletal muscle regeneration, there has been relatively little impact in the clinical approaches used to treat skeletal muscle injuries and wasting. The purpose of this review article is to provide an overview of the basic biology of satellite cell function in response to muscle loading and to relate these findings in the context of aging and neuromuscular pathology for the rehabilitation medicine specialist.

  • 8. Andersson, Christin
    et al.
    Blennow, Kaj
    Almkvist, Ove
    Andreasen, Niels
    Engfeldt, Peter
    Örebro universitet, Hälsoakademin.
    Johansson, Sven-Erik
    Lindau, Maria
    Eriksdotter-Jönhagen, Maria
    Increasing CSF phospho-tau levels during cognitive decline and progression to dementia2008Inngår i: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 29, nr 10, s. 1466-1473Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Little is known about longitudinal changes of cerebrospinal fluid (CSF) biomarkers during cognitive decline in neurodegenerative disease progression.

    OBJECTIVE: To investigate longitudinal changes in CSF biomarkers--total-tau (T-tau), phospho-tau (P-tau) and beta-amyloid (Abeta42)--during cognitive decline.

    METHODS: Forty memory clinic patients (47.5% females), aged 61.3+/-7.6 (S.D.) years, non-demented at baseline, underwent lumbar puncture and neuropsychological testing at two occasions. Baseline mean MMSE-score was 28.3+/-1.8. Patients were divided into three groups based on baseline memory functioning; severely impaired (SIM), moderately impaired (MIM) and no impairment (NIM).

    RESULTS: There was a significant increase in P-tau in the SIM-group during follow-up, while P-tau in MIM and NIM did not change. Eighty-three percent of the SIM-patients converted to dementia (80% AD), while most MIM- and NIM-patients remained non-demented. T-tau- and Abeta42-levels did not change in any of the memory groups during follow-up.

    CONCLUSION: Increasing P-tau levels during cognitive decline and conversion to dementia suggest that P-tau may be useful as a longitudinal marker of the neurodegenerative process.

  • 9.
    Anselmius, Johan
    et al.
    Örebro universitet, Hälsoakademin.
    Milton, Ludvig
    Örebro universitet, Hälsoakademin.
    Expand A Lung: Ett träningsverktyg för andningsmuskulaturen?2011Independent thesis Advanced level (degree of Master (One Year)), 10 poäng / 15 hpOppgave
    Abstract [sv]

     Abstrakt

     

    Syfte:

    Syftet var att undersöka om prestation och uthålligheten hade förbättrats vid användandet av Expand a lung.

     

    Metod:

    En intervention genomfördes på sju testpersoner (4 kvinnor & 3 män) som använde Expand a lung under fjorton dagar, som jämfördes mot en kontrollgrupp på fyra testpersoner (2 kvinnor & 2 män). Testpersonerna genomförde två tester, med en intervall på fjorton dagar. I undersökningen figurerade 4 kvinnor och 3 män (ålder: 22.7 ± 2, vikt: 68.5 ± 10, längd: 175.1 ± 8.5) i experimentgruppen. 2 kvinnor och 2 män (ålder: 22.5 ± 1.5, vikt: 69 ± 9, längd: 170.7 ± 5.5) ingick i kontrollgruppen. Hjärtfrekvens, respiratoriska kvoten och blodlaktat uppmättes med hjälp utav Jaeger Oxycon Pro och lungvolym (SVC & FEV1) uppmättes med hjälp av Spirare SPS 310.

     

    Resultat:

    Ingen signifikant skillnad existerade inom grupperna. Experimentgruppen: SVC före x 4.73, SVC efter x 4,77. FEV1 före x 4.31, FEV1 efter x 4.29, HF (vid OBLA) före x 156, HF efter 155, RQ (vid OBLA) före x 1.04, RQ efter 1.05. Kontrollgruppen: SVC före x 4.98, SVC efter x 4.95. FEV1 före 4.48, FEV1 efter x 4.49, HF (vid OBLA) före x 165, HF efter 163, RQ (vid OBLA) före x 0.99, RQ efter x 1.00. Det som gick att urskilja var att det fanns skillnader på individnivå.

     

    Diskussion:

    Vår undersökning visade ingen signifikant skillnad på gruppnivå efter 14 dagars användande av Expand a lung. Dock fanns det skillnader på individnivå. Detta resultat kan bland annat bero på för kort träningsperiod och för få deltagare. Om Expand a lung kan förbättra prestationen vid träning under längre tid kan vi inte uttala oss om utan krävs vidare forskning.

     

    Nyckelord:

    Expand a lung, andningsmuskulaturträning, laktat, lungvolym.

    Inledning:

    Det existerar träningsredskap som utlovar en ökning gällande prestation och uthållighet, i träningssammanhang, av människans andningsmuskulatur. Träningsredskapen isolerade träningen till att bara sätta andningsmuskulaturen i arbete. Expand a lung var en av dessa nya, mer obeprövade, träningsredskap som utlovade en förbättrad prestation och uthållighet vid ett frekvent användande. Samtidigt visade en befintlig del av forskning att det indirekt inte gick att träna andningsmuskulaturen. Vi påträffade aldrig granskade vetenskaplig forskning som kunde fastställa vad Expand a lung utlovade.

  • 10.
    Appelberg, Jonas
    et al.
    Department of Clinical Physiology, Sundsvall Hospital, Sundsvall, Sweden.
    Janson, Christer
    Department of Medical Sciences: Respiratory Medicine and Allergology, Uppsala University, Uppsala, Sweden.
    Lindberg, Eva
    Department of Medical Sciences: Respiratory Medicine and Allergology, Uppsala University, Uppsala, Sweden.
    Pavlenko, Tatjana
    Department of Statistics, Stockholm University, Stockholm, Sweden.
    Hedenstierna, Göran
    Department of Medical Sciences: Clinical Physiology, Uppsala University, Uppsala, Sweden.
    Lung aeration during sleep in patients with obstructive sleep apnoea2010Inngår i: Clinical Physiology and Functional Imaging, ISSN 1475-0961, E-ISSN 1475-097X, Vol. 30, nr 4, s. 301-307Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Previous studies have indicated that patients with obstructive sleep apnoea (OSA) have altered ventilation and lung volumes awake and the results suggest that this may be a determinant of severity of desaturations during sleep. However, little is known about regional lung aeration during sleep in patients with OSA.

    Methods: Twelve patients with OSA were included in the study. Computed tomography was used to study regional lung aeration during wakefulness and sleep. Lung aeration was calculated in ml gas/g lung tissue in four different regions of interest (ROI(1-4)), along the border of the lung from ventral to dorsal.

    Results: Lung aeration in the dorsal (dependent) lung region (ROI(4)) was lower during sleep compared to wakefulness 0.78 +/- 0.19 versus 0.88 +/- 0.19 (mean +/- SD) ml gas/g lung tissue (P = 0.005). Associations were found between awake expiratory reserve volume and change in lung aeration from wakefulness to sleep in ROI(4) (r = -0.69; P = 0.012). In addition, the change in lung aeration in the dorsal region correlated to sleep time (r = 0.69; P = 0.014) but not to time in supine position. The difference in lung aeration between inspiration and expiration (i.e. ventilation), was larger in the ventral lung region when expressed as ml gas per g lung tissue. In two patients it was noted that, during on-going obstructive apnoea, lung aeration tended to be increased rather than decreased.

    Conclusions: Aeration in the dorsal lung region is reduced during sleep in patients with OSA. The decrease is related to lung volume awake and to sleep time.

  • 11. Appelberg, Jonas
    et al.
    Lindberg, -
    Snarkning och obstruktivt sömnapnésyndrom2010Inngår i: Sömn och sömnstörningar / [ed] Jan Ulfberg, Nora: Circad bok , 2010Kapittel i bok, del av antologi (Annet vitenskapelig)
  • 12.
    Arinell, Karin
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Cardiology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden; Acute Internal Medicine, Centralsjukhuset, Karlstad, Sweden.
    Blanc, Stéphane
    CNRS UMR 7178, Institut Pluridisciplinaire Hubert Curien, Université de Strasbourg, Strasbourg, France.
    Welinder, Karen Gjesing
    Department of Chemistry and Bioscience, Aalborg University, Aalborg, Denmark.
    Støen, Ole Gunnar
    Norwegian Institute for Nature Research, Trondheim, Norway.
    Evans, Alina L.
    Department of Forestry and Wildlife Management, Inland Norway University of Applied Sciences, Koppang, Norway.
    Fröbert, Ole
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Cardiology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Physical inactivity and platelet function in humans and brown bears: A comparative study2018Inngår i: Platelets, ISSN 0953-7104, E-ISSN 1369-1635, Vol. 29, nr 1, s. 87-90Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Physical inactivity increases the risk of thromboembolism. However, good standardized human models on inactivity are in short supply and experimental models are few.

