miun.sePublications
Change search
Refine search result
1 - 11 of 11
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • 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.
    Cheng, Arthur J.
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden .
    Place, Nicolas
    Institute of Movement Sciences and Sports Medicine, Medicine Faculty, Geneva University, Geneva, Switzerland .
    Bruton, Joseph D.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden .
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Westerblad, Håkan
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden .
    Doublet discharge stimulation increases sarcoplasmic reticulum Ca2+ release and improves performance during fatiguing contractions in mouse muscle fibres2013In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 591, no 15, p. 3739-3748Article in journal (Refereed)
    Abstract [en]

    Double discharges (doublets) of motor neurones at the onset of contractions increase both force and rate of force development during voluntary submaximal contractions. The purpose of this study was to examine the role of doublet discharges on force and myoplasmic free [Ca2+] ([Ca2+](i)) during repeated fatiguing contractions, using a stimulation protocol mimicking the in vivo activation pattern during running. Individual intact fibres from the flexor digitorum brevis muscle of mice were stimulated at 33 degrees C to undergo 150 constant-frequency (five pulses at 70 Hz) or doublet (an initial, extra pulse at 200 Hz) contractions at 300 ms intervals. In the unfatigued state, doublet stimulation resulted in a transient (approximate to 10 ms) approximate doubling of [Ca2+](i), which was accompanied by a greater force-time integral (approximate to 70%) and peak force (approximate to 40%) compared to constant frequency contractions. Moreover, doublets markedly increased force-time integral and peak force during the first 25 contractions of the fatiguing stimulation. In later stages of fatigue, addition of doublets increased force production but the increase in force production corresponded to only a minor portion of the fatigue-induced reduction in force. In conclusion, double discharges at the onset of contractions effectively increase force production, especially in early stages of fatigue. This beneficial effect occurs without additional force loss in later stages of fatigue, indicating that the additional energy cost induced by doublet discharges to skeletal muscle is limited.

  • 2.
    Cheng, Arthur J.
    et al.
    Karolinska Institutet.
    Willis, Sarah J.
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Zinner, Christoph
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Chaillou, Thomas
    Karolinska Institutet; Örebro universitet.
    Ivarsson, Niklas
    Karolinska Institutet.
    Ørtenblad, Niels
    University of Southern Denmark, Odense, Denmark.
    Lanner, Johanna T.
    Karolinska Institutet.
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Karolinska Institutet.
    Westerblad, Håkan
    Karolinska Institutet.
    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]

    Key points: We investigated whether intramuscular temperature affects the acute recovery of exercise performance following fatigue-induced by endurance exercise. Mean power output was better preserved during an all-out arm-cycling exercise following a 2 h recovery period in which the upper arms were warmed to an intramuscular temperature of ˜ 38°C than when they were cooled to as low as 15°C, which suggested that recovery of exercise performance in humans is dependent on muscle temperature. Mechanisms underlying the temperature-dependent effect on recovery were studied in intact single mouse muscle fibres where we found that recovery of submaximal force and restoration of fatigue resistance was worsened by cooling (16-26°C) and improved by heating (36°C). Isolated whole mouse muscle experiments confirmed that cooling impaired muscle glycogen resynthesis. We conclude that skeletal muscle recovery from fatigue-induced by endurance exercise is impaired by cooling and improved by heating, due to changes in glycogen resynthesis rate.

    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 2 h 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 [Ca2+] (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 flexor digitorum brevis muscles. We conclude that recovery from exhaustive endurance exercise is accelerated by raising and slowed by lowering muscle temperature.

