Ingrid Marie Egner

• Gundersen, Kristian; Bruusgaard, Jo C.; Egner, Ingrid Marie; Eftestøl, Einar & Bengtsen, Mads (2018). Muscle memory: virtues of your youth?. Journal of Physiology.  ISSN 0022-3751.  596(18), s 4289- 4290 . doi: 10.1113/JP276354
• Markworth, James F.; D'Souza, Randall F.; Aasen, Kirsten M.M.; Mitchell, Sarah M.; Durainayagam, Brenan R.; Sinclair, Andrew J.; Peake, Jonathan M.; Egner, Ingrid Marie; Raastad, Truls; Cameron-Smith, David & Mitchell, Cameron J. (2018). Arachidonic acid supplementation transiently augments the acute inflammatory response to resistance exercise in trained men. Journal of applied physiology.  ISSN 8750-7587.  125(2), s 271- 286 . doi: 10.1152/japplphysiol.00169.2018 Vis sammendrag

  Strenuous exercise can result in skeletal muscle damage, leading to the systemic mobilization, activation, and intramuscular accumulation of blood leukocytes. Eicosanoid metabolites of arachidonic acid (ARA) are potent inflammatory mediators, but whether changes in dietary ARA intake influence exercise-induced inflammation is not known. This study investigated the effect of 4 wk of dietary supplementation with 1.5 g/day ARA (n = 9, 24 ± 1.5 yr) or corn-soy oil placebo (n = 10, 26 ± 1.3 yr) on systemic and intramuscular inflammatory responses to an acute bout of resistance exercise (8 sets each of leg press and extension at 80% one-repetition maximum) in previously trained men. Whole EDTA blood, serum, peripheral blood mononuclear cells (PMBCs), and skeletal muscle biopsies were collected before exercise, immediately postexercise, and at 2, 4, and 48 h of recovery. ARA supplementation resulted in higher exercise-stimulated serum creatine kinase activity [incremental area under the curve (iAUC) P = 0.046] and blood leukocyte counts (iAUC for total white cells, P < 0.001; neutrophils: P = 0.007; monocytes: P = 0.015). The exercise-induced fold change in peripheral blood mononuclear cell mRNA expression of interleukin-1β (IL1B), CD11b (ITGAM), and neutrophil elastase (ELANE), as well as muscle mRNA expression of the chemokines interleukin-8 (CXCL8) and monocyte chemoattractant protein 1 (CCL2) was also greater in the ARA group than placebo. Despite this, ARA supplementation did not influence the histological presence of leukocytes within muscle, perceived muscle soreness, or the extent and duration of muscle force loss. These data show that ARA supplementation transiently increased the inflammatory response to acute resistance exercise but did not impair recovery.

• Mitchell, Cameron J; D'Souza, Randall F; Figueiredo, Vandre C.; Chan, Alex; Aasen, Kirsten MM; Durainayagam, Brenan; Mitchell, Sarah M.; Sinclair, Andrew J.; Egner, Ingrid Marie; Raastad, Truls; Cameron-Smith, David & Markworth, James F. (2018). The effect of dietary arachidonic acid supplementation on acute muscle adaptive responses to resistance exercise in trained men: a randomized controlled trial. Journal of applied physiology.  ISSN 8750-7587.  124(4), s 1080- 1091 . doi: 10.1152/japplphysiol.01100.2017 Vis sammendrag

  Arachidonic acid (ARA), a polyunsaturated ω-6 fatty acid, acts as precursor to a number of prostaglandins with potential roles in muscle anabolism. It was hypothesized that ARA supplementation might enhance the early anabolic response to resistance exercise (RE) by increasing muscle protein synthesis (MPS) via mammalian target of rapamycin (mTOR) pathway activation, and/or the late anabolic response by modulating ribosome biogenesis and satellite cell expansion. Nineteen men with {greater than or equal to}1 year of resistance training experience were randomized to consume either 1.5 grams daily of ARA or a corn-soy oil placebo in a double-blind manner for 4-weeks. Participants then undertook fasted RE (8 sets each of leg press and extension at 80% 1RM), with vastus lateralis biopsies obtained before exercise, immediately post-exercise, and at 2, 4 and 48 hours of recovery. MPS (measured via stable isotope infusion) was not different between groups (P=0.212) over the 4-hour recovery period. mTOR pathway members p70S6K and rpS6 were phosphorylated post-exercise (P<0.05), with no difference between groups. 45S pre-ribosomal RNA (rRNA) increased 48 hours after exercise only in ARA (P=0.012). NCAM+ satellite cells per fibre were increased 48 hours after exercise (P=0.013), with no difference between groups (P=0.331). Prior ARA supplementation did not alter the acute anabolic response to RE in previously resistance trained men; however, at 48 of recovery, ribosome biogenesis was stimulated only in the ARA group. The findings do not support a mechanistic link between ARA and short-term anabolism, but ARA supplementation in conjunction with resistance training may stimulate increases in translational capacity.