    Our objective was to investigate how standardized bed rest affects platelet aggregation in humans and to investigate if aggregation is altered in a translational model system - the hibernating brown bear (Ursus arctos). We collected blood from (1) healthy male volunteers participating in a 21-day bed rest study in head-down tilt position (-6°) 24 h a day; (2) free-ranging brown bears captured during winter hibernation and again during active state in summer. We analyzed platelet function using multiple electrode platelet aggregometry. In total, 9 healthy male volunteers (age 31.0 ± 6.4 years) and 13 brown bears (7 females and 6 males, age 2.8 ± 0.6 years) were included. In hibernating bears adenosine diphosphate, arachidonic acid, thrombin receptor activating peptide, and collagen impedance aggregometry tests were all halved compared to summer active state. In human volunteers no statistically significant changes were found between baseline and the end of bed rest. In human male volunteers 3 weeks of bed rest did not affect platelet function. In hibernating brown bears platelet aggregation was halved compared to summer and we hypothesize that this is a protective measure to avoid formation of thrombi under periods of low blood flow.

  • 13.
    Aronson, D.
    et al.
    Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
    Wojtaszewski, J.
    Copenhagen Muscle Research Center, August Krogh Institute, University of Copenhagen, Copenhagen, Denmark.
    Thorell, A.
    Department of Surgery, Karolinska Hospital and Institute, Stockholm, Sweden.
    Nygren, J.
    Department of Surgery, Karolinska Hospital and Institute, Stockholm, Sweden.
    Zangen, A.
    Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
    Richter, E. A.
    Copenhagen Muscle Research Center, August Krogh Institute, University of Copenhagen, Copenhagen, Denmark.
    Ljungqvist, Olle
    Department of Surgery, Karolinska Hospital and Institute, Stockholm, Sweden.
    Fielding, R. A.
    Department of Health Sciences, Sargent Coll. All. Hlth. Professions, Boston University, Boston, MA , United States.
    Goodyear, L. J.
    Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA; Joslin Diabetes Center, One Joslin Place, Boston, MA, United States.
    Extracellular-regulated protein kinase cascades are activated in response to injury in human skeletal muscle1998Inngår i: American Journal of Physiology, ISSN 0002-9513, E-ISSN 2163-5773, Vol. 275, nr 2, s. C555-C561Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The mitogen-activated protein (MAP) kinase signaling pathways are believed to act as critical signal transducers between stress stimuli and transcriptional responses in mammalian cells. However, it is not known whether these signaling cascades also participate in the response to injury in human tissues. To determine whether injury to the vastus lateralis muscle activates MAP kinase signaling in human subjects, two needle biopsies or open muscle biopsies were taken from the same incision site 30-60 min apart. The muscle biopsy procedures resulted in striking increases in dual phosphorylation of the extracellular-regulated kinases (ERK1 and ERK2) and in activity of the downstream substrate, the p90 ribosomal S6 kinase. Raf-1 kinase and MAP kinase kinase, upstream activators of ERK, were also markedly stimulated in all subjects. In addition, c-Jun NH2-terminal kinase and p38 kinase, components of two parallel MAP kinase pathways, were activated following muscle injury. The stimulation of the three MAP kinase cascades was present only in the immediate vicinity of the injury, a finding consistent with a local rather than systemic activation of these signaling cascades in response to injury. These data demonstrate that muscle injury induces the stimulation of the three MAP kinase cascades in human skeletal muscle, suggesting a physiological relevance of these protein kinases in the immediate response to tissue injury and possibly in the initiation of wound healing.

  • 14.
    Arvidsson Lindvall, Mialinn
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper. University Health Care Research Centre, Region Örebro County, Örebro, Sweden.
    Anderzen-Carlsson, Agneta
    Örebro universitet, Institutionen för hälsovetenskaper. Region Örebro län. University Health Care Research Centre, Region Örebro County, Örebro, Sweden; Faculty of Health, Science, and Technology, Department of Health Sciences, Nursing, Karlstad University, Karlstad, Sweden.
    Appelros, Peter
    Faculty of Health, Science, and Technology, Department of Health Sciences, Nursing, Karlstad University, Karlstad, Sweden.
    Forsberg, Anette
    Örebro universitet, Institutionen för hälsovetenskaper. Region Örebro län. Department of Physiotherapy.
    Validity and test-retest reliability of the six-spot step test in persons after stroke2020Inngår i: Physiotherapy Theory and Practice, ISSN 0959-3985, E-ISSN 1532-5040, Vol. 36, nr 1, s. 211-218Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND AND PURPOSE: After stroke, asymmetric weight distribution is common with decreased balance control in standing and walking. The six-spot step test (SSST) includes a 5-m walk during which one leg shoves wooden blocks out of circles marked on the floor, thus assessing the ability to take load on each leg. The aim of the present study was to investigate the convergent and discriminant validity and test-retest reliability of the SSST in persons with stroke.

    METHODS: Eighty-one participants were included. A cross-sectional study was performed, in which the SSST was conducted twice, 3-7 days apart. Validity was investigated using measures of dynamic balance and walking. Reliability was assessed using intraclass correlation coefficient, standard error of the measurement (SEM), and smallest real difference (SRD).

    RESULTS: The convergent validity was strong to moderate, and the test-retest reliability was good. The SEM% was 14.7%, and the SRD% was 40.8% based on the mean of four walks shoving twice with the paretic and twice with the non-paretic leg.

    CONCLUSION: Values on random measurement error were high affecting the use of the SSST for follow-up evaluations but the SSST can be a complementary measure of gait and balance.

  • 15. Balagopal, P.
    et al.
    Ljungqvist, Olle
    Dept. of Surgery, Karolinska Institute and Hospital, Stockholm, Sweden.
    Nair, K. S.
    Endocrine Research Unit, Mayo Clinic and Foundation, Rochester, MN, United States.
    Skeletal muscle heavy-chain synthesis rate in healthy humans1997Inngår i: American Journal of Physiology, ISSN 0002-9513, E-ISSN 2163-5773, Vol. 272, nr 1, s. 45-50Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Mixed muscle protein synthetic rate has been measured in humans. These measurements represent the average of synthetic rates of all muscle proteins with variable rates. We determined to what extent the synthesis rate of mixed muscle protein in humans reflects that of myosin heavy chain (MHC), the main contractile protein responsible for the conversion of ATP to mechanical energy as muscle contraction. Fractional synthetic rates of MHC and mixed muscle protein were measured from the increment of [C-13]leucine in these proteins in vastus lateralis biopsy samples taken at 5 and 10 h during a primed continuous infusion of L-[1-C-13]leucine in 10 young healthy subjects. Calculations were done by use of plasma [C-13]ketoisocaproate (KIC) and muscle tissue fluid [C-13]leucine as surrogate measures of leucyl-tRNA. Fractional synthetic rate of MHC with plasma KIC (0.0299 +/- 0.0043%/h) and tissue fluid leucine (0.0443 +/- 0.0056%/h) were only 72 +/- 3% of that of mixed muscle protein (0.0408 +/- 0.0032 and 0.0603 +/- 0.0059%/h, respectively, with KIC and tissue fluid leucine). Contribution of MHC (7 +/- 1 mg . kg(-1) . h(-1)) to synthetic rates of whole body mixed muscle protein (36 +/- 5 mg . kg(-1) . h(-1)) and whole body protein (127 +/- 4 mg . kg(-1) . h(-1)) is only 18 +/- 1 and 5 +/- 1%, respectively. This relatively low contribution of MHC to whole body and mixed muscle protein synthesis warrants direct measurement of synthesis rate of MHC in conditions involving abnormalities of muscle contractile function.

  • 16.
    Bankole, Landry-Cyrille
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. University of Lyon, Saint- Etienne, France; University Hospital of Saint-Etienne, Saint- Etienne, France.
    Feasson, Leonard
    University of Lyon, Saint- Etienne, France; University Hospital of Saint-Etienne, Saint- Etienne, France.
    Ponsot, Elodie
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Kadi, Fawzi
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fibre type-specific satellite cell content in two models of muscle disease2013Inngår i: Histopathology, ISSN 0309-0167, E-ISSN 1365-2559, Vol. 63, nr 6, s. 826-832Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Aims: Muscle satellite cells (SCs) are responsible for the regenerative events following muscle fibre injury. This study aimed to improve our understanding of SC behaviour in two models of muscle disorder with different pathological mechanisms and onset of disease.