  • 3.
    Gejl, Kasper D.
    et al.
    Department of Sports Science and Clinical Biomechanics, SDU Muscle Research Cluster, University of Southern Denmark, Odense, Denmark.
    Ørtenblad, Niels
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Univ Southern Denmark, Denmark.
    Andersson, Erik
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Plomgaard, Peter
    Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Swedish Olymp Comm, Stockholm.
    Nielsen, Joachim
    Department of Pathology, SDU Muscle Research Cluster, Odense University Hospital, Odense.
    Local depletion of glycogen with supra-maximal exercise in human skeletal muscle fibres2017In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, no 9, p. 2809-2821Article in journal (Refereed)
    Abstract [en]

    Skeletal muscle glycogen is heterogeneous distributed in three separated compartments (intramyofibrillar, intermyofibrillar and subsarcolemmal). Although only constituting 4-15% of the total glycogen volume, the availability of intramyofibrillar glycogen has been shown to be of particular importance to muscle function. The present study was designed to investigate the depletion of these three sub-cellular glycogen compartments during repeated supra-maximal exercise in elite athletes. Ten elite cross-country skiers (age: 25 +/- 4 yrs., VO2 max : 65 +/- 4 ml kg-1 min-1 , mean +/- SD) performed four approximately 4-minute supra-maximal sprint time trials (STT 1-4) with 45 min recovery. The sub-cellular glycogen volumes in m. triceps brachii were quantified from electron microscopy images before and after both STT 1 and STT 4. During STT 1, the depletion of intramyofibrillar glycogen was higher in type I fibres (-52% [-89:-15%]) than type 2 fibres (-15% [-52:22%]) (P = 0.02), while the depletion of intermyofibrillar glycogen (main effect: -19% [-33:0], P = 0.006) and subsarcolemmal glycogen (main effect: -35% [-66:0%], P = 0.03) was similar between fibre types. In contrast, only intermyofibrillar glycogen volume was significantly reduced during STT 4, in both fibre types (main effect: -31% [-50:-11%], P = 0.002). Furthermore, for each of the sub-cellular compartments, the depletion of glycogen during STT 1 was associated with the volumes of glycogen before STT 1. In conclusion, the depletion of spatially distinct glycogen compartments differs during supra-maximal exercise. Furthermore, the depletion changes with repeated exercise and is fibre type-dependent. 

  • 4.
    Hostrup, M.
    et al.
    Department of Nutrition, Exercise and Sports, Section of Integrated Physiology, University of Copenhagen, Denmark .
    Kalsen, A.
    Department of Nutrition, Exercise and Sports, Section of Integrated Physiology, University of Copenhagen, Denmark .
    Ørtenblad, Niels
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Department of Sports Science and Biomechanics, University of Southern Denmark, Denmark .
    Juel, C.
    Department of Biology, University of Copenhagen, Denmark .
    Mørch, K.
    Department of Nutrition, Exercise and Sports, Section of Integrated Physiology, University of Copenhagen, Denmark .
    Rzeppa, S.
    Norwegian Doping Control Laboratory, Oslo University Hospital, Norway .
    Karlsson, S.
    Department of Respiratory Research, Bispebjerg University Hospital, Denmark .
    Backer, V.
    Department of Respiratory Research, Bispebjerg University Hospital, Denmark .
    Bangsbo, J.
    Department of Nutrition, Exercise and Sports, Section of Integrated Physiology, University of Copenhagen, Denmark .
    β2-Adrenergic stimulation enhances Ca2+ release and contractile properties of skeletal muscles, and counteracts exercise-induced reductions in Na+-K+-ATPase Vmax in trained men2014In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 592, no 24, p. 5445-5459Article in journal (Refereed)
    Abstract [en]

