Gymnastik- och idrottshögskolan, GIH

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  • 1.
    Adler, Dana
    et al.
    Bar Ilan University, Israel.
    Shapira, Zehavit
    Bar Ilan University, Israel.
    Weiss, Shimon
    Bar Ilan University, Israel ; University of California, Los Angeles, USA..
    Shainberg, Asher
    Bar Ilan University, Israel.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Weak Electromagnetic Fields Accelerate Fusion of Myoblasts.2021In: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 22, no 9, article id 4407Article in journal (Refereed)
    Abstract [en]

    Weak electromagnetic fields (WEF) alter Ca2+ handling in skeletal muscle myotubes. Owing to the involvement of Ca2+ in muscle development, we investigated whether WEF affects fusion of myoblasts in culture. Rat primary myoblast cultures were exposed to WEF (1.75 µT, 16 Hz) for up to six days. Under control conditions, cell fusion and creatine kinase (CK) activity increased in parallel and peaked at 4-6 days. WEF enhanced the extent of fusion after one and two days (by ~40%) vs. control, but not thereafter. Exposure to WEF also enhanced CK activity after two days (almost four-fold), but not afterwards. Incorporation of 3H-thymidine into DNA was enhanced by one-day exposure to WEF (~40%), indicating increased cell replication. Using the potentiometric fluorescent dye di-8-ANEPPS, we found that exposure of cells to 150 mM KCl resulted in depolarization of the cell membrane. However, prior exposure of cells to WEF for one day followed by addition of KCl resulted in hyperpolarization of the cell membrane. Acute exposure of cells to WEF also resulted in hyperpolarization of the cell membrane. Twenty-four hour incubation of myoblasts with gambogic acid, an inhibitor of the inward rectifying K+ channel 2.1 (Kir2.1), did not affect cell fusion, WEF-mediated acceleration of fusion or hyperpolarization. These data demonstrate that WEF accelerates fusion of myoblasts, resulting in myotube formation. The WEF effect is associated with hyperpolarization but WEF does not appear to mediate its effects on fusion by activating Kir2.1 channels.

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  • 2.
    Blackwood, Sarah J
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Horwath, Oscar
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Moberg, Marcus
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Pontén, Marjan
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Apro, William
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden..
    Ekblom, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Physical Activity and Health. Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden..
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Extreme Variations in Muscle Fiber Composition Enable Detection of Insulin Resistance and Excessive Insulin Secretion.2022In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 107, no 7, p. e2729-e2737, article id dgac221Article in journal (Refereed)
    Abstract [en]

    CONTEXT: Muscle fiber composition is associated with peripheral insulin action.

    OBJECTIVE: We investigated whether extreme differences in muscle fiber composition are associated with alterations in peripheral insulin action and secretion in young, healthy subjects who exhibit normal fasting glycemia and insulinemia.

    METHODS: Relaxation time following a tetanic contraction was used to identify subjects with a high or low expression of type I muscle fibers: group I (n=11), area occupied by type I muscle fibers = 61.0 ± 11.8%; group II (n=8), type I area = 36.0 ± 4.9% (P<0.001). Biopsies were obtained from the vastus lateralis muscle and analyzed for mitochondrial respiration on permeabilized fibers, muscle fiber composition and capillary density. An intravenous glucose tolerance test was performed and indices of glucose tolerance, insulin sensitivity and secretion were determined.

    RESULTS: Glucose tolerance was similar between groups, whereas whole-body insulin sensitivity was decreased by ~50% in group II vs group I (P=0.019). First phase insulin release (area under the insulin curve during 10 min after glucose infusion) was increased by almost 4-fold in group II vs I (P=0.01). Whole-body insulin sensitivity was correlated with % area occupied by type I fibers (r=0.54; P=0.018) and capillary density in muscle (r=0.61; P=0.005), but not with mitochondrial respiration. Insulin release was strongly related to % area occupied by type II fibers (r=0.93; P<0.001).

    CONCLUSIONS: Assessment of muscle contractile function in young healthy subjects may prove useful in identifying individuals with insulin resistance and enhanced glucose stimulated insulin secretion prior to onset of clinical manifestations.

  • 3.
    Blackwood, Sarah J
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Horwath, Oscar
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Moberg, Marcus
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden..
    Pontén, Marjan
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Apro, William
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
    Ekblom, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Physical Activity and Health. Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden..
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Insulin resistance after a 3-day fast is associated with an increased capacity of skeletal muscle to oxidize lipids.2023In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 324, no 5, p. E390-E401Article in journal (Refereed)
    Abstract [en]