    Methods and results: Pax7(+)SC content was assessed in types I and II fibres of patients with Duchenne muscular dystrophy (DMD; n=9; age 132years), polymyositis/dermatomyositis (PM/DM; n=9; age 52 +/- 12years) and in controls (n=5; age 26 +/- 5years). Pax7(+)SCs number in type I and II fibres was higher (P<0.05) in DMD and in PM/DM compared to controls. Type I fibres were associated with a higher number of Pax7(+)SCs compared to type II fibres only in DMD; Pax7(+)SCs number in type I fibres was about threefold higher in DMD compared to PM/DM (P<0.05). In DMD, Pax7(+)SC content in small regenerating fibres (0.09 +/- 0.09 SCs/fibre) was similar to that in fibres from healthy skeletal muscle. The proportion of activated SCs (Ki-67(+)SCs) was fivefold lower in DMD (0.4 +/- 0.4%) compared to PM/DM (2.8 +/- 2%). Pax7(+) cells located outside the basal lamina were observed in DMD muscles only.

    Conclusion: The capacity to generate new SCs is increased even in severely impaired muscles and a fibre type-specific enhancement of SC occurs in type I muscle fibres in DMD.

  • 17.
    Bark, Tor
    et al.
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Katouli, Mohammad
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Möllby, R.
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Svenberg, Torgny E.
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Glutamine supplementation does not prevent bacterial translocation after non-lethal haemorrhage in rats1995Inngår i: European Journal of Surgery, ISSN 1102-4151, E-ISSN 1741-9271, Vol. 161, nr 1, s. 3-8Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE:

    To find out whether supplementation of an enteral diet with glutamine would reduce translocation of bacteria to mesenteric lymph nodes or blood after major haemorrhage in rats.

    DESIGN:

    Open randomised study.

    SETTING:

    University departments of surgery and microbiology, Sweden.

    MATERIAL:

    49 Sprague-Dawley rats.

    INTERVENTIONS:

    Rats were fed enterally for 7 days on diets supplemented with either glutamine or an isonitrogenous amount of non-essential amino acids. After feeding, 8 experimental and 8 control rats underwent sham operation; 9 and 7, respectively, underwent moderate haemorrhage (to 65 mm Hg); and 9 and 8, respectively, underwent severe haemorrhage (50 mm Hg) without reinfusion.

    MAIN OUTCOME MEASURES:

    Microbiological analyses of samples of blood and mesenteric lymph nodes taken 24 hours after haemorrhage.

    RESULTS:

    The median (interquartile) number of colony forming units/mesenteric lymph nodes after moderate haemorrhage in animals who were given glutamine supplementation was 11 (0-34) and in control animals 20 (0-178). After severe haemorrhage the corresponding figures were 199 (10-310) and 22 (0-187). No pathogens were isolated from blood cultures.

    CONCLUSION:

    Glutamine supplementation before haemorrhage did not reduce bacterial translocation to mesenteric lymph nodes in this rat model.

  • 18.
    Bark, Tor
    et al.
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Katouli, Mohammad
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Svenberg, Torgny E.
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Food deprivation increases bacterial translocation after non-lethal haemorrhage in rats1995Inngår i: European Journal of Surgery, ISSN 1102-4151, E-ISSN 1741-9271, Vol. 161, nr 2, s. 67-71Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE:

    To investigate whether brief fasting before the induction of hypotension by non-lethal haemorrhage may induce translocation of enteric bacteria to mesenteric lymph nodes or blood in rats.

    DESIGN:

    Laboratory experiment.

    SETTING:

    University departments of surgery and microbiology, Sweden.

    MATERIAL:

    39 Male Sprague-Dawley rats.

    INTERVENTIONS:

    20 animals were fasted for 24 hours, all 39 then underwent controlled haemorrhage for 60 minutes that reduced the blood pressure to 55 mm Hg.

    MAIN OUTCOME MEASURES:

    Differences in blood loss, blood glucose concentrations, and packed cell volume; and aerobic cultures of mesenteric lymph nodes and blood.

    RESULTS:

    Fasted rats (n = 20) lost 2.3% of blood volume compared with 2.8% in fed rats(p < 0.001). Packed cell volume dropped by 11.3% in fasted rats and 16.5% in fed rats (p < 0.001). Glucose concentrations rose by 7.0 mmol/l in fasted rats compared with 21.0 mmol/l in fed rats (p < 0.001). Mesenteric lymph nodes contained enteric bacteria in 14/20 fasted rats compared with 6/19 fed rats (p < 0.05). In 4 fasted rats blood cultures grew pathogenic bacteria compared with no fed rats (p = 0.11). The number of bacteria found in mesenteric lymph nodes was significantly greater in fasted than in fed rats (p = 0.01).

    CONCLUSIONS:

    Brief fasting before hypotension caused by non-lethal haemorrhage was associated with significantly increased bacterial translocation compared with fed animals. Increases in blood glucose concentrations and plasma refill may have had a protective effect in fed rats. These experiments may be of clinical relevance as elective operations are usually preceded by overnight fasting.

  • 19.
    Bass, Joseph J.
    et al.
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    Kazi, Abid A.
    Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, United States of America.
    Deane, Colleen S.
    Department of Sport and Health Sciences, University of Exeter, Exeter, UK; Living Systems Institute, University of Exeter, Stocker Road, Exeter, UK.
    Nakhuda, Asif
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    Ashcroft, Stephen P.
    School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham, UK.
    Brook, Matthew S.
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    Wilkinson, Daniel J.
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    Phillips, Bethan E.
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    Philp, Andrew
    School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham, UK; Mitochondrial Metabolism & Ageing Laboratory, Diabetes and Metabolism Division, Garvan Institute of Medical Research, Sydney, Australia; St Vincent's Medical School, UNSW Medicine, UNSW Sydney, Sydney, Australia.
    Tarum, Janelle
    School of Health Sciences, Örebro University, Örebro, Sweden.
    Kadi, Fawzi
    Örebro universitet, Institutionen för hälsovetenskaper.
    Andersen, Ditte
    Molecular Physiology of Diabetes Laboratory, Dept. of Comparative Biomedical Sciences, Royal Veterinary College, UK.
    Garcia, Amadeo Muñoz
    Institute of Metabolism and Systems Research, The University of Birmingham, Birmingham, UK; Department of Bioinformatics - BiGCaT, NUTRIM School of Nutrition and Metabolism in Translational Research, Maastricht University, Maastricht, The Netherlands.
    Smith, Ken
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    Gallagher, Iain J.
    Physiology, Exercise and Nutrition Research Group, Faculty of Health Sciences and Sport, University of Stirling, Stirling, UK.
    Szewczyk, Nathaniel J.
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    Cleasby, Mark E.
    Molecular Physiology of Diabetes Laboratory, Dept. of Comparative Biomedical Sciences, Royal Veterinary College, UK.
    Atherton, Philip J.
    MRC/ARUK Centre for Musculoskeletal Ageing Research and National Institute for Health Research (NIHR), Nottingham Biomedical Research Centre (BRC), School of Medicine, University of Nottingham, Nottingham, UK.
    The mechanisms of skeletal muscle atrophy in response to transient knockdown of the vitamin D receptor in vivo2021Inngår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 599, nr 3, s. 963-979Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    KEY POINTS:

    • Reduced vitamin D receptor (VDR) expression prompts skeletal muscle atrophy.
    • Atrophy occurs through catabolic processes, namely the induction of autophagy, while anabolism remains unchanged.
    • In response to VDR-KD mitochondrial function and related gene-set expression is impaired.
    • In vitro VDR knockdown induces myogenic dysregulation occurring through impaired differentiation.
    • These results highlight the autonomous role the VDR has within skeletal muscle mass regulation.

    Objective: Vitamin-D deficiency is estimated to affect ∼40% of the world's population and has been associated with impaired muscle maintenance. Vitamin-D exerts its actions through the Vitamin-D-receptor (VDR), the expression of which was recently confirmed in skeletal muscle, and its down-regulation is linked to reduced muscle mass and functional decline. To identify potential mechanisms underlying muscle atrophy, we studied the impact of VDR knockdown (KD) on mature skeletal muscle in vivo, and myogenic regulation in vitro in C2C12 cells.

    Methods: Male Wistar rats underwent in vivo electrotransfer (IVE) to knock down the VDR in hind-limb tibialis anterior (TA) muscle for 10 days. Comprehensive metabolic and physiological analysis was undertaken to define the influence loss of the VDR on muscle fibre composition, protein synthesis, anabolic and catabolic signalling, mitochondrial phenotype, and gene expression. Finally, in vitro lentiviral transfection was used to induce sustained VDR-KD in C2C12 cells to analyse myogenic regulation.