• Peake, Jonathan M.; Roberts, Llion A.; Figueiredo, Vandré C.; Egner, Ingrid Marie; Krog Christensen, Simone; Aas, Sigve Nyvik; Suzuki, Katsuhiko; Markworth, James F.; Coombes, Jeff S.; Cameron-Smith, David & Raastad, Truls (2017). The effects of cold water immersion and active recovery on inflammation and cell stress responses in human skeletal muscle after resistance exercise. Journal of Physiology.  ISSN 0022-3751.  595(3), s 695- 711 . doi: 10.1113/JP272881 Vis sammendrag

  Cold water immersion and active recovery are common post-exercise recovery treatments. However, little is known about whether these treatments influence inflammation and cellular stress in human skeletal muscle after exercise. We compared the effects of cold water immersion versus active recovery on inflammatory cells, pro-inflammatory cytokines, neurotrophins and heat shock proteins (HSPs) in skeletal muscle after intense resistance exercise. Nine active men performed unilateral lower-body resistance exercise on separate days, at least 1 week apart. On one day, they immersed their lower body in cold water (10°C) for 10 min after exercise. On the other day, they cycled at a low intensity for 10 min after exercise. Muscle biopsies were collected from the exercised leg before, 2, 24 and 48 h after exercise in both trials. Exercise increased intramuscular neutrophil and macrophage counts, MAC1 and CD163 mRNA expression (P < 0.05). Exercise also increased IL1β, TNF, IL6, CCL2, CCL4, CXCL2, IL8 and LIF mRNA expression (P < 0.05). As evidence of hyperalgesia, the expression of NGF and GDNF mRNA increased after exercise (P < 0.05). The cytosolic protein content of αB-crystallin and HSP70 decreased after exercise (P < 0.05). This response was accompanied by increases in the cytoskeletal protein content of αB-crystallin and the percentage of type II fibres stained for αB-crystallin. Changes in inflammatory cells, cytokines, neurotrophins and HSPs did not differ significantly between the recovery treatments. These findings indicate that cold water immersion is no more effective than active recovery for reducing inflammation or cellular stress in muscle after a bout of resistance exercise.

