oru.sePublications
Change search
Refine search result
1234 1 - 50 of 166
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 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 diabetes2015In: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 115, no 12, p. 2599-2607Article in journal (Refereed)
    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 University, Örebro University School of Business.
    Objective assessment of Parkinson’s disease motor symptoms during leg agility test using motion sensors2018Conference paper (Refereed)
    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.

  • 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 University, Örebro University School of Business.
    Feasibility of a multi-sensor data fusion method for assessment of Parkinson’s disease motor symptoms2018Conference paper (Other academic)
    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.

  • 4.
    Almon, Ricardo
    et al.
    Örebro University, Department of Clinical Medicine.
    Alvarez-Leon, Eva E.
    Engfeldt, Peter
    Örebro University, Department of Clinical Medicine.
    Serra-Majem, Lluis
    Magnuson, Anders
    Nilsson, Torbjörn K.
    Associations between lactase persistence and the metabolic syndrome: a Mendelian randomization study in the Canary Islands2009Conference paper (Refereed)
  • 5.
    Almon, Ricardo
    et al.
    Örebro University, Department of Clinical Medicine.
    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 University, Department of Clinical Medicine.
    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 Islands2009In: European Journal of Nutrition, ISSN 1436-6207, E-ISSN 1436-6215, Vol. 49, no 3, p. 141-146Article in journal (Refereed)
    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.

  • 6. Ambrosio, Fabrisia
    et al.
    Kadi, Fawzi
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    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 pathology2009In: American Journal of Physical Medicine & Rehabilitation, ISSN 0894-9115, E-ISSN 1537-7385, Vol. 88, no 2, p. 145-155Article in journal (Refereed)
    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.

  • 7. Andersson, Christin
    et al.
    Blennow, Kaj
    Almkvist, Ove
    Andreasen, Niels
    Engfeldt, Peter
    Örebro University, School of Health and Medical Sciences.
    Johansson, Sven-Erik
    Lindau, Maria
    Eriksdotter-Jönhagen, Maria
    Increasing CSF phospho-tau levels during cognitive decline and progression to dementia2008In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 29, no 10, p. 1466-1473Article in journal (Refereed)
    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.

  • 8.
    Anselmius, Johan
    et al.
    Örebro University, School of Health and Medical Sciences.
    Milton, Ludvig
    Örebro University, School of Health and Medical Sciences.
    Expand A Lung: Ett träningsverktyg för andningsmuskulaturen?2011Independent thesis Advanced level (degree of Master (One Year)), 10 credits / 15 HE creditsStudent thesis
    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.

  • 9.
    Arinell, Karin
    et al.
    Örebro University, School of Medical Sciences. 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 University, School of Medical Sciences. 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 study2018In: Platelets, ISSN 0953-7104, E-ISSN 1369-1635, Vol. 29, no 1, p. 87-90Article in journal (Refereed)
    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.

  • 10.
    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 muscle1998In: American Journal of Physiology, ISSN 0002-9513, E-ISSN 2163-5773, Vol. 275, no 2, p. C555-C561Article in journal (Refereed)
    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.

  • 11.
    Arvidsson Lindvall, Mialinn
    et al.
    Örebro University, School of Health Sciences. University Health Care Research Centre, Region Örebro County, Örebro, Sweden.
    Anderzen-Carlsson, Agneta
    Örebro University, School of Health Sciences. Örebro University Hospital. 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 University, School of Health Sciences. Örebro University Hospital.
    Validity and test-retest reliability of the six-spot step test in persons after stroke2018In: Physiotherapy Theory and Practice, ISSN 0959-3985, E-ISSN 1532-5040Article in journal (Refereed)
    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.

  • 12. 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 humans1997In: American Journal of Physiology, ISSN 0002-9513, E-ISSN 2163-5773, Vol. 272, no 1, p. 45-50Article in journal (Refereed)
    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.

  • 13.
    Bark, Tor
    et al.
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Katouli, Mohammad
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro University, School of Medical Sciences. 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 rats1995In: European Journal of Surgery, ISSN 1102-4151, E-ISSN 1741-9271, Vol. 161, no 1, p. 3-8Article in journal (Refereed)
    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.

  • 14.
    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 University, School of Medical Sciences. Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Food deprivation increases bacterial translocation after non-lethal haemorrhage in rats1995In: European Journal of Surgery, ISSN 1102-4151, E-ISSN 1741-9271, Vol. 161, no 2, p. 67-71Article in journal (Refereed)
    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.