    Results: Muscle VDR-KD elicited atrophy through a reduction in total protein content, resulting in lower myofibre area. Activation of autophagic processes was observed, with no effect upon muscle protein synthesis or anabolic signalling. Furthermore, RNA-Seq analysis identified systematic down-regulation of multiple mitochondrial respiration related protein and genesets. Finally, in vitro VDR-knockdown impaired myogenesis (cell cycling, differentiation and myotube formation).

    Conclusion: Taken together, these data indicate a fundamental regulatory role of the VDR in the regulation of myogenesis and muscle mass; whereby it acts to maintain muscle mitochondrial function and limit autophagy.

  • 20. Bigard, X.
    et al.
    Chaillou, Thomas
    Université Grenoble Alpes, Saint-Martin-d'Heres, France .
    Sanchez, H.
    Malgoyre, A.
    Koulmann, N,
    How to build high oxidative skeletal muscle?: Interaction between energy stress and muscle growth2010Konferansepaper (Fagfellevurdert)
  • 21.
    Biratu, Maria
    Örebro universitet, Hälsoakademin.
    Jämförelse av lungfunktion, VO2max och muskelstyrka mellan rökare och icke-rökare. 2010Independent thesis Basic level (professional degree), 10 poäng / 15 hpOppgave
    Abstract [sv]

    Nikotin är världens tredje mest använda drog efter koffein och alkohol. Rökning utgör en av de absolut främsta orsakerna till en för tidig död i hela världen. Minst 10 000 svenskar dör varje år i förtid på grund av rökning. Syftet med denna studie var att jämföra skillnaden i lungfunktion, muskelstyrka och arbetsförmåga mellan rökare och icke-rökare. Till studien rekryterades totalt 20 frivilliga försökspersoner i åldrarna 27-56 år varav 10 var rökare och 10 icke-rökare. Mätning av lungfunktion genomfördes med en spirometer, där både VC och flöde-volym mätningar (FEV1, FEV % och PEF) registrerades. Muskelstyrkan mättes med en handdynamometer. Vid mätning av VO2max fick deltagarna utföra ett maxtest på en ergometercykel som kopplades till mätutrustningen Oxycon Pro-Jaeger. Resultatet visade att det fanns skillnad i lungfunktion mellan rökare och icke-rökare. VC, FEV1, FEV % och PEF var signifikant lägre hos rökare jämfört med icke-rökare (p < 0.05). Eftersom de flesta av testpersonerna inte uppnådde sitt VO2max användes istället peak VO2 vid jämförelsen. Det fanns ingen signifikant skillnad i peak VO2 och handstyrka mellan rökare och icke-rökare (p= 0.40 respektive 0.38). Det förelåg en signifikant korrelation mellan FEV1 och peak VO2 hos alla deltagare (p=0.0042). Däremot fanns det ingen korrelation mellan FEV1 och handstyrkan (p=0.579). Denna studie visar på att rökning påverkar lungfunktionen, att rökare har lägre lungfunktion än icke-rökare. Muskelstyrkan och arbetskapaciteten mätt som peak VO2 skiljde sig inte åt mellan rökare och icke-rökare men det krävs ett större testmaterial för att kunna dra några säkra slutsatser.

    Fulltekst (pdf)
    FULLTEXT02
  • 22.
    Boersma, Katja
    et al.
    Örebro universitet, Institutionen för juridik, psykologi och socialt arbete.
    Flink, Ida
    Örebro universitet, Institutionen för juridik, psykologi och socialt arbete.
    Linton, Steven J.
    Örebro universitet, Institutionen för juridik, psykologi och socialt arbete.
    Considering the interpersonal context of pain catastrophizing2019Inngår i: Scandinavian Journal of Pain, ISSN 1877-8860, E-ISSN 1877-8879, Vol. 20, nr 1, s. 9-10Artikkel i tidsskrift (Fagfellevurdert)
  • 23.
    Boija, Per Olov
    et al.
    Department. of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro universitet, Institutionen för medicinska vetenskaper. Department. of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Nylander, Gunnar
    Department. of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Ware, James
    Department. of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Hypovolaemic stress induced glycogenolysis, isolated liver perfusion study1987Inngår i: Research in experimental medicine, ISSN 0300-9130, E-ISSN 1433-8580, Vol. 187, nr 5, s. 315-322Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Intrinsic hepatic glycogenolysis was examined after hypovolemic stress. Hemorrhagic hypotension of 70 (P70) and 40 mm Hg (P40) for 60 min was inflicted for two postprandial groups and of 70 mm Hg (S70) in a 24-h starved group. The results were compared with three control groups; one postprandial (Pc), one 24-h starved (Sc), and one starved for 9 h (Sc: 9) to mimic the glycogen depletion produced by 70 mm Hg hemorrhagic hypotension. Glucose output was studied in vitro using av recirculating isolated liver perfusion system with a perfusate free of glucose and endocrine stimulation. Liver glycogen determination was made before perfusion start. Although the glycogen stores were decreased after hemorrhage glucose yield was increased (P70) and unchanged (P40) as compared to controls (Pc and Sc: 9). Both starved groups delivered small amounts of glucose, but the released fraction of the S70 group was more than twice that from the Sc group. These data suggest a liver enzyme activation with increased velocity of the enzymesubstrate reactions responsible for glycogen degradation, induced during in vivo hemorrhage and persisting for at least 30 min in vitro perfusion.

  • 24.
    Burgess, G.M.
    et al.
    Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
    Dooley, R.K.
    Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
    McKinney, J.S.
    Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
    Nånberg, Eewa
    Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
    Putney, J.W.
    Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
    Further studies on the interactions between the calcium mobilization and cyclic AMP pathways in guinea pig hepatocytes1986Inngår i: Molecular Pharmacology, ISSN 0026-895X, E-ISSN 1521-0111, Vol. 30, nr 4, s. 315-320Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Isoproterenol (50 nM) potentiated the effects of angiotensin (1-50 nM) on 86Rb efflux and 45Ca efflux from guinea pig hepatocytes. This effect occurred in the presence or absence of extracellular Ca2+ and required the simultaneous presence of both isoproterenol and angiotensin. Neither the divalent cationophore, A23187, nor 4 beta-phorbol dibutyrate could substitute for angiotensin. The effects of isoproterenol were greatest with submaximal concentrations of angiotensin, whereas maximal concentrations of angiotensin were affected little. Isoproterenol did not substantially increase the formation of [3H]inositol triphosphate or the ratio of isomers [3H]inositol 1,4,5-trisphosphate and [3H]inositol 1,3,4-trisphosphate formed in response to angiotensin. Isoproterenol also enhanced the phase of Ca2+ mobilization involving Ca2+ entry which is consistent with the previously proposed functional linkage between receptor-regulated Ca2+ release and Ca2+ entry. These findings suggest that isoproterenol may act by increasing the sensitivity of the endoplasmic reticulum to the Ca2+-releasing action of inositol 1,4,5-trisphosphate.

  • 25.
    Chaillou, Thomas
    Örebro universitet, Institutionen för hälsovetenskaper.
    Impaired ribosome biogenesis could contribute to anabolic resistance to strength exercise in the elderly2017Inngår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, nr 5, s. 1447-1448Artikkel, forskningsoversikt (Fagfellevurdert)
  • 26.
    Chaillou, Thomas
    Örebro universitet, Institutionen för hälsovetenskaper.
    Ribosome specialization and its potential role in the control of protein translation and skeletal muscle size2019Inngår i: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 127, nr 2, s. 599-607Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    The ribosome is typically viewed as a supramolecular complex with constitutive and invariant capacity in mediating translation of mRNA into protein. This view has been challenged by recent research revealing that ribosome composition could be heterogeneous, and this heterogeneity leads to functional ribosome specialization. This review presents the idea that ribosome heterogeneity results from changes in its various components, including variations in ribosomal protein (RP) composition, post-translational modifications of RPs, changes in ribosomal-associated proteins, alternative forms of rRNA and post-transcriptional modifications of rRNAs. Ribosome heterogeneity could be orchestrated at several levels and may depend on numerous factors, such as the subcellular location, cell type and tissue specificity, the development state, cell state, ribosome biogenesis, RP turnover, physiological stimuli and circadian rhythm. Ribosome specialization represents a completely new concept for the regulation of gene expression. Specialized ribosomes could modulate several aspects of translational control, such as mRNA translation selectivity, translation initiation, translational fidelity and translation elongation. Recent research indicates that the expression of Rpl3 is markedly increased, while that of Rpl3l is highly reduced during mouse skeletal muscle hypertrophy. Moreover, Rpl3l overexpression impairs the growth and myogenic fusion of myotubes. Although the function of Rpl3 and Rpl3l in the ribosome remains to be clarified, these findings suggest that ribosome specialization may be potentially involved in the control of protein translation and skeletal muscle size. Limited data concerning ribosome specialization are currently available in skeletal muscle. Future investigations have the potential to delineate the function of specialized ribosomes in skeletal muscle.