• van Velthoven, Cindy TJ; de Morree, Antoine; Egner, Ingrid Marie; Brett, Jamie O & Rando, Thomas A (2017). Transcriptional Profiling of Quiescent Muscle Stem Cells In Vivo. Cell reports.  ISSN 2211-1247.  21(7), s 1994- 2004 . doi: 10.1016/j.celrep.2017.10.037 Fulltekst i vitenarkiv.
• Eftestøl, Einar; Egner, Ingrid Marie; Lunde, Ida Gjervold; Ellefsen, Stian; Andersen, Tom; Sjåland, Cecilie; Gundersen, Kristian & Bruusgaard, Jo C. (2016). Increased hypertrophic response with increased mechanical load in skeletal muscles receiving identical activity patterns. American Journal of Physiology - Cell Physiology.  ISSN 0363-6143.  311(4), s C616- C629 . doi: 10.1152/ajpcell.00016.2016
• Egner, Ingrid Marie; Bruusgaard, Jo C. & Gundersen, Kristian (2016). Satellite cell depletion prevents fiber hypertrophy in skeletal muscle. Development.  ISSN 0950-1991.  143(16), s 2898- 2906 . doi: 10.1242/dev.134411
• Roberts, Llion A.; Raastad, Truls; Markworth, James F.; Figueiredo, Vandre C.; Egner, Ingrid Marie; Shield, Anthony; Cameron-Smith, David; Coombes, Jeff S. & Peake, Jonathan M. (2015). Post-exercise cold water immersion attenuates acute anabolic signalling and long-term adaptations in muscle to strength training. Journal of Physiology.  ISSN 0022-3751.  593(18), s 4285- 4301 . doi: 10.1113/JP270570
• Egner, Ingrid Marie; Bruusgaard, Jo C.; Eftestøl, Einar & Gundersen, Kristian (2013). A cellular memory mechanism aids overload hypertrophy in muscle long after an episodic exposure to anabolic steroids. Journal of Physiology.  ISSN 0022-3751.  591(24), s 6221- 6230 . doi: 10.1113/jphysiol.2013.264457
• Paulsen, Gøran; Egner, Ingrid Marie; Raastad, Truls; Reinholt, Finn P.; Owe, Simen Gylterud; Lauritzen, Fredrik; Brorson, Sverre Henning & Koskinen, Satu (2013). Inflammatory markers CD11b, CD16, CD66b, CD68, myeloperoxidase and neutrophil elastase in eccentric exercised human skeletal muscles. Histochemistry and Cell Biology.  ISSN 0948-6143.  139(5), s 691- 715 . doi: 10.1007/s00418-012-1061-x
• Bruusgaard, Jo C.; Egner, Ingrid Marie; Klungervik, Tove; Dupre-Aucouturier, S; Desplanches, D & Gundersen, Kristian (2012). No change in myonuclear number during muscle unloading and reloading. Journal of applied physiology.  ISSN 8750-7587.  113(2), s 290- 296 . doi: 10.1152/japplphysiol.00436.2012
• Bruusgaard, Jo C.; Johansen, Ida Beitnes; Egner, Ingrid Marie; Rana, Zaheer Ahmad & Gundersen, Kristian (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proceedings of the National Academy of Sciences of the United States of America.  ISSN 0027-8424.  107(34), s 15111- 15116 . doi: 10.1073/pnas.0913935107
• Paulsen, Gøran; Egner, Ingrid; Drange, Mads; Langberg, Henning; Benestad, Haakon Breien; Fjeld, Jan Gunnar; Hallén, Jostein & Raastad, Truls (2010). A COX-2 inhibitor reduces muscle soreness, but does not influence recovery and adaptation after eccentric exercise. Scandinavian Journal of Medicine & Science in Sports.  ISSN 0905-7188.  20(1, online), s 195 Vis sammendrag

  The aim of this study was to investigate the effect of a cyclooxygenase (COX)-2 inhibitor on the recovery of muscle function, inflammation, regeneration after, and adaptation to, unaccustomed eccentric exercise. Thirty-three young males and females participated in a double-blind, placebo-controlled experiment. Seventy unilateral, voluntary, maximal eccentric actions with the elbow flexors were performed twice (bouts 1 and 2) with the same arm, separated by 3 weeks. The test group participants were administered 400 mg/day of celecoxib for 9 days after bout 1. After both bouts 1 and 2, concentric and isometric force-generating capacity was immediately reduced ( approximately 40-50%), followed by the later appearance of muscle soreness and increased serum creatine kinase levels. Radiolabelled autologous leukocytes (detected by scintigraphy) and monocytes/macrophages (histology) accumulated in the exercised muscles, simultaneously with increased satellite cell activity. These responses were reduced and recovery was faster after bout 2 than 1, demonstrating a repeated-bout effect. No differences between the celecoxib and placebo groups were detected, except for muscle soreness, which was attenuated by celecoxib. In summary, celecoxib, a COX-2 inhibitor, did not detectably affect recovery of muscle function or markers of inflammation and regeneration after unaccustomed eccentric exercise, nor did the drug influence the repeated-bout effect. However, it alleviated muscle soreness.