  • 15. 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 growth2010Conference paper (Refereed)
  • 16.
    Biratu, Maria
    Örebro University, School of Health and Medical Sciences.
    Jämförelse av lungfunktion, VO2max och muskelstyrka mellan rökare och icke-rökare. 2010Independent thesis Basic level (professional degree), 10 credits / 15 HE creditsStudent thesis
    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.

  • 17.
    Boija, Per Olov
    et al.
    Department. of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro University, School of Medical Sciences. 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 study1987In: Research in experimental medicine, ISSN 0300-9130, E-ISSN 1433-8580, Vol. 187, no 5, p. 315-322Article in journal (Refereed)
    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.

  • 18.
    Chaillou, Thomas
    Örebro University, School of Health Sciences.
    Impaired ribosome biogenesis could contribute to anabolic resistance to strength exercise in the elderly2017In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, no 5, p. 1447-1448Article, review/survey (Refereed)
  • 19.
    Chaillou, Thomas
    Örebro University, School of Health Sciences.
    Skeletal Muscle Fiber Type in Hypoxia: Adaptation to High-Altitude Exposure and Under Conditions of Pathological Hypoxia2018In: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 9, article id 1450Article, review/survey (Refereed)
    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.

  • 20.
    Chaillou, Thomas
    et al.
    Örebro University, School of Health Sciences.
    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 humans2017In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 122, no 2, p. 410-410Article in journal (Refereed)
  • 21.
    Chaillou, Thomas
    et al.
    Örebro University, School of Health Sciences.
    Cheng, Arthur J.
    Faculty of Health, School of Kinesiology and Health Sciences, York University, Canada.
    Mechanisms of prolonged low-frequency force depression: in-vivo studies get us closer to the truth2019In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490Article in journal (Refereed)
  • 22.
    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 force2016Conference paper (Refereed)
  • 23.
    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 muscle2016In: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 100, no Suppl., p. S186-S186Article in journal (Refereed)
    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.

  • 24.
    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 function2015Conference paper (Refereed)
  • 25.
    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 regrowth2015In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 118, p. 86-97Article in journal (Refereed)
    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.

  • 26. Chaillou, Thomas
    et al.
    Koulmann, N.
    Beaudry, M.
    Bigard, X.
    Molecular mechanisms involved in the muscle mass control2011Conference paper (Refereed)
  • 27.
    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 overload2013In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 209, no 4, p. 272-282Article in journal (Refereed)
    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.

  • 28.
    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 injury2014In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 466, no 3, p. 587-598Article in journal (Refereed)
    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.

  • 29.
    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 injury2011Conference paper (Refereed)
  • 30.
    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 injury2011In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 25, no 1 Suppl.Article in journal (Refereed)
    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.

  • 31.
    Chaillou, Thomas
    et al.
    Örebro University, School of Health Sciences. Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Koulmann, N.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Simler, N.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Meunier, A.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Serrurier, B.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Chapot, R.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Peinnequin, A.
    Genomic Core Facility, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Beaudry, M.
    Laboratoire “Réponses cellulaires et fonctionnelles a` l’hypoxie”, Université Paris, Bobigny, France.
    Bigard, X.
    Operational environments, Institut de Recherche Biomédicale des Armées, La Tronche, France.
    Hypoxia transiently affects skeletal muscle hypertrophy in a functional overload model2012In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 302, p. R643-R654Article in journal (Refereed)
    Abstract [en]

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

  • 32. 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 rats2010Conference paper (Refereed)
  • 33.
    Chaillou, Thomas
    et al.
    Örebro University, School of Health Sciences. 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 chemotherapy2017In: Physiological Reports, E-ISSN 2051-817X, Vol. 5, no 11, article id e13261Article in journal (Refereed)
    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.

  • 34. Chaillou, Thomas
    et al.
    Zhang, X.
    McCarthy, J.
    Muscle-specific Ribosomal Protein L3-like Inhibits Myotube Growth2014Conference paper (Refereed)
  • 35.
    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 Growth2016In: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 231, no 9, p. 1894-1902Article in journal (Refereed)
    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.

  • 36. Charifi, N.
    et al.
    Kadi, Fawzi
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Féasson, L.
    Costes, F.
    Geyssant, A.
    Denis, C.
    Enhancement of microvessel tortuosity in the vastus lateralis muscle of old men in response to endurance training2004In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 554, no Pt 2, p. 559-569Article in journal (Refereed)
    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.

  • 37.
    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 ALS2017In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 219, no S710, p. 17-17, article id P-28Article in journal (Refereed)
    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.