  • 27.
    Chaillou, Thomas
    Örebro universitet, Institutionen för hälsovetenskaper.
    Skeletal Muscle Fiber Type in Hypoxia: Adaptation to High-Altitude Exposure and Under Conditions of Pathological Hypoxia2018Inngår i: Frontiers in Physiology, E-ISSN 1664-042X, Vol. 9, artikkel-id 1450Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Skeletal muscle is able to modify its size, and its metabolic/contractile properties in response to a variety of stimuli, such as mechanical stress, neuronal activity, metabolic and hormonal influences, and environmental factors. A reduced oxygen availability, called hypoxia, has been proposed to inducemetabolic adaptations and loss ofmass in skeletal muscle. In addition, several evidences indicate that muscle fiber-type composition could be affected by hypoxia. The main purpose of this review is to explore the adaptation of skeletal muscle fiber-type composition to exposure to high altitude (ambient hypoxia) and under conditions of pathological hypoxia, including chronic obstructive pulmonary disease (COPD), chronic heart failure (CHF) and obstructive sleep apnea syndrome (OSAS). The muscle fiber-type composition of both adult animals and humans is not markedly altered during chronic exposure to high altitude. However, the fast-to-slow fiber-type transition observed in hind limb muscles during post-natal development is impaired in growing rats exposed to severe altitude. A slow-to-fast transition in fiber type is commonly found in lower limb muscles from patients with COPD and CHF, whereas a transition toward a slower fiber-type profile is often found in the diaphragm muscle in these two pathologies. A slow-to-fast transformation in fiber type is generally observed in the upper airway muscles in rodent models of OSAS. The factors potentially responsible for the adaptation of fiber type under these hypoxic conditions are also discussed in this review. The impaired locomotor activity most likely explains the changes in fiber type composition in growing rats exposed to severe altitude. Furthermore, chronic inactivity and muscle deconditioning could result in the slow-to-fast fiber-type conversion in lower limb muscles during COPD and CHF, while the factors responsible for the adaptation of muscle fiber type during OSAS remain hypothetical. Finally, the role played by cellular hypoxia, hypoxia-inducible factor-1 alpha (HIF-1 alpha), and other molecular regulators in the adaptation of muscle fiber-type composition is described in response to high altitude exposure and conditions of pathological hypoxia.

  • 28.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper.
    Cheng, Arthur
    Karolinska Institutet, Stockholm, Sweden.
    A dose of 5,000 km.h of severe hypoxia (at > 5,000 m altitude) is probably required to induce skeletal muscle wasting in humans2017Inngår i: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 122, nr 2, s. 410-410Artikkel i tidsskrift (Fagfellevurdert)
  • 29.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper.
    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 truth2019Inngår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 316, nr 5, s. R502-R503Artikkel i tidsskrift (Fagfellevurdert)
  • 30.
    Chaillou, Thomas
    et al.
    Karolinska Institute, Stockholm, Sweden.
    Hynynen, H.
    University of Eastern Finland, Joensuu, Finland.
    Ferreira, D.
    Karolinska Institute, Stockholm, Sweden.
    Pironti, G.
    Karolinska Institute, Stockholm, Sweden.
    Andersson, D.C.
    Karolinska Institute, Stockholm, Sweden.
    Ruas, J.
    Karolinska Institute, Stockholm, Sweden.
    Tavi, P.
    University of Eastern Finland, Joensuu, Finland.
    Lanner, J.T.
    Karolinska Institute, Stockholm, Sweden.
    The mitochondrial NDUFA4L2 protein: a novel modulator of skeletal muscle mass and force2016Konferansepaper (Fagfellevurdert)
  • 31.
    Chaillou, Thomas
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Hynynen, H
    University of Eastern Finland, Joensuu, Finland.
    Ferreira, D
    Karolinska Institutet, Stockholm, Sweden.
    Pironti, G
    Karolinska Institutet, Stockholm, Sweden.
    Kenne, E
    Karolinska Institutet, Stockholm, Sweden.
    Andersson, D C
    Karolinska Institutet, Stockholm, Sweden; Karolinska University Hospital, Stockholm, Sweden.
    Ruas, J L
    Karolinska Institutet, Stockholm, Sweden.
    Tavi, P
    University of Eastern Finland, Joensuu, Finland.
    Lanner, J T
    Karolinska Institutet, Stockholm, Sweden.
    NDUFA4L2: Connecting metabolic signals and mitochondrial function in cardiac and skeletal muscle2016Inngår i: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 100, nr Suppl., s. S186-S186Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The nuclear-encoded mitochondrial protein NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 (NDUFA4L2) was recently identified. NDUFAe4L2 is shown to be induced by hypoxia via HIF1α and is thought to inhibit production of mitochondrial reactive oxygen species in fibroblasts exposed to hypoxia. Here the aim was to characterize the role of NDUFA4L2 in the mitochondria-rich tissues skeletal and cardiac muscle. We show hypoxia induced NDUFA4L2 expression in isolated muscle fibers and in cardiomyocytes with full activation after ~3-6 h in hypoxia. The half-maximal O2 level for NDUFA4L2 expression (~4.6 % of ambient O2) suggests sensitivity to changes in O2 tension that occur under physiological conditions (e.g. exercise, moderate ischemia). We identified that the NDUFA4L2 gene promoter has binding sites for transcription factors other than HIF-1α; repetitive sites for PPARα,γ and one for Nrf2. NDUFA4L2 overexpression resulted in functional effects on skeletal and cardiac muscle; e.g. it alters cellular Ca2+ signaling and the expression of Ca2+ handling genes. Further, NDUFA4L2 overexpression reduces muscle mass (~20%), leading to a decreased force production in skeletal muscle. The NDUFA4L2-induced loss of muscle mass was associated with increases in mRNA levels of e.g. MurF1, Mul1, caspase-3 and Bax. Additionally, femoral artery ligation (FAL) induced NDUFA4L2 expression, which correlates with the decreased force production eight days post-FAL in skeletal muscle. Moreover, NDUFA4L2 upregulates antioxidant gene expression and silencing NDUFA4L2 makes cardiac cells less tolerant to hypoxia/re-oxygenation. Our results suggest that NDUFA4L2 expression affects vital functions in muscle cells and at least part of this effect is mediated by a link between NDUFA4L2 and nuclear gene expression. Thus, NDUFA4L2 might act as an integrator of the nutritional, environmental and functional status in muscle cells.

  • 32.
    Chaillou, Thomas
    et al.
    Karolinska Institute, Stockholm, Sweden.
    Ivarsson, N
    Mijwel, S
    Cheng, A
    Rundqvist, H
    Lanner, J
    Breast-cancer-induced muscle weakness: benefits of physical exercise to restore muscle function2015Konferansepaper (Fagfellevurdert)
  • 33.
    Chaillou, Thomas
    et al.
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
    Jackson, J.R.
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA; Department of Rehabilitation Sciences, College of Health Sciences, University of Kentucky, Lexington, Kentucky, USA.
    England, J.H.
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
    Kirby, T.J.
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA; Department of Rehabilitation Sciences, College of Health Sciences, University of Kentucky, Lexington, Kentucky, USA.
    Richards-White, J.
    Department of Rehabilitation Sciences, College of Health Sciences, University of Kentucky, Lexington, Kentucky, USA.
    Esser, K.A.
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
    Dupont-Versteegden, E.E.
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA; Department of Rehabilitation Sciences, College of Health Sciences, University of Kentucky, Lexington, Kentucky, USA.
    McCarthy, J.J.
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
    Identification of a conserved set of upregulated genes in mouse skeletal muscle hypertrophy and regrowth2015Inngår i: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 118, s. 86-97Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The purpose of this study was to compare the gene expression profile of mouse skeletal muscle undergoing two forms of growth (hypertrophy and regrowth) with the goal of identifying a conserved set of differentially expressed genes. Expression profiling by microarray was performed on the plantaris muscle subjected to 1, 3, 5, 7, 10, and 14 days of hypertrophy or regrowth following 2 wk of hind-limb suspension. We identified 97 differentially expressed genes (≥2-fold increase or ≥50% decrease compared with control muscle) that were conserved during the two forms of muscle growth. The vast majority (∼90%) of the differentially expressed genes was upregulated and occurred at a single time point (64 out of 86 genes), which most often was on the first day of the time course. Microarray analysis from the conserved upregulated genes showed a set of genes related to contractile apparatus and stress response at day 1, including three genes involved in mechanotransduction and four genes encoding heat shock proteins. Our analysis further identified three cell cycle-related genes at day and several genes associated with extracellular matrix (ECM) at both days 3 and 10. In conclusion, we have identified a core set of genes commonly upregulated in two forms of muscle growth that could play a role in the maintenance of sarcomere stability, ECM remodeling, cell proliferation, fast-to-slow fiber type transition, and the regulation of skeletal muscle growth. These findings suggest conserved regulatory mechanisms involved in the adaptation of skeletal muscle to increased mechanical loading.