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• Egner, Ingrid Marie; Bruusgaard, Jo C. & Gundersen, Kristian (2017). An apparent lack of effect of satellite cell depletion on hypertrophy could be due to methodological limitations. Response to `Methodological issues limit interpretation of negative effects of satellite cell depletion on adult muscle hypertrophy?. Development.  ISSN 0950-1991.  144(8), s 1365- 1367 . doi: 10.1242/dev.148163
• Eftestøl, Einar; Egner, Ingrid Marie; Ellefsen, Stian; Andersen, Tom; Gundersen, Kristian & Bruusgaard, Jo C. (2016). The importance of mechanosensation in skeletal muscle hypertrophy.
• Egner, Ingrid Marie; Bruusgaard, Jo C.; Eftestøl, Einar & Gundersen, Kristian (2012). Effects of anabolic steroid on nuclear number and muscle mass.
• Gundersen, Kristian; Eftestøl, Einar; Egner, Ingrid Marie & Bruusgaard, Jo C. (2011). The effect of testosterone propionate on overloaded skeletal muscle.
• Bruusgaard, Jo C.; Johansen, Ida Beitnes; Egner, Ingrid Marie & Gundersen, Kristian (2009). Are myonuclei forever?. Journal of Muscle Research and Cell Motility.  ISSN 0142-4319.  30(1), s 307
• Egner, Ingrid Marie (2009). Steng dem ute!. Dagbladet.  ISSN 0805-3766.
• Egner, Ingrid; Paulsen, Gøran; Koskinen, Satu & Raastad, Truls (2007). LEUKOCYTE MYOFIBER-INFILTRATION IS NOT THE MAIN CAUSE OF HALTED RECOVERY OF FORCE GENERATION CAPACITY AFTER HIGH-FORCE ECCENTRIC EXERCISE. Vis sammendrag

  Unaccustomed maximal eccentric exercise is believed to cause muscle damage and inflammation characterized by leukocyte infiltration (Peake et al. 2005). The infiltration of leukocytes is suggested to deteriorate the damage caused during exercise, as the time course of radiolabelled leukocytes accumulation has shown a temporal relation with halted recovery of force-generation capacity (MacIntyre et al. 1996; Raastad et al. 2003). The purpose of this study was to investigate the time course of the accumulation of leukocytes directly in muscle tissue and indirectly by radiolabelled leukocytes after unaccustomed maximal eccentric exercise. Twenty-two young and healthy subjects performed 70 unilateral maximal eccentric repetitions with their elbow flexors. Autologous leukocytes were radiolabelled with 99mTc and monitored by a gamma camera at 6 and 20 hr. Muscle biopsies were taken 1, 48, 96 and 168 hours, and 3 weeks after exercise. Immunohistochemical staining with monoclonal antibodies to leukocytes (CD11b: granulocytes, monocytes, NK-cells and T-cells; CD16: NK-cells, neutrophils and basophiles; CD68: macrophages, monocytes, lymphocytes, mast cells and neutrophils) was used to detect the presence of leukocytes in the muscle tissue in both exercised and control arm. To quantify the presence of leukocytes, cells positive for the respective antibody and nuclei stain (DAPI) were counted. CD11b staining showed low numbers of positive cells at all time points, and there was no difference between exercised and control muscle. Staining with CD16 showed 4.3±1.6 positive cells pr 100 myofiber at 1 hr in exercised muscles. CD16+ cells increased modest to 48 and 96 hr, and peaked at 168 hr (180±92 positive cells pr 100 myofiber) after the exercise (p<0.01). The extensive accumulation of CD16+ cells in some subjects at this time points was related to necrotic myofibers and also peak concentration of CK in the blood. We observed that high radioactivity (labelled leukocytes) at 20 hr was related to a halted recovery of the force-generation capacity and, at later time points, necrotic myofibers. The number of CD16+ cells also increased in the control arm (p<0.05). Three weeks after the exercise there was still some CD16+ in the endomysium of regenerated myofibers. The increase in CD68+ cells followed the same pattern as with CD16, peak numbers at 168 hr with 275±129 cells pr 100 myofiber (p<0.05). We conclude that the infiltration of leukocytes into myofibers after eccentric exercise appears not as early as indicated with leukocyte radiolabelling. Evidently, it seems that the halted recovery of force-generation capacity and high radioactivity at earlier time points are not caused by leukocyte myofiber-infiltration, since the course of this event was found much later.

