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  • American Physiological Society  (14)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Cell Physiology Vol. 284, No. 6 ( 2003-06-01), p. C1362-C1373
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 284, No. 6 ( 2003-06-01), p. C1362-C1373
    Abstract: The present study illustrates elements of the signal cascades involved in the activation of taurine efflux pathways in myotubes derived from skeletal muscle cells. Exposing primary skeletal muscle cells, loaded with 14 C-taurine, to 1) hypotonic media, 2) the phospholipase A 2 (PLA 2 ) activator melittin, 3) anoxia, or 4) lysophosphatidyl choline (LPC) causes an increase in 14 C-taurine release and a concomitant production of reactive oxygen species (ROS). The antioxidants butulated hydroxy toluene and vitamin E inhibit the taurine efflux after cell swelling, anoxia, and addition of LPC. The muscle cells possess two separate taurine efflux pathways, i.e., a swelling- and melittin-induced pathway that requires 5-lipoxygenase activity for activation and a LPC-induced pathway. The two pathways are distinguished by their opposing sensitivity toward the anion channel blocker DIDS and cholesterol. These data provide evidence for PLA 2 products and ROS as key mediators of the signal cascade leading to taurine efflux in muscle.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2000
    In:  Journal of Applied Physiology Vol. 89, No. 1 ( 2000-07-01), p. 210-217
    In: Journal of Applied Physiology, American Physiological Society, Vol. 89, No. 1 ( 2000-07-01), p. 210-217
    Abstract: The purpose of the study was to characterize the sarcoplasmic reticulum (SR) function and contractile properties before and during recovery from fatigue in the rat extensor digitorum longus muscle. Fatiguing contractions (60 Hz, 150 ms/s for 4 min) induced a reduction of the SR Ca 2+ release rate to 66% that persisted for 1 h, followed by a gradual recovery to 87% of prefatigue release rate at 3 h recovery. Tetanic force and rate of force development (+dF/d t) and relaxation (−dF/d t) were depressed by ∼80% after stimulation. Recovery occurred in two phases: an initial phase, in which during the first 0.5–1 h the metabolic state recovered to resting levels, and a slow phase from 1–3 h characterized by a rather slow recovery of the mechanical properties. The recovery of SR Ca 2+ release rate was closely correlated to +dF/d t during the slow phase of recovery ( r 2 = 0.51; P 〈 0.05). Despite a slowing of the relaxation rate, we did not find any significant alterations in the SR Ca 2+ uptake function. These data demonstrate that the Ca 2+ release mechanism of SR is sensitive to repetitive in vitro muscle contraction. Moreover, the results indicate that +dF/d t to some extent depends on the rate of Ca 2+ release during the slow phase of recovery.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 3
    In: Journal of Applied Physiology, American Physiological Society, Vol. 109, No. 6 ( 2010-12), p. 1628-1634
    Abstract: Very little attention has been given to the combined effects of aging and disuse as separate factors causing deterioration in muscle mechanical function. Thus the purpose of this study was to investigate the effects of 2 wk of immobilization followed by 4 wk of retraining on knee extensor muscle mechanical function (e.g., maximal strength and rapid force capacity) and muscle fiber morphology in 9 old (OM: 67.3 ± 1.3 yr) and 11 young healthy men (YM: 24.4 ± 0.5 yr) with comparable levels of physical activity. Following immobilization, OM demonstrated markedly larger decreases in rapid force capacity (i.e., rate of force development, impulse) than YM (∼20–37 vs. ∼13–16%; P 〈 0.05). In contrast, muscle fiber area decreased in YM for type I, IIA, and IIx fibers (∼15–30%; P 〈 0.05), whereas only type IIa area decreased in OM (13.2%; P 〈 0.05). Subsequent retraining fully restored muscle mechanical function and muscle fiber area in YM, whereas OM showed an attenuated recovery in muscle fiber area and rapid force capacity (tendency). Changes in maximal isometric and dynamic muscle strength were similar between OM and YM. In conclusion, the present data reveal that OM may be more susceptible to the deleterious effects of short-term muscle disuse on muscle fiber size and rapid force capacity than YM. Furthermore, OM seems to require longer time to recover and regain rapid muscle force capacity, which may lead to a larger risk of falling in aged individuals after periods of short-term disuse.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 298, No. 3 ( 2010-03), p. E706-E713