  • 34. Chaillou, Thomas
    et al.
    Koulmann, N.
    Beaudry, M.
    Bigard, X.
    Molecular mechanisms involved in the muscle mass control2011Konferansepaper (Fagfellevurdert)
  • 35.
    Chaillou, Thomas
    et al.
    Département Environnements opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche, France.
    Koulmann, N.
    Département Environnements opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche, France; Ecole du Val-de-Grâce, Paris, France.
    Meunier, A.
    Département Environnements opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche, France.
    Malgoyre, A.
    Département Environnements opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche, France.
    Serrurier, B.
    Département Environnements opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche, France.
    Beaudry, M.
    Laboratoire Réponses cellulaires et fonctionnelles à l'hypoxie, Université Paris, Sorbonne-Paris-Cité, France.
    Bigard, X.
    Département Environnements opérationnels, Institut de Recherche Biomédicale des Armées Antenne de la Tronche, La Tronche, France; Ecole du Val-de-Grâce, Paris, France.
    Effect of hypoxia exposure on the phenotypic adaptation in remodelling skeletal muscle submitted to functional overload2013Inngår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 209, nr 4, s. 272-282Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Aim: To determine whether hypoxia influences the phenotypic adaptation of skeletal muscle induced by mechanical overload.

    Methods: Plantaris muscles of female rats were submitted to mechanical overload following synergist ablation. After 3 days of overload, rats were exposed to either hypobaric hypoxia (equivalent to 5500 m) or normoxia. Muscles were collected after 5, 12 and 56 days of overload (i.e. after 3, 9 and 53 days of hypoxia). We determined the myosin heavy chain (MHC) distribution, mRNA levels of myocyte-enriched calcineurin-integrating protein 1 (MCIP1) to indirectly assess calcineurin activity, the changes in oxidative capacity from the activities of citrate synthase (CS) and cytochrome c oxidase (COX), and the expression of regulators involved in mitochondrial biogenesis (Pgc-1α, NRF1 and Tfam) and degradation (BNIP-3).

    Results: Hypoxia did not alter the fast-to-slow MHC shift and the increase in calcineurin activity induced by overload; it only transiently slowed down the overload-induced transition in MHC isoforms. Hypoxia similarly decreased CS and COX activities in overloaded and control muscles. Nuclear respiratory factor 1 (NRF1) and transcription factor A (Tfam) mRNA and BNIP-3 protein were not influenced by hypoxia in overloaded muscles, whereas Pgc-1α mRNA and protein contents did not correlate with changes in oxidative capacity.

    Conclusion: Hypoxia is not a critical stimulus to modulate the fast-to-slow MHC transition associated with overload. Thus, the impairment of the fast-to-slow fibre shift often observed during post-natal development in hypoxia could be explained by the lower voluntary locomotor activity associated with hypoxia. Hypoxia alters mitochondrial oxidative capacity, but this adaptive response is similar in overloaded and control muscles.

  • 36.
    Chaillou, Thomas
    et al.
    Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées, Antenne de la Tronche, La Tronche, France; Center for Muscle Biology, Department of Physiology, University of Kentucky, Lexington KY, United States.
    Koulmann, N.
    Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées, Antenne de la Tronche, La Tronche, France; Ecole du Val-de-Grâce, Paris, France.
    Meunier, A.
    Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées, Antenne de la Tronche, La Tronche, France.
    Pugnière, P.
    Pôle Génomique, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    McCarthy, J.J.
    Center for Muscle Biology, Department of Physiology, University of Kentucky, Lexington KY, United States.
    Beaudry, M.
    Laboratoire Réponses Cellulaires et Fonctionnelles À l'Hypoxie, Sorbonne-Paris-Cité, Université Paris13, Paris, France.
    Bigard, X.
    Département Environnements Opérationnels, Institut de Recherche Biomédicale des Armées, Antenne de la Tronche, La Tronche, France; Ecole du Val-de-Grâce, Paris, France.
    Ambient hypoxia enhances the loss of muscle mass after extensive injury2014Inngår i: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 466, nr 3, s. 587-598Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Hypoxia induces a loss of skeletal muscle mass and alters myogenesis in vitro, but whether it affects muscle regeneration in vivo following injury remains to be elucidated. We hypothesized that hypoxia would impair the recovery of muscle mass during regeneration. To test this hypothesis, the soleus muscle of female rats was injured by notexin and allowed to recover for 3, 7, 14, and 28 days under normoxia or hypobaric hypoxia (5,500 m) conditions. Hypoxia impaired the formation and growth of new myofibers and enhanced the loss of muscle mass during the first 7 days of regeneration, but did not affect the final recovery of muscle mass at 28 days. The impaired regeneration under hypoxic conditions was associated with a blunted activation of mechanical target of rapamycin (mTOR) signaling as assessed by p70(S6K) and 4E-BP1 phosphorylation that was independent of Akt activation. The decrease in mTOR activity with hypoxia was consistent with the increase in AMP-activated protein kinase activity, but not related to the change in regulated in development and DNA response 1 protein content. Hypoxia increased the mRNA levels of the atrogene muscle ring finger-1 after 7 days of regeneration, though muscle atrophy F box transcript levels remained unchanged. The increase in MyoD and myogenin mRNA expression with regeneration was attenuated at 7 days with hypoxia. In conclusion, our results support the notion that the enhanced loss of muscle mass observed after 1 week of regeneration under hypoxic conditions could mainly result from the impaired formation and growth of new fibers resulting from a reduction in protein synthesis and satellite cell activity.

  • 37.
    Chaillou, Thomas
    et al.
    University of Grenoble, Grenoble, France.
    Koulmann, N.
    Simler, N.
    Meunier, A.
    Grégoire, C.
    Chapot, R.
    Serrurier, B.
    Beaudry, M.
    Bigard, X.
    Ambient hypoxia enhances the muscle-mass loss after extensive injury2011Konferansepaper (Fagfellevurdert)
  • 38.
    Chaillou, Thomas
    et al.
    Université Grenoble Alpes, Grenoble, France .
    Koulmann, N.
    Simler, N.
    Meunier, A.
    Grégoire, C.
    Serrurier, B.
    Beaudry, M.
    Bigard, X.
    Ambient hypoxia enhances the muscle-mass loss after extensive injury2011Inngår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 25, nr 1 Suppl.Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to examine the effect of ambient hypoxia on the main intracellular pathways involved in muscle regeneration. Left soleus muscles of female rats were degenerated by notexin injection before exposure to either normoxia (N) or ambient hypoxia (H) (10% O2) during 3, 7, 14 and 28 days (d). The expected muscle-mass loss of injured muscles was higher in H than in N rats at d3 and d7, whereas the recovery of muscle mass was similar in H and N rats at d28. The mammalian target of rapamycin (mTOR) activity, assessed from both eIF-4E binding protein (4E-BP1) and P70S6K phosphorylation, was markedly increased during the early period of regeneration, but remained two-fold lower in H than in N groups at d3. The hypoxia-induced alteration of mTOR activity, independently of Akt, was associated with an activation of AMP-activated kinase (AMPK) at d3. In contrast, REDD1, another negative regulator of mTOR, was markedly activated by H at d14 and d28 in intact muscles, but was blunted during the first days of regeneration (d3–7), independently of H. Taken together, we show for the first time, that hypoxia enhances the muscle-mass loss after extensive injury. This could be due to a specific impairment of mTOR activation during muscle regeneration, independently of Akt, at least partly related to AMPK activation, without detectable effect of REDD1.

  • 39.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper. 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 model2012Inngår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 302, s. R643-R654Artikkel i tidsskrift (Fagfellevurdert)
    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.