    There is a debate on whether lipid-mediated insulin resistance derives from an increased or decreased capacity of muscle to oxidize fats. Here we examine the involvement of muscle fiber composition in the metabolic responses to a 3-day fast (starvation, which results in increases in plasma lipids and insulin resistance) in two groups of healthy young subjects: 1, area occupied by type I fibers = 61.0 ± 11.8%; 2, type I area = 36.0 ± 4.9% (P<0.001). Muscle biopsies and intravenous glucose tolerance tests were performed after an overnight fast and after starvation. Biopsies were analyzed for muscle fiber composition and mitochondrial respiration. Indices of glucose tolerance and insulin sensitivity were determined. Glucose tolerance was similar in both groups after an overnight fast and deteriorated to a similar degree in both groups after starvation. In contrast, whole-body insulin sensitivity decreased markedly after starvation in group 1 (P<0.01), whereas the decrease in group 2 was substantially smaller (P=0.06). Non-esterified fatty acids and β-hydroxybutyrate levels in plasma after an overnight fast were similar between groups and increased markedly and comparably in both groups after starvation, demonstrating similar degrees of lipid load. The capacity of permeabilized muscle fibers to oxidize lipids was significantly higher in group 1 vs. 2, whereas there was no significant difference in pyruvate oxidation between groups. The data demonstrate that loss of whole-body insulin sensitivity after short-term starvation is a function of muscle fiber composition and is associated with an elevated rather than a diminished capacity of muscle to oxidize lipids.

  • 4.
    Blackwood, Sarah J
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Jude, Baptiste
    Karolinska Institutet, Sweden..
    Mader, Theresa
    Karolinska Institutet, Sweden..
    Lanner, Johanna T
    Karolinska Institutet, Sweden..
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Role of nitration in control of phosphorylase and glycogenolysis in mouse skeletal muscle.2021In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 320, no 4, p. E691-E701Article in journal (Refereed)
    Abstract [en]

    Phosphorylase is one of the most carefully studied proteins in history, but knowledge of its regulation during intense muscle contraction is incomplete. Tyrosine nitration of purified preparations of skeletal muscle phosphorylase results in inactivation of the enzyme and this is prevented by antioxidants. Whether an altered redox state affects phosphorylase activity and glycogenolysis in contracting muscle is not known. Here, we investigate the role of redox state in control of phosphorylase and glycogenolysis in isolated mouse fast-twitch (extensor digitorum longus, EDL) and slow-twitch (soleus) muscle preparations during repeated contractions. Exposure of crude muscle extracts to H2O2 had little effect on phosphorylase activity. However, exposure of extracts to peroxynitrite (ONOO-), a nitrating/oxidizing agent, resulted in complete inactivation of phosphorylase (half maximal inhibition at ~200 µM ONOO-), which was fully reversed by the presence of an ONOO-scavanger, dithiothreitol (DTT). Incubation of isolated muscles with ONOO- resulted in nitration of phosphorylase and marked inhibition of glycogenolysis during repeated contractions. ONOO- also resulted in large decreases in high-energy phosphates (ATP and phosphocreatine) in the rested state and following repeated contractions. These metabolic changes were associated with decreased force production during repeated contractions (to ~60% of control). In contrast, repeated contractions did not result in nitration of phosphorylase, nor did DTT or the general antioxidant N-acetylcysteine alter glycogenolysis during repeated contractions. These findings demonstrate that ONOO- inhibits phosphorylase and glycogenolysis in living muscle under extreme conditions. However, nitration does not play a significant role in control of phosphorylase and glycogenolysis during repeated contractions.

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  • 5.
    Blackwood, Sarah J
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Isoproterenol enhances force production in mouse glycolytic and oxidative muscle via separate mechanisms.2019In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 471, no 10, p. 1305-1316Article in journal (Refereed)
    Abstract [en]

    Fight or flight is a biologic phenomenon that involves activation of β-adrenoceptors in skeletal muscle. However, how force generation is enhanced through adrenergic activation in different muscle types is not fully understood. We studied the effects of isoproterenol (ISO, β-receptor agonist) on force generation and energy metabolism in isolated mouse soleus (SOL, oxidative) and extensor digitorum longus (EDL, glycolytic) muscles. Muscles were stimulated with isometric tetanic contractions and analyzed for metabolites and phosphorylase activity. Under conditions of maximal force production, ISO enhanced force generation markedly more in SOL (22%) than in EDL (8%). Similarly, during a prolonged tetanic contraction (30 s for SOL and 10 s for EDL), ISO-enhanced the force × time integral more in SOL (25%) than in EDL (3%). ISO induced marked activation of phosphorylase in both muscles in the basal state, which was associated with glycogenolysis (less in SOL than in EDL), and in EDL only, a significant decrease (16%) in inorganic phosphate (Pi). ATP turnover during sustained contractions (1 s EDL, 5 s SOL) was not affected by ISO in EDL, but essentially doubled in SOL. Under conditions of maximal stimulation, ISO has a minor effect on force generation in EDL that is associated with a decrease in Pi, whereas ISO has a marked effect on force generation in SOL that is associated with an increase in ATP turnover. Thus, phosphorylase functions as a phosphate trap in ISO-mediated force enhancement in EDL and as a catalyzer of ATP supply in SOL.