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 298, No. 3 ( 2010-03), p. E706-E713
    Abstract: The purpose of the study was to investigate the effect of aerobic training and type 2 diabetes on intramyocellular localization of lipids, mitochondria, and glycogen. Obese type 2 diabetic patients ( n = 12) and matched obese controls ( n = 12) participated in aerobic cycling training for 10 wk. Endurance-trained athletes ( n = 15) were included for comparison. Insulin action was determined by euglycemic-hyperinsulinemic clamp. Intramyocellular contents of lipids, mitochondria, and glycogen at different subcellular compartments were assessed by transmission electron microscopy in biopsies obtained from vastus lateralis muscle. Type 2 diabetic patients were more insulin resistant than obese controls and had threefold higher volume of subsarcolemmal (SS) lipids compared with obese controls and endurance-trained subjects. No difference was found in intermyofibrillar lipids. Importantly, following aerobic training, this excess SS lipid volume was lowered by ∼50%, approaching the levels observed in the nondiabetic subjects. A strong inverse association between insulin sensitivity and SS lipid volume was found ( r 2 =0.62, P = 0.002). The volume density and localization of mitochondria and glycogen were the same in type 2 diabetic patients and control subjects, and showed in parallel with improved insulin sensitivity a similar increase in response to training, however, with a more pronounced increase in SS mitochondria and SS glycogen than in other localizations. In conclusion, this study, estimating intramyocellular localization of lipids, mitochondria, and glycogen, indicates that type 2 diabetic patients may be exposed to increased levels of SS lipids. Thus consideration of cell compartmentation may advance the understanding of the role of lipids in muscle function and type 2 diabetes.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 279, No. 1 ( 2000-07-01), p. R152-R160
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 279, No. 1 ( 2000-07-01), p. R152-R160
    Abstract: To evaluate the effect of intermittent sprint training on sarcoplasmic reticulum (SR) function, nine young men performed a 5 wk high-intensity intermittent bicycle training, and six served as controls. SR function was evaluated from resting vastus lateralis muscle biopsies, before and after the training period. Intermittent sprint performance (ten 8-s all-out periods alternating with 32-s recovery) was enhanced 12% ( P 〈 0.01) after training. The 5-wk sprint training induced a significantly higher ( P 〈 0.05) peak rate of AgNO 3 -stimulated Ca 2+ release from 709 (range 560–877; before) to 774 (596–977) arbitrary units Ca 2+ ⋅ g protein − 1 ⋅ min − 1 (after). The relative SR density of functional ryanodine receptors (RyR) remained unchanged after training; there was, however, a 48% ( P 〈 0.05) increase in total number of RyR. No significant differences in Ca 2+ uptake rate and Ca 2+ -ATPase capacity were observed following the training, despite that the relative density of Ca 2+ -ATPase isoforms SERCA1 and SERCA2 had increased 41% and 55%, respectively ( P 〈 0.05). These data suggest that high-intensity training induces an enhanced peak SR Ca 2+ release, due to an enhanced total volume of SR, whereas SR Ca 2+ sequestration function is not altered.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 315, No. 5 ( 2018-11-01), p. E872-E884
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 315, No. 5 ( 2018-11-01), p. E872-E884
    Abstract: This study compared the effects of moderate-intensity endurance training and high-intensity interval training on fiber type-specific subcellular volumetric content and morphology of lipid droplets and mitochondria in skeletal muscles of type 2 diabetic patients. Sixteen sedentary type 2 diabetic patients (57 ± 7 yr old) were randomized to complete 11 wk of either 40-min cycling at 50% peak workload (Endurance, n = 8) or 10 1-min cycling intervals at 95% peak workload separated by 1 min of recovery (High-Intensity Interval, n = 8), three times per week. Assessments for cardiorespiratory fitness, body composition, glycemic control, together with muscle biopsies were performed before and after the intervention. Morphometric analyses of lipid droplets and mitochondria were conducted in the subcellular fractions of biopsied muscle fibers using quantitative electron microscopy. The training intervention increased cardiorespiratory fitness, lowered fat mass, and improved nonfasting glycemic control ( P 〈 