  • 40. Chaillou, Thomas
    et al.
    Koulmann, N.
    Simler, N.
    Serrurier, B.
    Meunier, A.
    Chapot, R.
    Peinnequin, A.
    Beaudry, M.
    Bigard, X.
    Ambient hypoxia transiently affects muscle growth in a functional overload model in rats2010Konferansepaper (Fagfellevurdert)
  • 41.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    McPeek, Ashley
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lanner, Johanna T.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Docetaxel does not impair skeletal muscle force production in a murine model of cancer chemotherapy2017Inngår i: Physiological Reports, E-ISSN 2051-817X, Vol. 5, nr 11, artikkel-id e13261Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Chemotherapy drugs such as docetaxel are commonly used to treat cancer. Cancer patients treated with chemotherapy experience decreased physical fitness, muscle weakness and fatigue. To date, it is unclear whether these symptoms result only from cancer-derived factors or from the combination of cancer disease and cancer treatments, such as chemotherapy. In this study, we aimed at determining the impact of chemotherapy per se on force production of hind limb muscles from healthy mice treated with docetaxel. We hypothesized that docetaxel will decrease maximal force, exacerbate the force decline during repeated contractions and impair recovery after fatiguing stimulations. We examined the function of soleus and extensor digitorum longus (EDL) muscles 24h and 72h after a single injection of docetaxel (acute treatment), and 7days after the third weekly injection of docetaxel (repeated treatment). Docetaxel was administrated by intravenous injection (20mg/kg) in female FVB/NRj mice and control mice were injected with saline solution. Our results show that neither acute nor repeated docetaxel treatment significantly alters force production during maximal contractions, repeated contractions or recovery. Only a tendency to decreased peak specific force was observed in soleus muscles 24h after a single injection of docetaxel (-17%, P=0.13). In conclusion, docetaxel administered intravenously does not impair force production in hind limb muscles from healthy mice. It remains to be clarified whether docetaxel, or other chemotherapy drugs, affect muscle function in subjects with cancer and whether the side effects associated with chemotherapy (neurotoxicity, central fatigue, decreased physical activity, etc.) are responsible for the experienced muscle weakness and fatigue.

  • 42.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper.
    Montiel Rojas, Diego
    Örebro universitet, Institutionen för hälsovetenskaper.
    Does the blunted stimulation of skeletal muscle protein synthesis by aging in response to mechanical load result from impaired ribosome biogenesis?2023Inngår i: Frontiers in aging, E-ISSN 2673-6217, Vol. 4, artikkel-id 1171850Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Age-related loss of skeletal muscle mass leads to a reduction of strength. It is likely due to an inadequate stimulation of muscle protein synthesis (MPS) in response to anabolic stimuli, such as mechanical load. Ribosome biogenesis is a major determinant of translational capacity and is essential for the control of muscle mass. This mini-review aims to put forth the hypothesis that ribosome biogenesis is impaired by aging in response to mechanical load, which could contribute to the age-related anabolic resistance and progressive muscle atrophy. Recent animal studies indicate that aging impedes muscle hypertrophic response to mechanical overload. This is associated with an impaired transcription of ribosomal DNA (rDNA) by RNA polymerase I (Pol I), a limited increase in total RNA concentration, a blunted activation of AKT/mTOR pathway, and an increased phosphorylation of AMPK. In contrast, an age-mediated impairment of ribosome biogenesis is unlikely in response to electrical stimulations. In human, the hypertrophic response to resistance exercise training is diminished with age. This is accompanied by a deficit in long-term MPS and an absence of increased total RNA concentration. The results addressing the acute response to resistance exercise suggest an impaired Pol I-mediated rDNA transcription and attenuated activation/expression of several upstream regulators of ribosome biogenesis in muscles from aged individuals. Altogether, emerging evidence indicates that impaired ribosome biogenesis could partly explain age-related anabolic resistance to mechanical load, which may ultimately contribute to progressive muscle atrophy. Future research should develop more advanced molecular tools to provide in-depth analysis of muscle ribosome biogenesis.

  • 43.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper.
    Sanna, Igor
    Department of Health Sciences, Örebro University, Örebro, Sweden.
    Kadi, Fawzi
    Örebro universitet, Institutionen för hälsovetenskaper.
    Glutamine-stimulated in vitro hypertrophy is preserved in muscle cells from older women2020Inngår i: Mechanisms of Ageing and Development, ISSN 0047-6374, E-ISSN 1872-6216, Vol. 187, artikkel-id 111228Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Age-related loss of muscle mass may result from reduced protein synthesis stimulation in response to anabolic stimuli, such as amino acid (AA) supplementation. The exact etiology of anabolic resistance to AA remains unclear. Therefore, the aim of this study was to investigate the anabolic response [cell size, protein synthesis and mechanistic target of rapamycin (mTOR) pathway] to the AA glutamine (a strong anabolic AA highly present in skeletal muscle) in myotubes obtained from 8 young (YW; 21-35 yrs) and 8 older (OW; 65-70 yrs) healthy women. This in vitro model of human primary myogenic cells explores the intrinsic behavior of muscle cells, while excluding potential influences of external factors. We showed that despite lower muscle mass, strength and cardiorespiratory fitness in OW compared to YW, myotube size (myotube diameter and area) and protein synthesis were not altered in OW, and glutamine-induced myotube hypertrophy and protein synthesis were preserved in OW. Apart from a lower glutamine-induced increase in P70S6 kinase phosphorylation in OW, no significant differences in other components of the mTOR pathway were observed between groups. Altogether, our data support the idea that the intrinsic capacity of muscle cells to respond to glutamine stimulation is preserved in healthy older women.

  • 44.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper.
    Treigyte, Viktorija
    Sports Science and Innovation Institute, Lithuanian Sports University, Kaunas, Lithuania.
    Cold water immersion puts the chill on muscle protein synthesis after resistance exercise2020Inngår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 598, nr 6, s. 1123-1124Artikkel i tidsskrift (Fagfellevurdert)
  • 45.
    Chaillou, Thomas
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper.
    Treigyte, Viktorija
    Eimantas, Nerijus
    Venckunas, Tomas
    Brazaitis, Marius
    Impact of acute and prolonged cooling on skeletal muscle force in young males2022Konferansepaper (Fagfellevurdert)
    Abstract [en]

    Introduction

    In athletes, exposure to cold during winter sports may impair physical performance. Severe muscle cooling appears to reduce maximal force and induces a shift towards a slower contractile profile. However, whether moderate muscle cooling and the duration of cooling affect muscle contractile profile (assessed from electrically evoked torque at low and high frequencies) and maximal voluntary force (isometric and isokinetic contractions) remains to be clarified. Therefore, the aim of this study was to investigate the impact of acute and prolonged cooling on electrically evoked torque and maximal voluntary contraction torque in young males. 

    Methods

    Twelve active males (27.2 ± 6.6 years old) were recruited for this study, consisting of 2 phases: acute and prolonged exposures. During each phase, participants were randomly exposed to cold water immersion (CWI, 10°C, up to the iliac crest) or passive resting (PR). Exposure to CWI was either continuous during 45min (acute CWI, A-CWI) or intermittent during a period of 300min [prolonged CWI (P-CWI) including immersions between baseline to 45min, 165 to 180min, and 255 to 270min]. Muscle (Tmu, average across 1, 2 and 3cm depth) and rectal (Trec) temperatures were assessed using thermo-sensors. Transcutaneous electrical stimulation of the quadriceps muscle was performed to determine torques at low (20 Hz: P20) and high (100 Hz: P100) frequencies, and P20/P100 ratio was calculated. Maximal voluntary isometric torque of the knee extensors (MVIC), as well as peak isokinetic torques (90°/s) of knee extensors (KE-IsoC) and flexors (KF-isoC) were determined. Neuromuscular tests were performed at baseline (BL) and 60min after BL during acute exposure, and at BL, 60, 90, 150 and 300min after BL during prolonged exposure.

    Results

    Trec did not change after A-CWI while it was reduced (0.8 ± 0.4°C, p<0.001) after P-CWI compared to BL. Tmu decreased during A-CWI and P-CWI compared to BL (6.1 ± 2.2°C and 4.6 ± 1.1°C, respectively, p<0.001), with larger reduction of Tmu after A-CWI than P-CWI (p<0.05). P20 was not affected by the conditions. P100 was lower after 60min in A-CWI and P-CWI compared to PR (p<0.05). After the last bath (60min in A-CWI and 300min in P-CWI), P100 was nearly significantly higher in A-CWI than P-CWI (p=0.05). P20/P100 was higher after 60min in A-CWI and P-CWI compared to PR (p<0.001), but this ratio was lower in P-CWI than A-CWI after the last bath (p<0.05). MVIC torque remained unchanged during A-CWI and P-CWI, while KE-IsoC and KF-IsoC torques were similarly reduced after A-CWI and P-CWI compared to PR (p<0.05).

    Conclusion

    Moderate muscle cooling preferentially impairs maximal force production of dynamic contractions, but not isometric contractions, regardless of exposure duration. A shift towards a slower contractile profile (i.e., increased P20/P100) is more evident after A-CWI than P-CWI, which may be partially explained by a larger reduction of Tmu rather than the exposure duration or reduced Trec.