    The aim of the present study was to examine the effect of β2-adrenergic stimulation on skeletal muscle contractile properties, sarcoplasmic reticulum (SR) rates of Ca2+ release and uptake, and Na+-K+-ATPase activity before and after fatiguing exercise in trained men. The study consisted of two experiments (EXP1, n = 10 males, EXP2, n = 20 males), where β2-adrenoceptor agonist (terbutaline) or placebo was randomly administered in double-blinded crossover designs. In EXP1, maximal voluntary isometric contraction (MVC) of m. quadriceps was measured, followed by exercise to fatigue at 120% of maximal oxygen uptake (V˙O2, max ). A muscle biopsy was taken after MVC (non-fatigue) and at time of fatigue. In EXP2, contractile properties of m. quadriceps were measured with electrical stimulations before (non-fatigue) and after two fatiguing 45 s sprints. Non-fatigued MVCs were 6 ± 3 and 6 ± 2% higher (P < 0.05) with terbutaline than placebo in EXP1 and EXP2, respectively. Furthermore, peak twitch force was 11 ± 7% higher (P < 0.01) with terbutaline than placebo at non-fatigue. After sprints, MVC declined (P < 0.05) to the same levels with terbutaline as placebo, whereas peak twitch force was lower (P < 0.05) and half-relaxation time was prolonged (P < 0.05) with terbutaline. Rates of SR Ca2+ release and uptake at 400 nm [Ca2+] were 15 ± 5 and 14 ± 5% (P < 0.05) higher, respectively, with terbutaline than placebo at non-fatigue, but declined (P < 0.05) to similar levels at time of fatigue. Na+-K+-ATPase activity was unaffected by terbutaline compared with placebo at non-fatigue, but terbutaline counteracted exercise-induced reductions in maximum rate of activity (Vmax) at time of fatigue. In conclusion, increased contractile force induced by β2-adrenergic stimulation is associated with enhanced rate of Ca2+ release in humans. While β2-adrenergic stimulation elicits positive inotropic and lusitropic effects on non-fatigued m. quadriceps, these effects are blunted when muscles fatigue.

  • 5.
    Koh, HE
    et al.
    Syddanskt universitet, Danmark.
    Nielsen, J
    Syddanskt universitet, Danmark.
    Saltin, B
    Köpenhamns universitet, Danmark.
    Holmberg, Hans-Christer
    UiT Arctic University of Norway, Tromsø, Norway.
    Örtenblad, Niels
    Syddanskt universitet, Danmark.
    Pronounced limb and fibre type differences in subcellular lipid droplet content and distribution in elite skiers before and after exhaustive exercise2017In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, no 17, p. 5781-5795Article in journal (Refereed)
    Abstract [en]

    KEY POINTS:

    Although lipid droplets in skeletal muscle are an important energy source during endurance exercise, our understanding of lipid metabolism in this context remains incomplete. Using transmission electron microscopy, two distinct subcellular pools of lipid droplets can be observed in skeletal muscle - one beneath the sarcolemma and the other between myofibrils. At rest, well-trained leg muscles of cross-country skiers contain 4- to 6-fold more lipid droplets than equally well-trained arm muscles, with a 3-fold higher content in type 1 than in type 2 fibres. During exhaustive exercise, lipid droplets between the myofibrils but not those beneath the sarcolemma are utilised by both type 1 and 2 fibres. These findings provide insight into compartmentalisation of lipid metabolism within skeletal muscle fibres.

    ABSTRACT:

    Although the intramyocellular lipid pool is an important energy store during prolonged exercise, our knowledge concerning its metabolism is still incomplete. Here, quantitative electron microscopy was used to examine subcellular distribution of lipid droplets in type 1 and 2 fibres of the arm and leg muscles before and after 1 h of exhaustive exercise. Intermyofibrillar lipid droplets accounted for 85-97% of the total volume fraction, while the subsarcolemmal pool made up 3-15%. Before exercise, the volume fractions of intermyofibrillar and subsarcolemmal lipid droplets were 4- to 6-fold higher in leg than in arm muscles (P < 0.001). Furthermore, the volume fraction of intermyofibrillar lipid droplets was 3-fold higher in type 1 than in type 2 fibres (P < 0.001), with no fibre type difference in the subsarcolemmal pool. Following exercise, intermyofibrillar lipid droplet volume fraction was 53% lower (P = 0.0082) in both fibre types in arm, but not leg muscles. This reduction was positively associated with the corresponding volume fraction prior to exercise (R2  = 0.84, P < 0.0001). No exercise-induced change in the subsarcolemmal pool could be detected. These findings indicate clear differences in the subcellular distribution of lipid droplets in the type 1 and 2 fibres of well-trained arm and leg muscles, as well as preferential utilisation of the intermyofibrillar pool during prolonged exhaustive exercise. Apparently, the metabolism of lipid droplets within a muscle fibre is compartmentalised.