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  • 6.
    Durrant, Christelle
    et al.
    Université de Paris, France.
    Fuehring, Jana I
    Hannover Medical School, Germany.
    Willemetz, Alexandra
    Université de Paris, France.
    Chrétien, Dominique
    Université Paris Decartes, Sorbonnes Paris Cité, Institut Imagine, France.
    Sala, Giusy
    University of Milan, Italy.
    Ghidoni, Riccardo
    University of Milan, Italy.
    Katz, Abram
    Karolinska institutet, Stockholm, Sweden.
    Rötig, Agnès
    Université Paris Decartes, Sorbonnes Paris Cité, Institut Imagine, France.
    Thelestam, Monica
    Karolinska institutet, Stockholm, Sweden.
    Ermonval, Myriam
    Institut Pasteur, Department of Virology, Paris, France.
    Moore, Stuart E H
    Université de Paris, France.
    Defects in Galactose Metabolism and Glycoconjugate Biosynthesis in a UDP-Glucose Pyrophosphorylase-Deficient Cell Line Are Reversed by Adding Galactose to the Growth Medium.2020In: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 21, no 6, article id E2028Article in journal (Refereed)
    Abstract [en]

    UDP-glucose (UDP-Glc) is synthesized by UGP2-encoded UDP-Glc pyrophosphorylase (UGP) and is required for glycoconjugate biosynthesis and galactose metabolism because it is a uridyl donor for galactose-1-P (Gal1P) uridyltransferase. Chinese hamster lung fibroblasts harboring a hypomrphic UGP(G116D) variant display reduced UDP-Glc levels and cannot grow if galactose is the sole carbon source. Here, these cells were cultivated with glucose in either the absence or presence of galactose in order to investigate glycoconjugate biosynthesis and galactose metabolism. The UGP-deficient cells display < 5% control levels of UDP-Glc/UDP-Gal and > 100-fold reduction of [6-3H]galactose incorporation into UDP-[6-3H]galactose, as well as multiple deficits in glycoconjugate biosynthesis. Cultivation of these cells in the presence of galactose leads to partial restoration of UDP-Glc levels, galactose metabolism and glycoconjugate biosynthesis. The Vmax for recombinant human UGP(G116D) with Glc1P is 2000-fold less than that of the wild-type protein, and UGP(G116D) displayed a mildly elevated Km for Glc1P, but no activity of the mutant enzyme towards Gal1P was detectable. To conclude, although the mechanism behind UDP-Glc/Gal production in the UGP-deficient cells remains to be determined, the capacity of this cell line to change its glycosylation status as a function of extracellular galactose makes it a useful, reversible model with which to study different aspects of galactose metabolism and glycoconjugate biosynthesis.

  • 7.
    Einstein, Ofira
    et al.
    Ariel University, Ariel, Israel.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ben-Hur, Tamir
    Hebrew University Medical Center, Jerusalem, Israel.
    Physical exercise therapy for autoimmune neuroinflammation: Application of knowledge from animal models to patient care.2022In: Autoimmunity Reviews, ISSN 1568-9972, E-ISSN 1873-0183, Vol. 21, no 4, article id 103033Article in journal (Refereed)
    Abstract [en]

    Physical exercise (PE) impacts various autoimmune diseases. Accordingly, clinical trials demonstrated the safety of PE in multiple sclerosis (MS) patients and indicated beneficial outcomes. There is also an increasing body of research on the beneficial effects of exercise on experimental autoimmune encephalomyelitis (EAE), the animal model of MS, and various mechanisms underlying these effects were suggested. However, despite the documented favorable impact of PE on our health, we still lack a thorough understanding of its effects on autoimmune neuroinflammation and specific guidelines of PE therapy for MS patients are lacking. To that end, current findings on the impact of PE on autoimmune neuroinflammation, both in human MS and animal models are reviewed. The concept of personalized PE therapy for autoimmune neuroinflammation is discussed, and future research for providing biological rationale for clinical trials to pave the road for precise PE therapy in MS patients is described.

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  • 8.
    Fainstein, Nina
    et al.
    Hadassah - Hebrew University Medical Center, Jerusalem, Israel.
    Tyk, Reuven
    Ariel University, Ariel, Israel.
    Touloumi, Olga
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Lagoudaki, Roza
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Goldberg, Yehuda
    Ariel University, Ariel, Israel.
    Agranyoni, Oryan
    Ariel University, Ariel, Israel.
    Navon-Venezia, Shiri
    Ariel University, Ariel, Israel.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Grigoriadis, Nikolaos
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Ben-Hur, Tamir
    Hadassah - Hebrew University Medical Center, Jerusalem, Israel.
    Einstein, Ofira
    Ariel University, Ariel, Israel..
    Exercise intensity-dependent immunomodulatory effects on encephalomyelitis.2019In: Annals of Clinical & Translational Neurology, ISSN 2328-9503, Vol. 6, no 9, p. 1647-1658Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Exercise training (ET) has beneficial effects on multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the intensity-dependent effects of ET on the systemic immune system in EAE remain undefined.

    OBJECTIVE: (1) To compare the systemic immune modulatory effects of moderate versus high-intensity ET protocols in protecting against development of EAE; (2) To investigate whether ET affects autoimmunity selectively, or causes general immunosuppression.