  • 38.
    Cheng, Arthur J.
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Willis, Sarah J.
    Swedish Winter Sports Research Centre, Mid Sweden University, Östersund, Sweden.
    Zinner, Christoph
    Swedish Winter Sports Research Centre, Mid Sweden University, Östersund, Sweden.
    Chaillou, Thomas
    Örebro University, School of Health Sciences. Karolinska Institutet, Stockholm, Sweden.
    Ivarsson, Niklas
    Karolinska Institutet, Stockholm, Sweden.
    Ørtenblad, Niels
    University of Southern Denmark, Odense, Denmark.
    Lanner, Johanna T.
    Karolinska Institutet, Stockholm, Sweden.
    Holmberg, Hans-Christer
    Karolinska Institutet, Stockholm, Sweden; Swedish Winter Sports Research Centre, Mid Sweden University, Östersund, Sweden.
    Westerblad, Håkan
    Karolinska Institutet, Stockholm, Sweden.
    Post-exercise recovery of contractile function and endurance in humans and mice is accelerated by heating and slowed by cooling skeletal muscle2017In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, no 24, p. 7413-7426Article in journal (Refereed)
    Abstract [en]

    Manipulation of muscle temperature is believed to improve post-exercise recovery, with cooling being especially popular among athletes. However, it is unclear whether such temperature manipulations actually have positive effects. Accordingly, we studied the effect of muscle temperature on the acute recovery of force and fatigue resistance after endurance exercise. One hour of moderate-intensity arm cycling exercise in humans was followed by two hours recovery in which the upper arms were either heated to 38°C, not treated (33°C), or cooled to ∼15°C. Fatigue resistance after the recovery period was assessed by performing 3 × 5 min sessions of all-out arm cycling at physiological temperature for all conditions (i.e. not heated or cooled). Power output during the all-out exercise was better maintained when muscles were heated during recovery, whereas cooling had the opposite effect. Mechanisms underlying the temperature-dependent effect on recovery were tested in mouse intact single muscle fibres, which were exposed to ∼12 min of glycogen-depleting fatiguing stimulation (350 ms tetani given at 10 s interval until force decreased to 30% of the starting force). Fibres were subsequently exposed to the same fatiguing stimulation protocol after 1-2 h of recovery at 16-36°C. Recovery of submaximal force (30 Hz), the tetanic myoplasmic free [Ca(2+) ] (measured with the fluorescent indicator indo-1), and fatigue resistance were all impaired by cooling (16-26°C) and improved by heating (36°C). In addition, glycogen resynthesis was faster at 36°C than 26°C in whole FDB muscles. We conclude that recovery from exhaustive endurance exercise is accelerated by raising and slowed by lowering muscle temperature.

  • 39.
    Degens, Hans
    et al.
    Department of Clinical Neuroscience, Karolinska Hospital, Stockholm, Sweden; Department of Anatomy, MDC Box 6, University of South Florida, Tampa FL, United States; Department of Anatomy, MDC 6, University of South Florida, Tampa, United States.
    Soop, Mattias
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Höök, Peter
    Department of Clinical Neuroscience, Karolinska Hospital, Stockholm, Sweden; Department of Clinical Neuroscience, Karolinska Hospital, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro University, School of Medical Sciences. Department of Surgery, Huddinge University Hospital, Huddinge, Sweden.
    Larsson, Lars E.I.
    Department of Clinical Neuroscience, Karolinska Hospital, Stockholm, Sweden; Department of Clinical Neuroscience, Karolinska Hospital, Stockholm, Sweden.
    Post-operative effects on insulin resistance and specific tension of single skeletal muscle fibres1999In: Clinical Science, ISSN 0143-5221, E-ISSN 1470-8736, Vol. 97, no 4, p. 449-455Article in journal (Refereed)
    Abstract [en]

    Surgery and accidental trauma are associated with a transient period of insulin resistance, substrate catabolism and muscle weakness. In the present study, we evaluated the changes in the force-generating capacity of chemically skinned single muscle fibresfollowing abdominal surgery. Biopsies of the m. vastus lateralis were obtained in three patients 1 day before and 3 or 6 days after surgery. Part of the biopsy was frozen for histochemical analysis of the fibre cross-sectional area (FCSA) and myofibrillar protein content, and another part was used for single-fibre contractile measurements. All patients developed insulin resistance following surgery. The maximum velocity of unloaded shortening of single muscle fibres did not change following surgery. The FCSA did not decrease after surgery, as determined either from histochemical sections or from singlefibres measured at a fixed sarcomere length of 2.76+/-0.09 microm (mean+/-S.D.). Further, the force-generating capacity of the single fibres, measured as maximal Ca(2+)-activated force (P(0)) or as P(0) normalized to FCSA (specific tension), remained unchanged, as did the myofibrillar protein content of the muscle. In conclusion, the muscle weakness associated with post-operative insulin resistance is not related to a decreased specifictension or a loss of myofibrillar proteins. Other potential cellular mechanisms underlying post-operative weakness are discussed.