  • 6.
    Nielsen, J.
    et al.
    Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.
    Holmberg, H. -C
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Schröder, H. D.
    Institute of Pathology, University of Southern Denmark, Odense, Denmark.
    Saltin, B.
    Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark .
    Örtenblad, N.
    Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.
    Human skeletal muscle glycogen utilization in exhaustive exercise: Role of subcellular localization and fibre type2011In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 589, no 11, p. 2871-2885Article in journal (Refereed)
    Abstract [en]

    Although glycogen is known to be heterogeneously distributed within skeletal muscle cells, there is presently little information available about the role of fibre types, utilization and resynthesis during and after exercise with respect to glycogen localization. Here, we tested the hypothesis that utilization of glycogen with different subcellular localizations during exhaustive arm and leg exercise differs and examined the influence of fibre type and carbohydrate availability on its subsequent resynthesis. When 10 elite endurance athletes (22 ± 1 years, = 68 ± 5 ml kg-1 min-1, mean ± SD) performed one hour of exhaustive arm and leg exercise, transmission electron microscopy revealed more pronounced depletion of intramyofibrillar than of intermyofibrillar and subsarcolemmal glycogen. This phenomenon was the same for type I and II fibres, although at rest prior to exercise, the former contained more intramyofibrillar and subsarcolemmal glycogen than the latter. In highly glycogen-depleted fibres, the remaining small intermyofibrillar and subsarcolemmal glycogen particles were often found to cluster in groupings. In the recovery period, when the athletes received either a carbohydrate-rich meal or only water the impaired resynthesis of glycogen with water alone was associated primarily with intramyofibrillar glycogen. In conclusion, after prolonged high-intensity exercise the depletion of glycogen is dependent on subcellular localization. In addition, the localization of glycogen appears to be influenced by fibre type prior to exercise, as well as carbohydrate availability during the subsequent period of recovery. These findings provide insight into the significance of fibre type-specific compartmentalization of glycogen metabolism in skeletal muscle during exercise and subsequent recovery. © 2011 The Authors. Journal compilation © 2011 The Physiological Society.

  • 7.
    Nielsen, Joachim
    et al.
    Department of Sports Science and Clinical Biomechanics, SDU Muscle Research Cluster (SMRC), University of Southern Denmark, Odense M, DK-5230, Denmark .
    Cheng, Arthur J.
    Department of Physiology and Pharmacology, Karolinska Institutet, SE-171 77, Stockholm, Sweden .
    Ørtenblad, Niels
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Department of Sports Science and Clinical Biomechanics, SDU Muscle Research Cluster (SMRC), University of Southern Denmark, Odense M, DK-5230, Denmark .
    Westerblad, Håkan
    Department of Physiology and Pharmacology, Karolinska Institutet, SE-171 77, Stockholm, Sweden .
    Subcellular distribution of glycogen and decreased tetanic Ca2+ in fatigued single intact mouse muscle fibres2014In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 592, no 9, p. 2003-2012Article in journal (Refereed)
    Abstract [en]