0.05), with no difference between training modalities. In the subsarcolemmal space, training decreased lipid droplet volume ( P = 0.003), and high-intensity interval, but not endurance, training reduced the size of lipid droplets, specifically in type 2 fibers ( P 〈 0.001). No training-induced change in intermyofibrillar lipid droplets was observed in both fiber types. Subsarcolemmal mitochondrial volume was increased by high-intensity interval ( P = 0.02), but not endurance, training ( P = 0.79). Along with improvement in glycemic control, low-volume high-intensity interval training is an alternative time-saving training modality that affects subcellular morphology and volumetric content of lipid droplets in skeletal muscle of type 2 diabetic patients.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 7
    In: Journal of Applied Physiology, American Physiological Society, Vol. 129, No. 6 ( 2020-12-01), p. 1355-1364
    Abstract: The objective was to determine whether skeletal muscle molecular markers and SC number were influenced differently in users and nonusers of oral contraceptives (OCs) following 10 wk of resistance training. Thirty-eight young healthy untrained users ( n = 20) and nonusers of OC ( n = 18) completed a 10-wk supervised progressive resistance training program. Before and after the intervention, a muscle tissue sample was obtained from the vastus lateralis muscle for analysis of muscle fiber cross-sectional area (fCSA) and satellite cell (SC) and myonuclei number using immunohistochemistry, gene expression using PCR, protein expression, and myosin heavy chain composition. Following the training period, quadriceps fCSA ( P 〈 0.05), SCs/type I fiber ( P = 0.05), and MURF-1 mRNA ( P 〈 0.01) were significantly increased with no difference between the groups. However, SCs/total fiber and SCs/type II fiber increased in OC users only, and SCs/type II fCSA tended ( P = 0.055) to be greater in the OC users. Furthermore, in OC users there were a fiber type shift from myosin heavy chain (MHC) IIx to MHC IIa ( P 〈 0.01), and expression of muscle regulatory factor 4 (MRF4) mRNA ( P 〈 0.001) was significantly greater than in non-OC users. Use of second-generation OCs in young untrained women increased skeletal muscle MRF4 expression and SC number following 10 wk of resistance training compared with nonusers. NEW & NOTEWORTHY The effect of oral contraceptive use on the skeletal muscle regulatory pathways in response to resistance training has not been investigated previously. Here we present novel data, demonstrating that use of second-generation oral contraceptives in young untrained women increased skeletal muscle regulatory factor 4 expression and satellite cell number following 10 wk of resistance training compared with nonusers.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2020
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 299, No. 6 ( 2010-12), p. E1053-E1060
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 299, No. 6 ( 2010-12), p. E1053-E1060
    Abstract: Previous studies have shown that skeletal muscle glycogen and mitochondria are distributed in distinct subcellular localizations, but the role and regulation of these subcellular localizations are unclear. In the present study, we used transmission electron microscopy to investigate the effect of disuse and aging on human skeletal muscle glycogen and mitochondria content in subsarcolemmal (SS), intermyofibrillar (IMF), and intramyofibrillar (intra) localizations. Five young (∼23 yr) and five old (∼66 yr) recreationally active men had their quadriceps muscle immobilized for 2 wk by whole leg casting. Biopsies were obtained from m. vastus lateralis before and after the immobilization period. Immobilization induced a decrement of intra glycogen content by 54% ( P 〈 0.001) in both age groups and in two ultrastructurally distinct fiber types, whereas the content of IMF and SS glycogen remained unchanged. A localization-dependent decrease ( P = 0.03) in mitochondria content following immobilization was found in both age groups, where SS mitochondria decreased by 33% ( P = 0.02), superficial IMF mitochondria decreased by 20% ( P = 0.05), and central IMF mitochondria remained unchanged. In conclusion, our findings demonstrate a localization-dependent adaptation to immobilization in glycogen and mitochondria content of skeletal muscles of both young and old individuals. Specifically, this suggests that short-term disuse preferentially affects glycogen particles located inside the myofibrils and that mitochondria volume plasticity can be dependent on the distance to the fiber border.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 9