  • 40.
    Doeltgen, Sebastian H.
    et al.
    Speech Pathology and Audiology, School of Health Sciences, Flinders University, Adelaide, Australia.
    Omari, Taher I.
    Human Physiology, Medical Science and Technology, School of Medicine, Flinders University, Adelaide, Australia.
    Savilampi, Johanna
    Örebro University, School of Medical Sciences. Department of Anaesthesiology and Intensive Care, Örebro University Hospital, Örebro, Sweden.
    Remifentanil alters sensory neuromodulation of swallowing in healthy volunteers: Quantification by a novel pressure-impedance analysis2016In: American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, E-ISSN 1522-1547, Vol. 310, no 11, p. G1176-G1182Article in journal (Refereed)
    Abstract [en]

    Exposure to remifentanil contributes to an increased risk of pulmonary aspiration, likely through reduced pharyngeal contractile vigour and diminished bolus propulsion during swallowing. Here, we employed a novel high resolution pressure-flow analysis to quantify the biomechanical changes across the upper esophageal sphincter (UES). Eleven healthy young participants (mean age 23.3±3.1 years, 7 male) received remifentanil via intravenous target controlled infusion with an effect-site concentration of 3 ng/ml. Before and 30 min following commencement of remifentanil administration, participants performed ten 10 ml saline swallows while pharyngo-esophageal manometry and electrical impedance data were recorded using a 4.2 mm diameter catheter housing 36 circumferential pressure sensors. Remifentanil significantly shortened the time period of UES opening (p<0.001) and increased residual UES pressure (p=0.003). At the level of the hypopharynx, remifentanil significantly shortened the time latency from maximum bolus distension to peak contraction (p=0.004) and significantly increased intrabolus distension pressure (p=0.024). Novel mechanical states analysis revealed that the latencies between the different phases of the stereotypical UES relaxation sequence were shortened by remifentanil. Reduced duration of bolus flow during shortened UES opening in concert with increased hypopharyngeal distension pressures are mechanically consistent with increased flow resistance due to a more rapid bolus flow rate. These biomechanical changes are congruent with modification of the physiologic neuro-regulatory mechanism governing accommodation to bolus volume.

  • 41.
    D'Souza, K.
    et al.
    Dalhousie Medicine New Brunswick, United States.
    Nzirorera, C.
    Dalhousie Medicine New Brunswick, United States.
    Cowie, A.M.
    Dalhousie Medicine New Brunswick, United States.
    Paramel Varghese, Geena
    Dalhousie Medicine New Brunswick, United States.
    Trivedi, P.
    Dalhousie Medicine New Brunswick, United States.
    Eichmann, T.O.
    Department of Biochemistry and Molecular Biology, Dalhousie University, Institute of Molecular Biosciences, Saint John, Canada.
    Biswas, D.
    Dalhousie Medicine New Brunswick, United States.
    Touaibia, M.
    University of Graz, Center for Explorative Lipidomics, BioTechMed-Graz, Department of Chemistry and Biochemistry, Graz, Austria.
    Morris, A.J.
    Dalhousie Medicine New Brunswick, United States; Université de Moncton, Division of Cardiovascular Medicine, Moncton, Canada.
    Aidinis, V.
    University of Kentucky, Lexington Veterans Affairs Medical Center, Division of Immunology, Lexington, United States.
    Kane, D.A.
    Biomedical Sciences Research Center “Alexander Fleming”, Department of Human Kinetics, Athens, Greece.
    Pulinilkunnil, T.
    Dalhousie Medicine New Brunswick, United States.
    Kienesberger, P.C.
    Dalhousie Medicine New Brunswick, United States.
    Autotaxin-Lysophosphatidic Acid Signaling Contributed to Obesity-Induced Insulin Resistance in Muscle and Impairs Mitochondrial Metabolism2018In: Journal of Lipid Research, ISSN 0022-2275, E-ISSN 1539-7262, Vol. 59, no 10, p. 1805-1817Article in journal (Refereed)
    Abstract [en]