• Egner, Ingrid; Paulsen, Gøran; Koskinen, Satu & Raastad, Truls (2007). Leukocyte myofiber-infiltration is not the main cause of halted recovery of force generation capacity after high-force eccentric exercise, In  Book of abstracts : 12th Annual Congress of the European College of Sport Science.  Likes Research Center.  s 293 Vis sammendrag

  Unaccustomed maximal eccentric exercise is believed to cause muscle damage and inflammation characterized by leukocyte infiltration (Peake et al. 2005). The infiltration of leukocytes is suggested to deteriorate the damage caused during exercise, as the time course of radiolabelled leukocytes accumulation has shown a temporal relation with halted recovery of force-generation capacity (MacIntyre et al. 1996; Raastad et al. 2003). The purpose of this study was to investigate the time course of the accumulation of leukocytes directly in muscle tissue and indirectly by radiolabelled leukocytes after unaccustomed maximal eccentric exercise. Twenty-two young and healthy subjects performed 70 unilateral maximal eccentric repetitions with their elbow flexors. Autologous leukocytes were radiolabelled with 99mTc and monitored by a gamma camera at 6 and 20 hr. Muscle biopsies were taken 1, 48, 96 and 168 hours, and 3 weeks after exercise. Immunohistochemical staining with monoclonal antibodies to leukocytes (CD11b: granulocytes, monocytes, NK-cells and T-cells; CD16: NK-cells, neutrophils and basophiles; CD68: macrophages, monocytes, lymphocytes, mast cells and neutrophils) was used to detect the presence of leukocytes in the muscle tissue in both exercised and control arm. To quantify the presence of leukocytes, cells positive for the respective antibody and nuclei stain (DAPI) were counted. CD11b staining showed low numbers of positive cells at all time points, and there was no difference between exercised and control muscle. Staining with CD16 showed 4.3±1.6 positive cells pr 100 myofiber at 1 hr in exercised muscles. CD16+ cells increased modest to 48 and 96 hr, and peaked at 168 hr (180±92 positive cells pr 100 myofiber) after the exercise (p<0.01). The extensive accumulation of CD16+ cells in some subjects at this time points was related to necrotic myofibers and also peak concentration of CK in the blood. We observed that high radioactivity (labelled leukocytes) at 20 hr was related to a halted recovery of the force-generation capacity and, at later time points, necrotic myofibers. The number of CD16+ cells also increased in the control arm (p<0.05). Three weeks after the exercise there was still some CD16+ in the endomysium of regenerated myofibers. The increase in CD68+ cells followed the same pattern as with CD16, peak numbers at 168 hr with 275±129 cells pr 100 myofiber (p<0.05). We conclude that the infiltration of leukocytes into myofibers after eccentric exercise appears not as early as indicated with leukocyte radiolabelling. Evidently, it seems that the halted recovery of force-generation capacity and high radioactivity at earlier time points are not caused by leukocyte myofiber-infiltration, since the course of this event was found much later.

• Paulsen, Gøran; Egner, Ingrid; Drange, Mads; Langberg, Henning; Ugelstad, Ingrid; Hallén, Jostein & Raastad, Truls (2007). VIL INNTAK AV EN COX-2-HEMMER PÅVIRKE SKADEOMFANG OG RESTITUSJON AV SKJELETTMUSKULATUR ETTER ARBEIDSINDUSERTE MUSKELSKADER?. Vis sammendrag

  ¿NSAIDs¿ (COX-1 og COX-2-hemmere) er vist å ha både positiv og negativ effekt på restitusjons- og adaptasjonsprosesser i skjelettmuskulatur. Dette er den første humanstudien som har sett på effekten av en selektiv COX-2-hemmer på restitusjons- og adaptasjonsprosesser etter eksentrisk muskelarbeid. Elleve kvinner og 22 menn (26±5 år) ble tilfeldig valgt til å innta Celebra® (400 mg celecoxib pr dag) eller placebo i ni dager etter å ha gjennomført 70 unilaterale, maksimale, eksentriske aksjoner med albuefleksorene. Den andre armen fungerte som kontroll. Før og etter arbeidet ble det utført repeterte målinger av maksimal isometrisk styrke og muskelstølhet. Biopsier av biceps brachii ble tatt én, 48, 96 og 168 timer etter arbeidet. Det ble også gjennomført mikrodialyse i biceps brachii to, 24 og 48 timer etter arbeidet. Biopsiene ble analysert ved immunohistokjemi for identifisering av makrofager og satellittceller. Muskeldialysatet ble analysert for prostaglandiner (PGE2) ved hjelp av et immunoassay. Etter tre uker ble arbeidsprotokollen gjennomført på nytt, men uten medikamentell intervensjon. Hos 30% av forsøkspersonene (i begge grupper) ble det observert nekrotiske muskelfibre og akkumulering av makrofager. Celecoxib hadde verken effekt på restitusjonen av muskelfunksjonen eller på akkumuleringen av makrofager og antall satellittceller i muskulaturen. Det ble heller ikke registrert noen medikamenteffekt på vevsvæskekonsentrasjonen av PGE2, men celecoxib viste en tendens til å redusere muskelstølhet. Celecoxib så ikke ut til å påvirke adaptasjonsprosessene, fordi det var ingen forskjell i restitusjonsforløpet mellom placebo- og celecoxib-gruppen da arbeidsprotokollen ble gjentatt. Celecoxib hadde i denne studien ingen registrerbar effekt på muskulaturen etter et eksentrisk muskelarbeid. Muligens skyldes dette at COX-2-enzymet ikke har en sentral rolle i responsen på slikt muskelarbeid hos mennesker. Den stølhetsdempende effekten kan skyldes at medikamentet virket på smerteledningsbanen i nervesystemet. Følgelig, inntak av COX-2- hemmeren celecoxib så ikke ut til å påvirke restitusjons- og adaptasjonsprosessene etter et muskelødeleggende arbeid, men kan redusere smerter.