    METHODS: Healthy mice performed moderate or high-intensity treadmill running programs. Proteolipid protein (PLP)-induced transfer EAE was utilized to examine ET effects specifically on the systemic immune system. Lymph node (LN)-T cells from trained versus sedentary donor mice were transferred to naïve recipients and EAE severity was assessed, by clinical assessment and histopathological analysis. LN-T cells derived from donor trained versus sedentary PLP-immunized mice were analyzed in vitro for proliferation assays by flow cytometry analysis and cytokine and chemokine receptor gene expression using real-time PCR. T cell-dependent immune responses of trained versus sedentary mice to the nonautoantigen ovalbumin and susceptibility to Escherichia coli-induced acute peritonitis were examined.

    RESULTS: High-intensity training in healthy donor mice induced significantly greater inhibition than moderate-intensity training on proliferation and generation of encephalitogenic T cells in response to PLP-immunization, and on EAE severity upon their transfer into recipient mice. High-intensity training also inhibited LN-T cell proliferation in response to ovalbumin immunization. E. coli bacterial counts and dissemination were not affected by training.

    INTERPRETATION: High-intensity training induces superior effects in preventing autoimmunity in EAE, but does not alter immune responses to E. coli infection.

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  • 9.
    Flockhart, Mikael
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Tischer, Dominik
    School of Health Sciences, Örebro University, Örebro, Sweden.
    Nilsson, Lina
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Blackwood, Sarah J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Physical Activity and Health.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Apro, William
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    THREE HOURS OF MODERATE INTENSITY EXERCISE TRAINING REDUCES GLUCOSE TOLERANCE IN ENDURANCE TRAINED ATHLETES2022Conference paper (Other academic)
    Abstract [en]

    BACKGROUND

    It is well accepted that exercise training improves glucose uptake and insulin sensitivity, and that endurance trained athletes in general show a high capacity for these parameters and excellent metabolic control. However, some studies fail to observe positive effects on glucose regulation in healthy, trained subjects the day after exercise. These, often unexpected, results have been postulated to be caused by excessive training loads, muscle damage, energy deficit, differences in glucose uptake in the exercised and non-exercised musculature and a metabolic interaction through increased fatty acid metabolism which suppresses glucose oxidation and uptake. The mode or volume of exercise that can lead to glucose intolerance in trained athletes as well as mechanistic insights and its relevance for health and performance are, however, not fully understood.

    AIM

    We studied the metabolic response to a glucose load the day after a session of high intensity interval training (HIIT) or three hours of continuous exercise (3h) in endurance trained athletes and compared the results with measurements during rest.

    METHOD

    Nine endurance trained athletes (5 females, 4 males) underwent oral glucose tolerance tests (OGTT) after rest and ~14 hours after exercise on a cycle ergometer (HIIT 5x4 minutes at ~95% of VO2max or 3h at 65% of VO2max). Venous blood was sampled at 15-minute intervals for 120 minutes and concentrations of glucose, insulin, free fatty acids (FFA) and ketones (β-hydroxybutyrate) were measured. Statistical analysis was performed using a RM one-way ANOVA with the Giesser-Greenhouse correction and Dunnett’s test was used to compare the exercise conditions to the resting condition.

    RESULTS

    The area under the curve (AUC) during the OGTT increased greatly after 3h (668±124 mM · min) (p<0.01) compared to rest (532±89) but was found to be unchanged after HIIT (541±96). Resting values of FFA and ketones were increased after 3h (p<0.01 and p<0.05, respectively) but not after HIIT. Insulin was found to be unaltered during all conditions.

    CONCLUSIONS AND RELEVANCE

    Here, we show manifestation of glucose intolerance in endurance trained athletes together with concomitant increases in plasma concentrations of FFA and ketones the day after a session of prolonged exercise training but not after HIIT. This could be a protective response for securing glucose delivery to the brain and therefore have a positive effect on endurance. It also has the potential to reduce the recovery of glycogen depots, glucose uptake during exercise and performance at higher work rates.

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    THREE HOURS OF MODERATE INTENSITY EXERCISE TRAINING REDUCES GLUCOSE TOLERANCE IN ENDURANCE TRAINED ATHLETES
  • 10.
    Flockhart, Mikael
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Tischer, Dominik
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Nilsson, Lina
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Blackwood, Sarah J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Apro, William
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Three hours of moderate intensity exercise training reduces glucose tolerance in endurance trained athletes2022In: Svensk idrottsmedicin 2022:2, Svensk förening för fysisk aktivitet och idrottsmedicin , 2022, p. 28-Conference paper (Other academic)
  • 11.
    Flockhart, Mikael
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Tischer, Dominik
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Nilsson, Lina C.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Blackwood, Sarah J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Apro, William
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Reduced glucose tolerance and insulin sensitivity after prolonged exercise in endurance athletes.2023In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 238, no 4, article id e13972Article in journal (Refereed)
    Abstract [en]

    AIM: The purpose of this study was to 1. investigate if glucose tolerance is affected after one acute bout of different types of exercise; 2. assess if potential differences between two exercise paradigms are related to changes in mitochondrial function; and 3. determine if endurance athletes differ from nonendurance-trained controls in their metabolic responses to the exercise paradigms.