    Autotaxin (ATX) is an adipokine that generates the bioactive lipid, lysophosphatidic acid (LPA). ATX-LPA signaling has been implicated in diet-induced obesity and systemic insulin resistance. However, it remains unclear whether the ATX-LPA pathway influences insulin function and energy metabolism in target tissues, particularly skeletal muscle, the major site of insulin-stimulated glucose disposal. The objective of this study was to test whether the ATX-LPA pathway impacts tissue insulin signaling and mitochondrial metabolism in skeletal muscle during obesity. Male mice with heterozygous ATX deficiency (ATX +/-) were protected from obesity, systemic insulin resistance, and cardiomyocyte dysfunction following high-fat high-sucrose (HFHS) feeding. HFHS-fed ATX +/- mice also had improved insulin-stimulated AKT phosphorylation in white adipose tissue, liver, heart, and skeletal muscle. Preserved insulin-stimulated glucose transport in muscle from HFHS fed ATX +/- mice was associated with improved mitochondrial pyruvate oxidation in the absence of changes in fat oxidation and ectopic lipid accumulation. Similarly, incubation with LPA decreased insulin-stimulated AKT phosphorylation and mitochondrial energy metabolism in C2C12 myotubes at baseline and following palmitate-induced insulin resistance. Taken together, our results suggest that the ATX-LPA pathway contributes to obesity-induced insulin resistance in metabolically relevant tissues. Our data also suggest that LPA directly impairs skeletal muscle insulin signaling and mitochondrial function. Preserved insulin-stimulated glucose transport in muscle from HFHS fed ATX +/- mice was associated with improved mitochondrial pyruvate oxidation in the absence of changes in fat oxidation and ectopic lipid accumulation. Similarly, incubation with LPA decreased insulin-stimulated AKT phosphorylation and mitochondrial energy metabolism in C2C12 myotubes at baseline and following palmitate-induced insulin resistance. Taken together, our results suggest that the ATX-LPA pathway contributes to obesity-induced insulin resistance in metabolically relevant tissues. Our data also suggest that LPA directly impairs skeletal muscle insulin signaling and mitochondrial function. Preserved insulin-stimulated glucose transport in muscle from HFHS fed ATX +/- mice was associated with improved mitochondrial pyruvate oxidation in the absence of changes in fat oxidation and ectopic lipid accumulation. Similarly, incubation with LPA decreased insulin-stimulated AKT phosphorylation and mitochondrial energy metabolism in C2C12 myotubes at baseline and following palmitate-induced insulin resistance. Taken together, our results suggest that the ATX-LPA pathway contributes to obesity-induced insulin resistance in metabolically relevant tissues. Our data also suggest that LPA directly impairs skeletal muscle insulin signaling and mitochondrial function. incubation with LPA decreased insulin-stimulated AKT phosphorylation and mitochondrial energy metabolism in C2C12 myotubes at baseline and following palmitate-induced insulin resistance. Taken together, our results suggest that the ATX-LPA pathway contributes to obesity-induced insulin resistance in metabolically relevant tissues. Our data also suggest that LPA directly impairs skeletal muscle insulin signaling and mitochondrial function. incubation with LPA decreased insulin-stimulated AKT phosphorylation and mitochondrial energy metabolism in C2C12 myotubes at baseline and following palmitate-induced insulin resistance. Taken together, our results suggest that the ATX-LPA pathway contributes to obesity-induced insulin resistance in metabolically relevant tissues. Our data also suggest that LPA directly impairs skeletal muscle insulin signaling and mitochondrial function.

  • 42.
    Echaniz-Laguna, Andoni
    et al.
    Département de Neurologie, Hopital Civil de Strasbourg, 1 Place de l’Hopital, Strasbourg, France; INSERM U-692, Faculté de Médecine, Strasbourg, France.
    Zoll, Joffrey
    Département de Physiologie, Faculté de Médecine, Strasbourg, France.
    Ponsot, Elodie
    Département de Physiologie, Faculté de Médecine, Strasbourg, France.
    N'guessan, Benoit
    Département de Physiologie, Faculté de Médecine, Strasbourg, France.
    Tranchant, Christine
    Département de Neurologie, Hopital Civil de Strasbourg, 1 Place de l’Hospital, Strasbourg, France.
    Loeffler, Jean-Philippe
    INSERM U-692, Faculté de Médecine, Strasbourg, France.
    Lampert, Eliane
    Département de Physiologie, Faculté de Médecine, Strasbourg, France.
    Muscular mitochondrial function in amyotrophic lateral sclerosis is progressively altered as the disease develops: A temporal study in man2006In: Experimental Neurology, ISSN 0014-4886, E-ISSN 1090-2430, Vol. 198, no 1, p. 25-30Article in journal (Refereed)
    Abstract [en]