    Key points Muscle glycogen (the storage form of glucose) is consumed during muscle work and the depletion of glycogen is thought to be a main contributor to muscle fatigue. In this study, we used a novel approach to first measure fatigue-induced reductions in force and tetanic Ca2+ in isolated single mouse muscle fibres following repeated contractions and subsequently quantify the subcellular distribution of glycogen in the same fibre. Using this approach, we investigated whether the decreased tetanic Ca2+ induced by repeated contractions was associated with glycogen depletion in certain subcellular regions. The results show a positive correlation between depletion of glycogen located within the myofibrils and low tetanic Ca2+ after repetitive stimulation. We conclude that subcellular glycogen depletion has a central role in the decrease in tetanic Ca2+ that occurs during repetitive contractions. In skeletal muscle fibres, glycogen has been shown to be stored at different subcellular locations: (i) between the myofibrils (intermyofibrillar); (ii) within the myofibrils (intramyofibrillar); and (iii) subsarcolemmal. Of these, intramyofibrillar glycogen has been implied as a critical regulator of sarcoplasmic reticulum Ca2+ release. The aim of the present study was to test directly how the decrease in cytoplasmic free Ca2+ ([Ca2+](i)) during repeated tetanic contractions relates to the subcellular glycogen distribution. Single fibres of mouse flexor digitorum brevis muscles were fatigued with 70Hz, 350ms tetani given at 2s (high-intensity fatigue, HIF) or 10s (low-intensity fatigue, LIF) intervals, while force and [Ca2+](i) were measured. Stimulation continued until force decreased to 30% of its initial value. Fibres were then prepared for analyses of subcellular glycogen distribution by transmission electron microscopy. At fatigue, tetanic [Ca2+](i) was reduced to 70 +/- 4% and 54 +/- 4% of the initial in HIF (P<0.01, n=9) and LIF (P<0.01, n=5) fibres, respectively. At fatigue, the mean inter- and intramyofibrillar glycogen content was 60-75% lower than in rested control fibres (P<0.05), whereas subsarcolemmal glycogen was similar to control. Individual fibres showed a good correlation between the fatigue-induced decrease in tetanic [Ca2+](i) and the reduction in intermyofibrillar (P=0.051) and intramyofibrillar (P=0.0008) glycogen. In conclusion, the fatigue-induced decrease in tetanic [Ca2+](i), and hence force, is accompanied by major reductions in inter- and intramyofibrillar glycogen. The stronger correlation between decreased tetanic [Ca2+](i) and reduced intramyofibrillar glycogen implies that sarcoplasmic reticulum Ca2+ release critically depends on energy supply from the intramyofibrillar glycogen pool.

  • 8.
    Nielsen, Joachim
    et al.
    Univ Southern Denmark, Denmark.
    Gejl, Kasper D.
    Univ Southern Denmark, Denmark.
    Hey-Mogensen, Martin
    Univ Southern Denmark, Denmark.
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Suetta, Charlotte
    Univ Copenhagen, Denmark.
    Krustrup, Peter
    Univ Southern Denmark, Denmark; Univ Exeter, England.
    Elemans, Coen P. H.
    Univ Southern Denmark, Denmark.
    Ørtenblad, Niels
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Univ Southern Denmark, Denmark.
    Plasticity in mitochondrial cristae density allows metabolic capacity modulation in human skeletal muscle2017In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, no 9, p. 2839-2847Article in journal (Refereed)
    Abstract [en]

    Mitochondrial energy production involves the movement of protons down a large electrochemical gradient via ATP synthase located on the folded inner membrane, known as cristae. In mammalian skeletal muscle, the density of cristae in mitochondria is assumed to be constant. However, recent experimental studies have shown that respiration per mitochondria varies. Modelling studies have hypothesized that this variation in respiration per mitochondria depends on plasticity in cristae density, although current evidence for such a mechanism is lacking. In the present study, we confirm this hypothesis by showing that, in human skeletal muscle, and in contrast to the current view, the mitochondrial cristae density is not constant but, instead, exhibits plasticity with long-term endurance training. Furthermore, we show that frequently recruited mitochondria-enriched fibres have significantly increased cristae density and that, at the whole-body level, muscle mitochondrial cristae density is a better predictor of maximal oxygen uptake rate than muscle mitochondrial volume. Our findings establish an elevating mitochondrial cristae density as a regulatory mechanism for increasing metabolic power in human skeletal muscle. We propose that this mechanism allows evasion of the trade-off between cell occupancy by mitochondria and other cellular constituents, as well as improved metabolic capacity and fuel catabolism during prolonged elevated energy requirements.