    METHODS: Nine endurance athletes (END) and eight healthy nonendurance-trained controls (CON) were studied. Oral glucose tolerance tests (OGTT) and mitochondrial function were assessed on three occasions: in the morning, 14 h after an overnight fast without prior exercise (RE), as well as after 3 h of prolonged continuous exercise at 65% of VO2 max (PE) or 5 × 4 min at ~95% of VO2 max (HIIT) on a cycle ergometer.

    RESULTS: Glucose tolerance was markedly reduced in END after PE compared with RE. END also exhibited elevated fasting serum FFA and ketones levels, reduced insulin sensitivity and glucose oxidation, and increased fat oxidation during the OGTT. CON showed insignificant changes in glucose tolerance and the aforementioned measurements compared with RE. HIIT did not alter glucose tolerance in either group. Neither PE nor HIIT affected mitochondrial function in either group. END also exhibited increased activity of 3-hydroxyacyl-CoA dehydrogenase activity in muscle extracts vs. CON.

    CONCLUSION: Prolonged exercise reduces glucose tolerance and increases insulin resistance in endurance athletes the following day. These findings are associated with an increased lipid load, a high capacity to oxidize lipids, and increased fat oxidation.

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  • 12.
    Goldberg, Yehuda
    et al.
    Ariel University, Ariel, Israel.
    Fainstein, Nina
    Hebrew University Medical Center, Jerusalem, Israel.
    Zaychik, Yifat
    Ariel University, Ariel, Israel.
    Hamdi, Liel
    Ariel University, Ariel, Israel.
    Segal, Shir
    Ariel University, Ariel, Israel.
    Nabat, Hanan
    Ariel University, Ariel, Israel.
    Touloumi, Olga
    AHEPA University Hospital of Thessaloniki, Greece..
    Zoidou, Sofia
    AHEPA University Hospital of Thessaloniki, Greece..
    Grigoriadis, Nikolaos
    AHEPA University Hospital of Thessaloniki, Greece..
    Hoffman, Jay R
    Ariel University, Ariel, Israel.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ben-Hur, Tamir
    Hebrew University Medical Center, Jerusalem, Israel..
    Einstein, Ofira
    Ariel University, Ariel, Israel.
    Continuous and interval training attenuate encephalomyelitis by separate immunomodulatory mechanisms.2021In: Annals of Clinical and Translational Neurology, E-ISSN 2328-9503, Vol. 8, no 1, p. 190-200Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Studies have reported beneficial effects of exercise training on autoimmunity, and specifically on multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). However, it is unknown whether different training paradigms affect disease course via shared or separate mechanisms.

    OBJECTIVE: To compare the effects and mechanism of immune modulation of high intensity continuous training (HICT) versus high intensity interval training (HIIT) on systemic autoimmunity in EAE.

    METHODS: We used the proteolipid protein (PLP)-induced transfer EAE model to examine training effects on the systemic autoimmune response. Healthy mice performed HICT or HIIT by running on a treadmill. Lymph-node (LN)-T cells from PLP-immunized trained- versus sedentary donor mice were transferred to naïve recipients and EAE clinical and pathological severity were assessed. LN cells derived from donor trained and sedentary PLP-immunized mice were analyzed in vitro for T-cell activation and proliferation, immune cell profiling, and cytokine mRNA levels and cytokine secretion measurements.

    RESULTS: Both HICT and HIIT attenuated the encephalitogenicity of PLP-reactive T cells, as indicated by reduced EAE clinical severity and inflammation and tissue pathology in the central nervous system, following their transfer into recipient mice. HICT caused a marked inhibition of PLP-induced T-cell proliferation without affecting the T-cell profile. In contrast, HIIT did not alter T-cell proliferation, but rather inhibited polarization of T cells into T-helper 1 and T-helper 17 autoreactive populations.

    INTERPRETATION: HICT and HIIT attenuate systemic autoimmunity and T cell encephalitogenicity by distinct immunomodulatory mechanisms.

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  • 13.
    Goldberg, Yehuda
    et al.
    Ariel University, Ariel, Israel.
    Segal, Shir
    Ariel University, Ariel, Israel.
    Hamdi, Liel
    Ariel University, Ariel, Israel.
    Nabat, Hanan
    Ariel University, Ariel, Israel.
    Fainstein, Nina
    Ariel University, Ariel, Israel; Hadassah - Hebrew University Medical Center, Jerusalem, Israel..
    Mediouni, Efrat
    Ariel University, Ariel, Israel.
    Asis, Yarden
    Ariel University, Ariel, Israel.
    Theotokis, Paschalis
    Salamotas, Ilias
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece.
    Grigoriadis, Nikolaos
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ben-Hur, Tamir
    Hadassah - Hebrew University Medical Center, Jerusalem, Israel..
    Einstein, Ofira
    Ariel University, Ariel, Israel..
    High-intensity interval training attenuates development of autoimmune encephalomyelitis solely by systemic immunomodulation.2023In: Scientific Reports, E-ISSN 2045-2322, Vol. 13, no 1, article id 16513Article in journal (Refereed)
    Abstract [en]