    We performed repeated analysis of mitochondrial respiratory function in skeletal muscle (SM) of patients with early-stage sporadic amyotrophic lateral sclerosis (SALS) to determine whether mitochondrial function was altered as the disease advanced. SM biopsies were obtained from 7 patients with newly diagnosed SALS, the same 7 patients 3 months later, and 7 sedentary controls. Muscle fibers were permeabilized with saponin, then skinned and placed in an oxygraphic chamber to measure basal and maximal adenosine diphosphate (ADP)-stimulated respiration rates and to assess mitochondrial regulation by ADP. We found that the maximal oxidative phosphorylation capacity of muscular mitochondria significantly increased, and muscular mitochondrial respiratory complex IV activity significantly decreased as the disease advanced. This temporal study demonstrates for the first time that mitochondrial function in SM in human SALS is progressively altered as the disease develops.

  • 43.
    Edholm, Peter
    et al.
    Örebro University, School of Health Sciences.
    Strandberg, Emelie
    Örebro University, School of Health Sciences.
    Kadi, Fawzi
    Örebro University, School of Health Sciences.
    A healthy diet rich in N-3 PUFAS enhances the effects of resistance training in elderly women2017Conference paper (Refereed)
  • 44.
    Edholm, Peter
    et al.
    Örebro University, School of Health Sciences.
    Strandberg, Emelie
    Örebro University, School of Health Sciences.
    Kadi, Fawzi
    Örebro University, School of Health Sciences.
    A healthy diet rich in N-3 PUFAS enhances the effects of resistance training in elderly women2017Conference paper (Refereed)
  • 45.
    Ekelund, Ulf
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Huddinge, Sweden.
    Poortvliet, Eric
    Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Huddinge, Sweden.
    Nilsson, Andreas
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Huddinge, Sweden.
    Yngve, Agneta
    Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Huddinge, Sweden.
    Holmberg, Anders
    Department of Statistics, Örebro University, 701 82 Örebro, Sweden.
    Sjöström, Michael
    Department of Physical Education and Health, Örebro University, Örebro, Sweden; Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Huddinge, Sweden.
    Physical activity in relation to aerobic fitness and body fat in 14- to 15-year-old boys and girls2001In: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 85, no 3-4, p. 195-201Article in journal (Refereed)
    Abstract [en]

    The purpose of this study was to examine the strength of the relationship between different variables of physical activity and aerobic fitness and body fat in adolescent boys and girls. Activity energy expenditure (AEE), time spent in a sedentary state, and time spent engaged in moderate and vigorous physical activity (MVPA, > or = 50% peak oxygen uptake, VO2peak) were assessed by the minute-by-minute heart rate monitoring method in 82 randomly selected 14- to 15-year olds (42 boys, 40 girls). Body fat was determined by measuring skinfold thicknesses. VO2peak was measured by indirect calorimetry. Somatic maturity level was determined by percentages of adult (i.e. 18 years) height attained at examination. AEE was related to aerobic fitness for both genders (boys, r = 0.30, P = 0.056; girls, r = 0.45, P = 0.003). For boys, there was a significant relationship between maturity level and VO2peak (r = 0.48, P < 0.001). For both genders, body fat was significantly and negatively related to VO2peak (r = -0.48 and r = -0.43, P < 0.01). Body fat and maturity explained 47% of the variation in VO2peak in boys, whereas AEE and body fat explained 22% of the variation in VO2peak in girls. No significant associations between physical activity variables and the data on body fat were observed. The total amount of physical activity (AEE) was related to VO2peak, at least in adolescent girls. Although VO2peak seems to be influenced by the maturity level in adolescent boys, the data support the promotion of a daily active lifestyle among young people.

  • 46.
    Ekelund, Ulf
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Sjöström, Michael
    Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Yngve, Agneta
    Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Poortvliet, Eric
    Unit for Preventive Nutrition, Department of Medical Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Nilsson, Andreas
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Fröberg, Karsten
    Institute of Sport Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.
    Wedderkopp, Niels
    Institute of Sport Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.
    Westerterp, Klaas
    Department of Human Biology, Maastricht University, Maastricht, The Netherlands.
    Physical activity assessed by activity monitor and doubly labeled water in children2001In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 33, no 2, p. 275-281Article in journal (Refereed)
    Abstract [en]

    PURPOSE: To validate the Computer Science and Application's (CSA) activity monitor for assessment of the total amount of physical activity during two school-weeks in 9-yr-old children and to develop equations to predict total energy expenditure (TEE) and activity energy expenditure (AEE) from activity counts and anthropometric variables.