  • 46. Chaillou, Thomas
    et al.
    Zhang, X.
    McCarthy, J.
    Muscle-specific Ribosomal Protein L3-like Inhibits Myotube Growth2014Konferansepaper (Fagfellevurdert)
  • 47.
    Chaillou, Thomas
    et al.
    Center for Muscle Biology, University of Kentucky, Lexington KY, USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky.
    Zhang, Xiping
    Center for Muscle Biology, University of Kentucky, Lexington KY,USA; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky.
    McCarthy, John J
    Center for Muscle Biology, University of Kentucky, Lexington, Kentucky; Department of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky.
    Expression of Muscle-Specific Ribosomal Protein L3-Like Impairs Myotube Growth2016Inngår i: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 231, nr 9, s. 1894-1902Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The ribosome has historically been considered to have no cell-specific function but rather serve in a "housekeeping" capacity. This view is being challenged by evidence showing that heterogeneity in the protein composition of the ribosome can lead to the functional specialization of the ribosome. Expression profiling of different tissues revealed that ribosomal protein large 3-like (Rpl3l) is exclusively expressed in striated muscle. In response to a hypertrophic stimulus, Rpl3l expression in skeletal muscle was significantly decreased by 82% whereas expression of the ubiquitous paralog Rpl3 was significantly increased by ∼fivefold. Based on these findings, we developed the hypothesis that Rpl3l functions as a negative regulator of muscle growth. To test this hypothesis, we used the Tet-On system to express Rpl3l in myoblasts during myotube formation. In support of our hypothesis, RPL3L expression significantly impaired myotube growth as assessed by myotube diameter (-23%) and protein content (-14%). Further analysis showed that the basis of this impairment was caused by a significant decrease in myoblast fusion as the fusion index was significantly lower (-17%) with RPL3L expression. These findings are the first evidence to support the novel concept of ribosome specialization in skeletal muscle and its role in the regulation of skeletal muscle growth.

  • 48. Charifi, N.
    et al.
    Kadi, Fawzi
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Féasson, L.
    Costes, F.
    Geyssant, A.
    Denis, C.
    Enhancement of microvessel tortuosity in the vastus lateralis muscle of old men in response to endurance training2004Inngår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 554, nr Pt 2, s. 559-569Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Muscle microvascularization is usually quantified in transverse sections, in absolute terms (capillaries around fibres, CAF, or capillary-to-fibre ratio, C/F) or as CAF related to fibre area (CAF/area, CAFA). The capillary-to-fibre perimeter exchange ratio (CFPE) has been introduced in order to assess the role of the capillary-to-fibre interface in resistance to O(2) diffusion. The ratio between the length of capillaries in contact with fibres and fibre perimeter (LC/PF) has also been used as an index for capillary tortuosity. The possibility of change in capillary tortuosity with endurance training was not considered in previous studies. Consequently, this study investigated the effect of 14 weeks of endurance training on muscle microvascularization, including microvessel tortuosity, in 11 elderly men (8th decade). Microvessels were analysed using the CD31 antibody. Together with the significant increase in peak oxygen exchange and citrate synthase activity, there was a significant increase in C/F. While CFPE and CAFA remained unchanged, an important finding was the clear increase in LC/PF (56%; P < 0.001) for a same sarcomere length. We also found a strong correlation between oxidative enzyme activity and LC/PF both before and after training. These results indicate that endurance training induces significant remodelling in the microvessel network in elderly men and that an increase in the degree of microvessel tortuosity would be an important mechanism of adaptation to endurance training.

  • 49.
    Cheng, A
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Allodi, I
    Karolinska Institutet, Stockholm, Sweden.
    Chaillou, Thomas
    Karolinska Institutet, Stockholm, Sweden.
    Thams, S
    Karolinska Institutet, Stockholm, Sweden.
    Ivarsson, N
    Karolinska Institutet, Stockholm, Sweden.
    Schlittler, M
    Karolinska Institutet, Stockholm, Sweden.
    Lanner, J
    Karolinska Institutet, Stockholm, Sweden.
    Hedlund, E
    Karolinska Institutet, Stockholm, Sweden.
    Andersson, D
    Karolinska Institutet, Stockholm, Sweden.
    Increased fatigue resistance and preserved specific force in intact single muscle fibres from the SOD1G93A mouse model of ALS2017Inngår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 219, nr S710, s. 17-17, artikkel-id P-28Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Introduction: Amyotrophic lateral sclerosis (ALS) is a motor neurone disease characterized by degeneration and loss of motor neurones, leading to severe muscle weakness and paralysis. Although motor neurone degeneration is already a well-characterized symptom that contributes to muscle weakness in the SOD1G93A mouse model of ALS, the purpose of the current study was to determine whether muscle weakness in ALS can be attributed to impaired intrinsic force generation in skeletal muscles of SOD1G93A mice.

    Methods: Experiments were performed on whole muscles and mechanically dissected intact single fibres from the flexor digitorum brevis (FDB) muscle of SOD1G93A mice at three age groups of 50, 125 and 150 days of age (P50, P125 and P150). Myoplasmic free [Ca2+] ([Ca2+]i) was measured using the fluorescent indicator, indo-1.

    Results: Motor neurone loss and decreased force were evident in whole FDB muscles of P125–150 mice. In the intact single muscle fibres however, specific force, tetanic [Ca2+]iand resting [Ca2+]i were similar in single FDB fibres from symptomatic P125–150 SOD1G93A and age-matched wild-type littermates. The most intriguing finding was a markedly greater fatigue resistance in single fibres from P125–150 SOD1G93A vs. wild-type mice, which was not present in asymptomatic young P50 SOD1G93A mice. No shift in fibre-type distribution was observed in whole FDB muscles to explain the increased fatigue resistance of single fibres from P125–150 SOD1G93A mice.

    Conclusion: These results support the hypothesis that muscle weakness in ALS is not attributed to intrinsicdefects in skeletal muscle fibre force generation.

  • 50.
    Cheng, Arthur J.
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; School of Kinesiology and Health Sciences, York University, Toronto, Canada.
    Allodi, Ilary
    Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Chaillou, Thomas
    Örebro universitet, Institutionen för hälsovetenskaper. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Schlittler, Maja
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Sports Science and Innovation Institute, Lithuanian Sports University, Kaunas, Lithuania.
    Ivarsson, Niklas
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lanner, Johanna T.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Thams, Sebastian
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Hedlund, Eva
    Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Andersson, Daniel C.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Heart and Vascular Theme; Section for Heart Failure, Arrhythmia and GUCH; Karolinska University Hospital, Stockholm, Sweden.
    Intact single muscle fibres from SOD1(G93A) amyotrophic lateral sclerosis mice display preserved specific force, fatigue resistance and training-like adaptations2019Inngår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 597, nr 12, s. 3133-3146Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Key points:

    • How defects in muscle contractile function contribute to weakness in amyotrophic lateral sclerosis (ALS) were systematically investigated.
    • Weakness in whole muscles from late stage SOD1G93A mice was explained by muscle atrophy as seen by reduced mass and maximal force.
    • On the other hand, surviving single muscle fibres in late stage SOD1G93A have preserved intracellular Ca2+ handling, normal force-generating capacity and increased fatigue resistance.
    • These intriguing findings provide a substrate for therapeutic interventions to potentiate muscular capacity and delay the progression of the ALS phenotype.

    Amyotrophic lateral sclerosis (ALS) is a motor neuron disease characterized by degeneration and loss of motor neurons, leading to severe muscle weakness and paralysis. The SOD1G93A mouse model of ALS displays motor neuron degeneration and a phenotype consistent with human ALS. The purpose of this study was to determine whether muscle weakness in ALS can be attributed to impaired intrinsic force generation in skeletal muscles. In the current study, motor neuron loss and decreased force were evident in whole flexor digitorum brevis (FDB) muscles of mice in the late stage of disease (125–150 days of age). However, in intact single muscle fibres, specific force, tetanic myoplasmic free [Ca2+] ([Ca2+]i), and resting [Ca2+]i remained unchanged with disease. Fibre-type distribution was maintained in late-stage SOD1G93A FDB muscles, but remaining muscle fibres displayed greater fatigue resistance compared to control and showed increased expression of myoglobin and mitochondrial respiratory chain proteins that are important determinants of fatigue resistance. Expression of genes central to both mitochondrial biogenesis and muscle atrophy where increased, suggesting that atrophic and compensatory adaptive signalling occurs simultaneously within the muscle tissue. These results support the hypothesis that muscle weakness in SOD1G93A is primarily attributed to neuromuscular degeneration and not intrinsic muscle fibre defects. In fact, surviving muscle fibres displayed maintained adaptive capacity with an exercise training-like phenotype, which suggests that compensatory mechanisms are activated that can function to delay disease progression.

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