    The impact of high-intensity interval training (HIIT) on the central nervous system (CNS) in autoimmune neuroinflammation is not known. The aim of this study was to determine the direct effects of HIIT on the CNS and development of experimental autoimmune encephalomyelitis (EAE). Healthy mice were subjected to HIIT by treadmill running and the proteolipid protein (PLP) transfer EAE model was utilized. To examine neuroprotection, PLP-reactive lymph-node cells (LNCs) were transferred to HIIT and sedentary (SED) mice. To examine immunomodulation, PLP-reactive LNCs from HIIT and SED donor mice were transferred to naïve recipients and analyzed in vitro. HIIT in recipient mice did not affect the development of EAE following exposure to PLP-reactive LNCs. HIIT mice exhibited enhanced migration of systemic autoimmune cells into the CNS and increased demyelination. In contrast, EAE severity in recipient mice injected with PLP-reactive LNCs from HIIT donor mice was significantly diminished. The latter positive effect was associated with decreased migration of autoimmune cells into the CNS and inhibition of very late antigen (VLA)-4 expression in LNCs. Thus, the beneficial effect of HIIT on EAE development is attributed solely to systemic immunomodulatory effects, likely because of systemic inhibition of autoreactive cell migration and reduced VLA-4 integrin expression.

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  • 14.
    Hamdi, Liel
    et al.
    Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel, Israel..
    Nabat, Hanan
    Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel, Israel..
    Goldberg, Yehuda
    Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel, Israel..
    Fainstein, Nina
    Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah - Hebrew University Medical Center, Jerusalem, Israel..
    Segal, Shir
    Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel, Israel..
    Mediouni, Efrat
    Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel, Israel..
    Asis, Yarden
    Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel, Israel..
    Touloumi, Olga
    B' Department of Neurology, AHEPA University Hospital of Thessaloniki, Greece..
    Grigoriadis, Nikolaos
    B' Department of Neurology, AHEPA University Hospital of Thessaloniki, Greece..
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ben-Hur, Tamir
    Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah - Hebrew University Medical Center, Jerusalem, Israel..
    Einstein, Ofira
    Department of Physical Therapy, Faculty of Health Sciences, Ariel University, Ariel, Israel..
    Exercise training alters autoimmune cell invasion into the brain in autoimmune encephalomyelitis.2022In: Annals of Clinical and Translational Neurology, E-ISSN 2328-9503, Vol. 9, no 11, p. 1792-1806Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The mechanisms by which exercise training (ET) elicits beneficial effects on the systemic immune system and the central nervous system (CNS) in autoimmune neuroinflammation are not fully understood.

    OBJECTIVES: To investigate (1) the systemic effects of high-intensity continuous training (HICT) on the migratory potential of autoimmune cells; (2) the direct effects of HICT on blood-brain-barrier (BBB) properties.

    METHODS: Healthy mice were subjected to high-intensity continuous training (HICT) by treadmill running. The proteolipid protein (PLP) transfer EAE model was utilized to examine the immunomodulatory effects of training, where PLP-reactive lymph-node cells (LNCs) from HICT and sedentary donor mice were analyzed in vitro and transferred to naïve recipients that developed EAE. To examine neuroprotection, encephalitogenic LNCs from donor mice were transferred into HICT or sedentary recipient mice and the BBB was analyzed.

    RESULTS: Transfer of PLP-reactive LNCs obtained from HICT donor mice attenuated EAE severity and inflammation in recipient mice. HICT markedly inhibited very late antigen (VLA)-4 and lymphocyte function-associated antigen (LFA)-1 expression in LNCs. Transfer of encephalitogenic LNCs into HICT recipients resulted in milder EAE and attenuated CNS inflammation. HICT reduced BBB permeability and the expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in CNS blood vessels.

    INTERPRETATION: HICT attenuates EAE development by both immunomodulatory and neuroprotective effects. The reduction in destructive CNS inflammation in EAE is attributed to systemic inhibition of autoreactive cell migratory potential, as well as reduction in BBB permeability, which are associated with reduced VLA-4/VCAM-1 and LFA-1/ICAM-1 interactions.