    METHODS: A total of 26 children (15 boys and 11 girls, mean age 9.1 +/- 0.3 yr) were monitored for 14 consecutive days. TEE was simultaneously measured by the doubly labeled water method. Averaged activity counts (counts.min(-1)) were compared with data on: 1) TEE, 2) AEE = TEE minus basal metabolic rate (BMR; estimated from predictive equations), and 3) daily physical activity level (PAL = TEE/BMR).

    RESULTS: Physical activity determined by activity counts was significantly related to the data on energy expenditures: TEE (r = 0.39; P < 0.05), AEE (r = 0.54; P < 0.01), and PAL (r = 0.58; P < 0.01). Multiple stepwise regression analysis showed that TEE was significantly influenced by gender, body composition (body weight or fat free mass), and activity counts (R(2) = 0.54--0.60). AEE was significantly influenced by activity counts and gender (R(2) = 0.45). There were no significant differences between activity counts and PAL in discriminating among activity levels with "low" (PAL < 1.56), "moderate" (1.57 < or = PAL > or = 1.81), and "high" (PAL > 1.81) intensity.

    CONCLUSION: Activity counts from the CSA activity monitor seems to be a useful measure of the total amount of physical activity in 9-yr-old children. Activity counts contributed significantly to the explained variation in TEE and was the best predictor of AEE.

  • 47.
    Eliason, Gabriella
    et al.
    Örebro University, School of Health and Medical Sciences.
    Abdel-Halim, S.
    Örebro University, School of Health and Medical Sciences.
    Arvidsson, B.
    Kadi, Fawzi
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Piehl-Aulin, Karin
    Örebro University, School of Health and Medical Sciences.
    Physical performance and muscular characteristics in different stages of COPD2009In: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 19, no 6, p. 865-870Article in journal (Refereed)
    Abstract [en]

    This study has examined exercise capacity and muscle morphology in patients with different severities of chronic obstructive pulmonary disease (COPD). Twenty-three patients and 12 healthy matched controls were recruited. Based on the severity of airflow obstruction, patients were divided into two subgroups. Exercise capacity was determined using a 6-min walk test. Muscle fiber composition, fiber area and number of satellite cells/muscle fiber were determined in muscle biopsies using immunohistochemistry. A progressive decline in exercise capacity was noted with ascending disease severity. Furthermore, a correlation between reduction in exercise capacity and changes in muscle fiber composition was observed in COPD. The group with severe and very severe COPD had a lower proportion of type I and a higher proportion of type IIa fibers compared with the other groups. In severe and very severe COPD, a reduction in fiber area of type IIa fibers was also seen. The number of satellite cells/muscle fiber did not differ between the groups. In conclusion, a decline in exercise capacity occurs already in mild and moderate COPD, indicating that the 6-min walk test is a reliable indicator of disease severity. Furthermore, changes in skeletal muscle morphology are associated with disease severity while muscle regenerative capacity is not altered.

  • 48.
    Eliason, Gabriella
    et al.
    Örebro University, School of Health and Medical Sciences.
    Abdel-Halim, Samy M.
    School of Health and Medical Sciences, Örebro University, Örebro, Sweden; Department of Medical Sciences, Respiratory Medicine and Allergology, Uppsala University, Uppsala, Sweden.
    Piehl-Aulin, Karin
    School of Health and Medical Sciences, Örebro University, Örebro, Sweden; Department of Rheumatology, Danderyds hospital, Stockholm, Sweden.
    Kadi, Fawzi
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Alterations in the muscle-to-capillary interface in patients with different degrees of chronic obstructive pulmonary disease2010In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 11, article id 97Article in journal (Refereed)
    Abstract [en]

    Background: It is hypothesized that decreased capillarization of limb skeletal muscle is implicated in the decreased exercise tolerance in COPD patients. We have recently demonstrated decreased number of capillaries per muscle fibre (CAF) but no changes in CAF in relation to fibre area (CAFA), which is based on the diffusion distance between the capillary and muscle fibre. The aim of the current study is to investigate the muscle-to-capillary interface which is an important factor involved in oxygen supply to the muscle that has previously been suggested to be a more sensitive marker for changes in the capillary bed compared to CAF and CAFA.