    In: Journal of Applied Physiology, American Physiological Society, Vol. 119, No. 5 ( 2015-09-01), p. 475-486
    Abstract: The study was a randomized placebo-controlled trial investigating mechanisms by which chronic β 2 -adrenergic stimulation enhances muscle force and power output during maximal cycle ergometer exercise in young men. Eighteen trained men were assigned to an experimental group [oral terbutaline 5 mg/30 kg body weight (bw) twice daily (TER); n = 9] or a control group [placebo (PLA); n = 9] for a 4-wk intervention. No changes were observed with the intervention in PLA. Isometric muscle force of the quadriceps increased ( P ≤ 0.01) by 97 ± 29 N (means ± SE) with the intervention in TER compared with PLA. Peak and mean power output during 30 s of maximal cycling increased ( P ≤ 0.01) by 32 ± 8 and 25 ± 9 W, respectively, with the intervention in TER compared with PLA. Maximal oxygen consumption (V̇o 2max ) and time to fatigue during incremental cycling did not change with the intervention. Lean body mass increased by 1.95 ± 0.8 kg ( P ≤ 0.05) with the intervention in TER compared with PLA. Change in single fiber cross-sectional area of myosin heavy chain (MHC) I (1,205 ± 558 μm 2 ; P ≤ 0.01) and MHC II fibers (1,277 ± 595 μm 2 ; P ≤ 0.05) of the vastus lateralis muscle was higher for TER than PLA with the intervention, whereas no changes were observed in MHC isoform distribution. Expression of muscle proteins involved in growth, ion handling, lactate production, and clearance increased ( P ≤ 0.05) with the intervention in TER compared with PLA, with no change in oxidative enzymes. Our observations suggest that muscle hypertrophy is the primary mechanism underlying enhancements in muscle force and peak power during maximal cycling induced by chronic β 2 -adrenergic stimulation in humans.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 10
    Online Resource
    Online Resource
    American Physiological Society ; 2021
    In:  Journal of Applied Physiology Vol. 131, No. 1 ( 2021-07-01), p. 388-400
    In: Journal of Applied Physiology, American Physiological Society, Vol. 131, No. 1 ( 2021-07-01), p. 388-400
    Abstract: The maintenance of healthy and functional mitochondria is the result of a complex mitochondrial turnover and herein quality-control program that includes both mitochondrial biogenesis and autophagy of mitochondria. The aim of this study was to examine the effect of an intensified training load on skeletal muscle mitochondrial quality control in relation to changes in mitochondrial oxidative capacity, maximal oxygen consumption, and performance in highly trained endurance athletes. Elite endurance athletes ( n = 27) performed high-intensity interval exercise followed by moderate-intensity continuous exercise 3 days per week for 4 wk in addition to their usual volume of training. Mitochondrial oxidative capacity, abundance of mitochondrial proteins, markers of autophagy, and antioxidant capacity of skeletal muscle were assessed in skeletal muscle biopsies before and after the intensified training period. The intensified training period increased several autophagy markers suggesting an increased turnover of mitochondrial and cytosolic proteins. In permeabilized muscle fibers, mitochondrial respiration was ∼20% lower after training although some markers of mitochondrial density increased by 5%–50%, indicative of a reduced mitochondrial quality by the intensified training intervention. The antioxidative proteins UCP3, ANT1, and SOD2 were increased after training, whereas we found an inactivation of aconitase. In agreement with the lower aconitase activity, the amount of mitochondrial LON protease that selectively degrades oxidized aconitase was doubled. Together, this suggests that mitochondrial respiratory function is impaired during the initial recovery from a period of intensified endurance training whereas mitochondrial quality control is slightly activated in highly trained skeletal muscle. NEW & NOTEWORTHY We show that mitochondrial respiration is temporarily impaired after a period of intensified exercise training in elite athletes. In parallel, proteins involved in the antioxidative response including SOD2, UCP3, and ANT2 were upregulated, whereas mitochondrial biogenesis was slightly activated. Despite the mitochondrial respiratory impairments, physical performance was improved a few days after the intense training period.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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