  • 9.
    Nielsen, Joachim
    et al.
    Univ Southern Denmark, Denmark.
    Gejl, Kasper D.
    Univ Southern Denmark, Denmark.
    Ørtenblad, Niels
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Univ Southern Denmark, Denmark.
    Is there plasticity in mitochondrial cristae density with endurance training?: Reply2017In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 595, no 9, p. 2987-2988Article in journal (Refereed)
  • 10.
    Ørtenblad, Niels
    et al.
    University of Southern Denmark, Odense, Denmark.
    Nielsen, Joachim
    University of Southern Denmark, Odense, Denmark.
    Saltin, Bengt
    Copenhagen Muscle Research Centre, Copenhagen, Denmark.
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Role of glycogen availability in sarcoplasmic reticulum Ca(2+) kinetics in human skeletal muscle2011In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 589, no 3, p. 711-725Article in journal (Refereed)
    Abstract [en]

    Little is known about the precise mechanism that relates skeletal muscle glycogen to muscle fatigue. The aim of the present study was to examine the effect of glycogen on sarcoplasmic reticulum (SR) function in the arm and leg muscles of elite cross-country skiers (n = 10, (V) over dot(O2 max) 72 +/- 2 ml kg(-1) min(-1)) before, immediately after, and 4 h and 22 h after a fatiguing 1 h ski race. During the first 4 h recovery, skiers received either water or carbohydrate (CHO) and thereafter all received CHO-enriched food. Immediately after the race, arm glycogen was reduced to 31 +/- 4% and SR Ca2+ release rate decreased to 85 +/- 2% of initial levels. Glycogen noticeably recovered after 4 h recovery with CHO (59 +/- 5% initial) and the SR Ca2+ release rate returned to pre-exercise levels. However, in the absence of CHO during the first 4 h recovery, glycogen and the SR Ca2+ release rate remained unchanged (29 +/- 2% and 77 +/- 8%, respectively), with both parameters becoming normal after the remaining 18 h recovery with CHO. Leg muscle glycogen decreased to a lesser extent (71 +/- 10% initial), with no effects on the SR Ca2+ release rate. Interestingly, transmission electron microscopy (TEM) analysis revealed that the specific pool of intramyofibrillar glycogen, representing 10-15% of total glycogen, was highly significantly correlated with the SR Ca2+ release rate. These observations strongly indicate that low glycogen and especially intramyofibrillar glycogen, as suggested by TEM, modulate the SR Ca2+ release rate in highly trained subjects. Thus, low glycogen during exercise may contribute to fatigue by causing a decreased SR Ca2+ release rate.

  • 11.
    Ørtenblad, Niels
    et al.
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Univ Southern Denmark, Inst Sports Sci & Clin Biomech, SDU Muscle Res Cluster SMRC, DK-5230 Odense M, Denmark.
    Westerblad, Håkan
    Karolinska Inst, Dept Physiol & Pharmacol, SE-17177 Stockholm, Sweden.
    Nielsen, Joachim
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Univ Southern Denmark, Inst Sports Sci & Clin Biomech, SDU Muscle Res Cluster SMRC, DK-5230 Odense M, Denmark.
    Muscle glycogen stores and fatigue2013In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 591, no 18, p. 4405-4413Article, review/survey (Refereed)
    Abstract [en]

    Studies performed at the beginning of the last century revealed the importance of carbohydrate as a fuel during exercise, and the importance of muscle glycogen on performance has subsequently been confirmed in numerous studies. However, the link between glycogen depletion and impaired muscle function during fatigue is not well understood and a direct cause-and-effect relationship between glycogen and muscle function remains to be established. The use of electron microscopy has revealed that glycogen is not homogeneously distributed in skeletal muscle fibres, but rather localized in distinct pools. Furthermore, each glycogen granule has its own metabolic machinery with glycolytic enzymes and regulating proteins. One pool of such glycogenolytic complexes is localized within the myofibrils in close contact with key proteins involved in the excitation-contraction coupling and Ca2+ release from the sarcoplasmic reticulum (SR). We and others have provided experimental evidence in favour of a direct role of decreased glycogen, localized within the myofibrils, for the reduction in SR Ca2+ release during fatigue. This is consistent with compartmentalized energy turnover and distinctly localized glycogen pools being of key importance for SR Ca2+ release and thereby affecting muscle contractility and fatigability.

1 - 11 of 11
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • 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