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  • 15.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    A century of exercise physiology: key concepts in regulation of glycogen metabolism in skeletal muscle.2022In: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 122, no 8, p. 1751-1772Article in journal (Refereed)
    Abstract [en]

    Glycogen is a branched, glucose polymer and the storage form of glucose in cells. Glycogen has traditionally been viewed as a key substrate for muscle ATP production during conditions of high energy demand and considered to be limiting for work capacity and force generation under defined conditions. Glycogenolysis is catalyzed by phosphorylase, while glycogenesis is catalyzed by glycogen synthase. For many years, it was believed that a primer was required for de novo glycogen synthesis and the protein considered responsible for this process was ultimately discovered and named glycogenin. However, the subsequent observation of glycogen storage in the absence of functional glycogenin raises questions about the true role of the protein. In resting muscle, phosphorylase is generally considered to be present in two forms: non-phosphorylated and inactive (phosphorylase b) and phosphorylated and constitutively active (phosphorylase a). Initially, it was believed that activation of phosphorylase during intense muscle contraction was primarily accounted for by phosphorylation of phosphorylase b (activated by increases in AMP) to a, and that glycogen synthesis during recovery from exercise occurred solely through mechanisms controlled by glucose transport and glycogen synthase. However, it now appears that these views require modifications. Moreover, the traditional roles of glycogen in muscle function have been extended in recent years and in some instances, the original concepts have undergone revision. Thus, despite the extensive amount of knowledge accrued during the past 100 years, several critical questions remain regarding the regulation of glycogen metabolism and its role in living muscle.

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  • 16.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    The role of glycogen phosphorylase in glycogen biogenesis in skeletal muscle after exercise2023In: Sports Medicine and Health Science, ISSN 2666-3376, Vol. 5, no 1, p. 29-33Article in journal (Refereed)
    Abstract [en]

    Initially it was believed that phosphorylase was responsible for both glycogen breakdown and synthesis in the living cell. The discovery of glycogen synthase and McArdle's disease (lack of phosphorylase activity), together with the high Pi/glucose 1-P ratio in skeletal muscle, demonstrated that glycogen synthesis could not be attributed to reversal of the phosphorylase reaction. Rather, glycogen synthesis was attributable solely to the activity of glycogen synthase, subsequent to the transport of glucose into the cell. However, the well-established observation that phosphorylase was inactivated (i.e., dephosphorylated) during the initial recovery period after prior exercise, when the rate of glycogen accumulation is highest and independent of insulin, suggested that phosphorylase could play an active role in glycogen accumulation. But the quantitative contribution of phosphorylase inactivation was not established until recently, when studying isolated murine muscle preparations during recovery from repeated contractions at temperatures ranging from 25 to 35 °C. Thus, in both slow-twitch, oxidative and fast-twitch, glycolytic muscles, inactivation of phosphorylase accounted for 45%–75% of glycogen accumulation during the initial hours of recovery following repeated contractions. Such data indicate that phosphorylase inactivation may be the most important mechanism for glycogen accumulation under defined conditions. These results support the initial belief that phosphorylase plays a quantitative role in glycogen formation in the living cell. However, the mechanism is not via activation of phosphorylase, but rather via inactivation of the enzyme.

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  • 17.
    Moberg, Marcus
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Physiology and Pharmacology, Karolinska Institute, Sweden.
    Apro, William
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Clinical Science, Intervention and Technology, Karolinska Institute, Sweden.
    Horwath, Oscar
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    van Hall, Gerrit
    University of Copenhagen, Denmark.; Rigshospitalet, Copenhagen, Denmark..
    Blackwood, Sarah J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Acute normobaric hypoxia blunts contraction-mediated mTORC1- and JNK-signaling in human skeletal muscle.2022In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 234, no 2, article id e13771Article in journal (Refereed)
    Abstract [en]

    AIM: Hypoxia has been shown to reduce resistance exercise-induced stimulation of protein synthesis and long-term gains in muscle mass. However, the mechanism whereby hypoxia exerts its effect is not clear. Here we examine the effect of acute hypoxia on the activity of several signaling pathways involved in regulation of muscle growth following a bout of resistance exercise.

    METHODS: Eight men performed two sessions of leg resistance exercise in Normoxia or Hypoxia (12% O2 ) in a randomized crossover fashion. Muscle biopsies were obtained at rest and at 0, 90,180 min after exercise. Muscle analyses included levels of signaling proteins and metabolites associated with energy turnover.

    RESULTS: Exercise during Normoxia induced a 5-10-fold increase of S6K1Thr389 phosphorylation throughout the recovery period, but Hypoxia blunted the increases by ~50%. Phosphorylation of JNKThr183/Tyr185 and the JNK target SMAD2Ser245/250/255 was increased by 30-40-fold immediately after exercise in Normoxia, but Hypoxia blocked almost 70% of the activation. Throughout recovery, phosphorylation of JNK and SMAD2 remained elevated following exercise in Normoxia, but the effect of Hypoxia was lost at 90-180 min post-exercise. Hypoxia had no effect on exercise induced Hippo- or autophagy-signaling and ubiquitin-proteasome related protein levels. Nor did Hypoxia alter the changes induced by exercise in high energy phosphates, glucose 6-P, lactate, or phosphorylation of AMPK or ACC.

    CONCLUSION: We conclude that acute severe hypoxia inhibits resistance exercise induced mTORC1- and JNK signaling in human skeletal muscle, effects that do not appear to be mediated by changes in the degree of metabolic stress in the muscle.

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  • 18.
    Nordström, Fabian
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Liegnell, Rasmus
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Apro, William
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Clinical Science, Intervention and Technology, Karolinska Institute, Sweden.
    Blackwood, Sarah J
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Moberg, Marcus
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Physiology and Pharmacology, Karolinska Institute, Sweden.
    The lactate receptor GPR81 is predominantly expressed in type II human skeletal muscle fibers: potential for lactate autocrine signaling.2023In: American Journal of Physiology - Cell Physiology, ISSN 0363-6143, E-ISSN 1522-1563, Vol. 324, no 2, p. C477-C487Article in journal (Refereed)
    Abstract [en]

    GPR81 was first identified in adipocytes as a receptor for L-lactate, which upon binding inhibits cAMP-PKA-CREB signaling. Moreover, incubation of myotubes with lactate augments expression of GPR81 and genes and proteins involved in lactate- and energy metabolism. However, characterization of GPR81 expression and investigation of related signaling in human skeletal muscle under conditions of elevated circulating lactate levels are lacking. Muscle biopsies were obtained from healthy men and women at rest, after leg extension exercise, with or without venous infusion of sodium lactate, and 90 and 180 min after exercise (8 men and 8 women). Analyses included protein and mRNA levels of GPR81, as well as GPR81-dependent signaling molecules. GPR81 expression was 2.5-fold higher in type II glycolytic compared with type I oxidative muscle fibers, and the expression was inversely related to the percentage of type I muscle fibers. Muscle from women expressed about 25% more GPR81 protein than from men. Global PKA-activity increased by 5-8% after exercise, with no differences between trials. CREBS133 phosphorylation was reduced by 30% after exercise and remained repressed during the entire trials, with no influence of the lactate infusion. The mRNA expression of VEGF and PGC-1α were increased by 2.5 - 6-fold during recovery, and that of LDH reduced by 15% with no differences between trials for any gene at any time point. The high expression of GPR81-protein in type II fibers suggests that lactate functions as an autocrine signaling molecule in muscle; however, lactate does not appear to regulate CREB signaling during exercise.

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  • 19.
    Zaychik, Yifat
    et al.
    Ariel University, Ariel, Israel..
    Fainstein, Nina
    Hadassah-Hebrew University Medical Center, Jerusalem, Israel..
    Touloumi, Olga
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Goldberg, Yehuda
    Ariel University, Ariel, Israel..
    Hamdi, Liel
    Ariel University, Ariel, Israel..
    Segal, Shir
    Ariel University, Ariel, Israel..
    Nabat, Hanan
    Ariel University, Ariel, Israel..
    Zoidou, Sofia
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Grigoriadis, Nikolaos
    AHEPA University Hospital of Thessaloniki, Thessaloniki, Greece..
    Katz, Abram
    Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.
    Ben-Hur, Tamir
    Hadassah-Hebrew University Medical Center, Jerusalem, Israel..
    Einstein, Ofira
    Ariel University, Ariel, Israel..
    High-Intensity Exercise Training Protects the Brain Against Autoimmune Neuroinflammation: Regulation of Microglial Redox and Pro-inflammatory Functions.2021In: Frontiers in Cellular Neuroscience, E-ISSN 1662-5102, Vol. 15, article id 640724Article in journal (Refereed)
    Abstract [en]

    Background: Exercise training induces beneficial effects on neurodegenerative diseases, and specifically on multiple sclerosis (MS) and it's model experimental autoimmune encephalomyelitis (EAE). However, it is unclear whether exercise training exerts direct protective effects on the central nervous system (CNS), nor are the mechanisms of neuroprotection fully understood. In this study, we investigated the direct neuroprotective effects of high-intensity continuous training (HICT) against the development of autoimmune neuroinflammation and the role of resident microglia. Methods: We used the transfer EAE model to examine the direct effects of training on the CNS. Healthy mice performed HICT by treadmill running, followed by injection of encephalitogenic proteolipid (PLP)-reactive T-cells to induce EAE. EAE severity was assessed clinically and pathologically. Brain microglia from sedentary (SED) and HICT healthy mice, as well as 5-days post EAE induction (before the onset of disease), were analyzed ex vivo for reactive oxygen species (ROS) and nitric oxide (NO) formation, mRNA expression of M1/M2 markers and neurotrophic factors, and secretion of cytokines and chemokines. Results: Transfer of encephalitogenic T-cells into HICT mice resulted in milder EAE, compared to sedentary mice, as indicated by reduced clinical severity, attenuated T-cell, and neurotoxic macrophage/microglial infiltration, and reduced loss of myelin and axons. In healthy mice, HICT reduced the number of resident microglia without affecting their profile. Isolated microglia from HICT mice after transfer of encephalitogenic T-cells exhibited reduced ROS formation and released less IL-6 and monocyte chemoattractant protein (MCP) in response to PLP-stimulation. Conclusions: These findings point to the critical role of training intensity in neuroprotection. HICT protects the CNS against autoimmune neuroinflammation by reducing microglial-derived ROS formation, neurotoxicity, and pro-inflammatory responses involved in the propagation of autoimmune neuroinflammation.

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