• Paulsen, Gøran; Egner, Ingrid; Drange, Mads; Langberg, Henning; Ugelstad, Ingrid; Hallén, Jostein & Raastad, Truls (2007). Vil inntak av en COX-2-hemmer påvirke skadeomfang og restitusjon av skjelettmuskulatur etter arbeidsinduserte muskelskader?. Norsk idrettsmedisin.  ISSN 0806-9328.  (3), s 24 Vis sammendrag

  ¿NSAIDs¿ (COX-1 og COX-2-hemmere) er vist å ha både positiv og negativ effekt på restitusjons- og adaptasjonsprosesser i skjelettmuskulatur. Dette er den første humanstudien som har sett på effekten av en selektiv COX-2-hemmer på restitusjons- og adaptasjonsprosesser etter eksentrisk muskelarbeid. Elleve kvinner og 22 menn (26±5 år) ble tilfeldig valgt til å innta Celebra® (400 mg celecoxib pr dag) eller placebo i ni dager etter å ha gjennomført 70 unilaterale, maksimale, eksentriske aksjoner med albuefleksorene. Den andre armen fungerte som kontroll. Før og etter arbeidet ble det utført repeterte målinger av maksimal isometrisk styrke og muskelstølhet. Biopsier av biceps brachii ble tatt én, 48, 96 og 168 timer etter arbeidet. Det ble også gjennomført mikrodialyse i biceps brachii to, 24 og 48 timer etter arbeidet. Biopsiene ble analysert ved immunohistokjemi for identifisering av makrofager og satellittceller. Muskeldialysatet ble analysert for prostaglandiner (PGE2) ved hjelp av et immunoassay. Etter tre uker ble arbeidsprotokollen gjennomført på nytt, men uten medikamentell intervensjon. Hos 30% av forsøkspersonene (i begge grupper) ble det observert nekrotiske muskelfibre og akkumulering av makrofager. Celecoxib hadde verken effekt på restitusjonen av muskelfunksjonen eller på akkumuleringen av makrofager og antall satellittceller i muskulaturen. Det ble heller ikke registrert noen medikamenteffekt på vevsvæskekonsentrasjonen av PGE2, men celecoxib viste en tendens til å redusere muskelstølhet. Celecoxib så ikke ut til å påvirke adaptasjonsprosessene, fordi det var ingen forskjell i restitusjonsforløpet mellom placebo- og celecoxib-gruppen da arbeidsprotokollen ble gjentatt. Celecoxib hadde i denne studien ingen registrerbar effekt på muskulaturen etter et eksentrisk muskelarbeid. Muligens skyldes dette at COX-2-enzymet ikke har en sentral rolle i responsen på slikt muskelarbeid hos mennesker. Den stølhetsdempende effekten kan skyldes at medikamentet virket på smerteledningsbanen i nervesystemet. Følgelig, inntak av COX-2- hemmeren celecoxib så ikke ut til å påvirke restitusjons- og adaptasjonsprosessene etter et muskelødeleggende arbeid, men kan redusere smerter.

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