    Methods: 23 COPD patients and 12 age-matched healthy subjects participated in the study. Muscle-to-capillary interface was assessed in muscle biopsies from the tibialis anterior muscle using the following parameters:

    1) The capillary-to-fibre ratio (C:Fi) which is defined as the sum of the fractional contributions of all capillary contacts around the fibre

    2) The ratio between C:Fi and the fibre perimeter (CFPE-index)

    3) The ratio between length of capillary and fibre perimeter (LC/PF) which is also referred to as the index of tortuosity.

    Exercise capacity was determined using the 6-min walking test.

    Results: A positive correlation was found between CFPE-index and ascending disease severity with CFPE-index for type I fibres being significantly lower in patients with moderate and severe COPD. Furthermore, a positive correlation was observed between exercise capacity and CFPE-index for both type I and type IIa fibres.

    Conclusion: It can be concluded that the muscle-to-capillary interface is disturbed in the tibialis anterior muscle in patients with COPD and that interface is strongly correlated to increased disease severity and to decreased exercise capacity in this patient group.

     

  • 49.
    Eliason, Gabriella
    et al.
    Örebro University, School of Health and Medical Sciences.
    Zakrisson, Ann-Britt
    Örebro University, School of Health and Medical Sciences.
    Piehl-Aulin, Karin
    Department of pheumatology, danderyds hospital, Stockholm, Sweden.
    Hurtig-Wennlöf, Anita
    Örebro University, School of Health and Medical Sciences.
    Physical activity patterns in patients with different degrees of chronic obstructive pulmonary diseaseManuscript (preprint) (Other academic)
    Abstract [en]

    Purpose: It has previously been suggested that exercise capacity is decreased in COPD patients and that it is associated with degree of disease. The reduced exercise capacity may plausibly be due to low levels of physical activity in this patient group. In the present study we aimed to assess exercise capacity and physical activity in different stages of COPD and to examine the associations between exercise capacity, pulmonary function and degree of physical activity.

    Methods: 44 COPD patients and 17 healthy subjects participated in the study. Exercise capacity was assessed using the 6 minute walking test and physical activity was assessed using a uniaxial accelerometer worn all waking hours during seven days.

    Results: Mean exercise capacity was significantly lower in COPD patients compared to healthy subjects. Mean physical activity level and time spent at least moderately active were significantly lower in patients with moderate and severe COPD compared to healthy subjects while no differences in time spent sedentary were observed between the study groups. Pulmonary function, mean physical activity level and time spent at least moderately physically active were significantly associated with exercise capacity in the patients.

    Conclusions: Patients with moderate and severe COPD are significantly less physically active compared to healthy subjects. Furthermore, mean physical activity level as well as physical activity of at least moderate intensity are positively associated with exercise capacity in COPD patients while time spent sedentary is not which stresses an important role of physical activity on exercise capacity in this patient group. 

  • 50.
    Emilsson, Kent
    Department of Clinical Physiology, Karlskoga Hospita, Karlskoga, Swede.
    Right ventricular long-axis function in relation to left ventricular systolic function2004In: Clinical Physiology and Functional Imaging, ISSN 1475-0961, E-ISSN 1475-097X, Vol. 24, no 4, p. 212-215Article in journal (Refereed)
    Abstract [en]

    A decrease in left ventricular (LV) systolic function is accompanied by a decrease in maximal relaxation velocity in LV long-axis direction, but is it also accompanied by a decrease in right ventricular (RV) long-axis function? To study this 35 consecutive patients were examined by echocardiography. Ejection fraction (LVEF) and mitral annulus motion (MAM) were used as indices of LV systolic function and tricuspid annulus motion (TAM), that is the systolic shortening in RV long-axis direction, was used as an index of RV systolic long-axis function. In the same way the maximal relaxation velocity in LV long-axis direction, that is the maximal diastolic velocity of MAM (MDV MAM), has been suggested as an index of LV diastolic function the maximal diastolic velocity of TAM (MDV TAM) can be supposed to be an index of RV diastolic function measuring the maximal relaxation velocity in the RV long-axis direction. A significant positive correlation was found between MDV TAM and MAM (r = 0.64, P<0001) and LVEF (r = 0.54, P = 0.001) and between TAM and the two studied indices of LV systolic function, with the highest correlation to MAM (r = 0.68, P<0.001) and the lowest to LVEF (r = 0.57, P<0.001). Thus, a decrease in LV systolic function is accompanied by a decrease in both systolic and diastolic RV long-axis function, findings that probably are due to the close anatomical connection between the ventricles and to changes that occur in afterload of the RV secondary to LV systolic dysfunction.

1234 1 - 50 of 166
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf