Gymnastik- och idrottshögskolan, GIH

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Horwath, O., Nordström, F., von Walden, F., Apro, W. & Moberg, M. (2023). Acute hypoxia attenuates resistance exercise-induced ribosome signaling but does not impact satellite cell pool expansion in human skeletal muscle.. The FASEB Journal, 37(3), Article ID e22811.
Öppna denna publikation i ny flik eller fönster >>Acute hypoxia attenuates resistance exercise-induced ribosome signaling but does not impact satellite cell pool expansion in human skeletal muscle.
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2023 (Engelska)Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 37, nr 3, artikel-id e22811Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Cumulative evidence supports the hypothesis that hypoxia acts as a regulator of muscle mass. However, the underlying molecular mechanisms remain incompletely understood, particularly in human muscle. Here we examined the effect of hypoxia on signaling pathways related to ribosome biogenesis and myogenic activity following an acute bout of resistance exercise. We also investigated whether hypoxia influenced the satellite cell response to resistance exercise. Employing a randomized, crossover design, eight men performed resistance exercise in normoxia (FiO2 21%) or normobaric hypoxia (FiO2 12%). Muscle biopsies were collected in a time-course manner (before, 0, 90, 180 min and 24 h after exercise) and were analyzed with respect to cell signaling, gene expression and satellite cell content using immunoblotting, RT-qPCR and immunofluorescence, respectively. In normoxia, resistance exercise increased the phosphorylation of RPS6, TIF-1A and UBF above resting levels. Hypoxia reduced the phosphorylation of these targets by ~37%, ~43% and ~ 67% throughout the recovery period, respectively (p < .05 vs. normoxia). Resistance exercise also increased 45 S pre-rRNA expression and mRNA expression of c-Myc, Pol I and TAF-1A above resting levels, but no differences were observed between conditions. Similarly, resistance exercise increased mRNA expression of myogenic regulatory factors throughout the recovery period and Pax7+ cells were elevated 24 h following exercise in mixed and type II muscle fibers, with no differences observed between normoxia and hypoxia. In conclusion, acute hypoxia attenuates ribosome signaling, but does not impact satellite cell pool expansion and myogenic gene expression following a bout of resistance exercise in human skeletal muscle.

Ort, förlag, år, upplaga, sidor
John Wiley & Sons, 2023
Nyckelord
Pax7, muscle fiber, myogenesis, resistance exercise, ribosome biogenesis
Nationell ämneskategori
Fysiologi Idrottsvetenskap
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7523 (URN)10.1096/fj.202202065RR (DOI)000936598200001 ()36786723 (PubMedID)
Forskningsfinansiär
Centrum för Idrottsforskning, D2017- 0012, D2019- 0050, D2019- 0035
Tillgänglig från: 2023-03-06 Skapad: 2023-03-06 Senast uppdaterad: 2023-03-23
Blackwood, S. J., Horwath, O., Moberg, M., Pontén, M., Apro, W., Ekblom, M., . . . Katz, A. (2023). Insulin resistance after a 3-day fast is associated with an increased capacity of skeletal muscle to oxidize lipids.. American Journal of Physiology. Endocrinology and Metabolism, 324(5), E390-E401
Öppna denna publikation i ny flik eller fönster >>Insulin resistance after a 3-day fast is associated with an increased capacity of skeletal muscle to oxidize lipids.
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2023 (Engelska)Ingår i: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 324, nr 5, s. E390-E401Artikel i tidskrift (Refereegranskat) Published
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.

Ort, förlag, år, upplaga, sidor
American Physiological Society, 2023
Nyckelord
glucose tolerance, insulin resistance, mitochondrial respiration, muscle fiber composition, starvation
Nationell ämneskategori
Fysiologi Endokrinologi och diabetes
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7521 (URN)10.1152/ajpendo.00317.2022 (DOI)000974241700002 ()36791323 (PubMedID)
Tillgänglig från: 2023-03-03 Skapad: 2023-03-03 Senast uppdaterad: 2024-01-11
Lilja, M., Moberg, M., Apro, W., Martínez-Aranda, L. M., Rundqvist, H., Langlet, B., . . . Lundberg, T. R. (2023). Limited effect of over-the-counter doses of ibuprofen on mechanisms regulating muscle hypertrophy during resistance training in young adults.. Journal of applied physiology, 134(3), 753-765
Öppna denna publikation i ny flik eller fönster >>Limited effect of over-the-counter doses of ibuprofen on mechanisms regulating muscle hypertrophy during resistance training in young adults.
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2023 (Engelska)Ingår i: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 134, nr 3, s. 753-765Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

We have previously shown that maximal over-the-counter doses of ibuprofen, compared with low doses of acetylsalicylic acid, reduce muscle hypertrophy in young individuals after 8 weeks of resistance training. Because the mechanism behind this effect has not been fully elucidated, we here investigated skeletal muscle molecular responses and myofiber adaptations in response to acute and chronic resistance training with concomitant drug intake. Thirty-one young (aged 18-35 years) healthy men (n=17) and women (n=14) were randomized to receive either ibuprofen (IBU;1200mg daily; n=15) or acetylsalicylic acid (ASA; 75mg daily; n=16) while undergoing 8 weeks of knee extension training. Muscle biopsies from the vastus lateralis were obtained before, at week 4 after an acute exercise session, and after 8 weeks of resistance training and analyzed for mRNA markers and mTOR signaling, as well as quantification of total RNA content (marker of ribosome biogenesis) and immunohistochemical analyzes of muscle fiber size, satellite cell content, myonuclear accretion, and capillarization. There were only two treatment ´ time interaction in selected molecular markers after acute exercise (atrogin-1 and MuRF1 mRNA), but several exercise effects. Muscle fiber size, satellite cell and myonuclear accretion, and capillarization were not affected by chronic training or drug intake. RNA content increased comparably (~14%) in both groups. Collectively, these data suggest that established acute and chronic hypertrophy regulators (including mTOR signaling, ribosome biogenesis, satellite cell content, myonuclear accretion, and angiogenesis) were not differentially affected between groups and therefore do not explain the deleterious effects of ibuprofen on muscle hypertrophy in young adults.

Ort, förlag, år, upplaga, sidor
American Physiological Society, 2023
Nyckelord
Non-steroidal anti-inflammatory drugs, Resistance exercise, Ribosome biogenesis, Satellite cells, Skeletal muscle
Nationell ämneskategori
Idrottsvetenskap
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7522 (URN)10.1152/japplphysiol.00698.2022 (DOI)000972694300002 ()36794689 (PubMedID)
Tillgänglig från: 2023-03-03 Skapad: 2023-03-03 Senast uppdaterad: 2023-06-12
Nordström, F., Liegnell, R., Apro, W., Blackwood, S. J., Katz, A. & Moberg, M. (2023). The lactate receptor GPR81 is predominantly expressed in type II human skeletal muscle fibers: potential for lactate autocrine signaling.. Paper presented at 324(2):C477-C487. American Journal of Physiology - Cell Physiology, 324(2), C477-C487
Öppna denna publikation i ny flik eller fönster >>The lactate receptor GPR81 is predominantly expressed in type II human skeletal muscle fibers: potential for lactate autocrine signaling.
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2023 (Engelska)Ingår i: American Journal of Physiology - Cell Physiology, ISSN 0363-6143, E-ISSN 1522-1563, Vol. 324, nr 2, s. C477-C487Artikel i tidskrift (Refereegranskat) Published
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.

Ort, förlag, år, upplaga, sidor
American Physiological Society, 2023
Nyckelord
CREB, HCAR1, PGC-1alpha, PKA, Resistance exercise
Nationell ämneskategori
Idrottsvetenskap Fysiologi
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7464 (URN)10.1152/ajpcell.00443.2022 (DOI)000959663400012 ()36622074 (PubMedID)
Konferens
324(2):C477-C487
Tillgänglig från: 2023-01-11 Skapad: 2023-01-11 Senast uppdaterad: 2023-05-18
Nilsson, J., Ekblom, M., Moberg, M. & Lövdén, M. (2023). The role of acute changes in mBDNF, cortisol and pro-BDNF in predicting cognitive performance in old age.. Scientific Reports, 13(1), Article ID 9418.
Öppna denna publikation i ny flik eller fönster >>The role of acute changes in mBDNF, cortisol and pro-BDNF in predicting cognitive performance in old age.
2023 (Engelska)Ingår i: Scientific Reports, E-ISSN 2045-2322, Vol. 13, nr 1, artikel-id 9418Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The interplay between biomarkers of relevance to neuroplasticity and its association with learning and cognitive ability in old age remains poorly understood. The present study investigated acute changes in plasma concentrations of mature brain-derived neurotrophic factor (mBDNF), its precursor protein (pro-BDNF), and cortisol, in response to acute physical exercise and cognitive training interventions, their covariation and role in predicting cognitive performance. Confirmatory results provided no support for mBDNF, pro-BDNF and cortisol co-varying over time, as the acute interventions unfolded, but did confirm a positive association between mBDNF and pro-BDNF at rest. The confirmatory results did not support the hypothesis that mBDNF change following physical exercise were counteracted by temporally coupled changes in cortisol or pro-BDNF, or by cortisol at rest, in its previously demonstrated faciliatory effect on cognitive training outcome. Exploratory results instead provided indications of a general and trait-like cognitive benefit of exhibiting greater mBDNF responsiveness to acute interventions when coupled with lesser cortisol responsiveness, greater pro-BDNF responsiveness, and lower cortisol at rest. As such, the results call for future work to test whether certain biomarker profiles are associated with preserved cognition in old age.

Ort, förlag, år, upplaga, sidor
Nature Publishing Group, 2023
Nyckelord
E-PABS, EPABS, hjärnhälsa, brain health
Nationell ämneskategori
Neurovetenskaper
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7671 (URN)10.1038/s41598-023-35847-5 (DOI)001006690200060 ()37296176 (PubMedID)
Tillgänglig från: 2023-06-26 Skapad: 2023-06-26 Senast uppdaterad: 2024-03-22
Ekblom, M., Bojsen-Møller, E., Blom, V., Tarassova, O., Moberg, M., Pontén, M., . . . Ekblom, Ö. (2022). Acute effects of physical activity patterns on plasma cortisol and brain-derived neurotrophic factor in relation to corticospinal excitability.. Behavioural Brain Research, 430, Article ID 113926.
Öppna denna publikation i ny flik eller fönster >>Acute effects of physical activity patterns on plasma cortisol and brain-derived neurotrophic factor in relation to corticospinal excitability.
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2022 (Engelska)Ingår i: Behavioural Brain Research, ISSN 0166-4328, E-ISSN 1872-7549, Vol. 430, artikel-id 113926Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Brain-derived neurotrophic factor (BDNF) and cortisol are both capable of modulating synaptic plasticity, but it is unknown how physical activity-induced changes in their plasma levels relate to corticospinal plasticity in humans. Sixteen inactive middle-aged men and women participated in three separate interventions consisting of 3hours prolonged sitting (SIT); 3hours sitting interrupted every 30minutes with frequent short physical activity breaks (FPA); and 2.5hours prolonged sitting followed by 25minutes of moderate intensity exercise (EXE). These 3hour sessions were each followed by a 30min period of paired associative stimulation over the primary motor cortex (PAS). Blood samples were taken and corticospinal excitability measured at baseline, pre PAS, 5min and 30min post PAS. Here we report levels of plasma BDNF and cortisol over three activity conditions and relate these levels to previously published changes in corticospinal excitability of a non-activated thumb muscle. There was no interaction between time and condition in BDNF, but cortisol levels were significantly higher after EXE compared to after SIT and FPA. Higher cortisol levels at pre PAS predicted larger increases in corticospinal excitability from baseline to all subsequent time points in the FPA condition only, while levels of BDNF at pre PAS did not predict such changes in any of the conditions. Neither BDNF nor cortisol modified changes from pre PAS to the subsequent time points, suggesting that the increased corticospinal excitability was not mediated though an augmented effect of the PAS protocol. The relationship between cortisol and plasticity has been suggested to be U-shaped. This is possibly why the moderately high levels of cortisol seen in the FPA condition were positively associated with changes AURC, while the higher cortisol levels seen after EXE were not. A better understanding of the mechanisms for how feasible physical activity breaks affect neuroplasticity can inform the theoretical framework for how work environments and schedules should be designed. DATA AVAILABILITY: Data are available from the corresponding author upon reasonable request.

Ort, förlag, år, upplaga, sidor
Elsevier, 2022
Nyckelord
BDNF, attention, cortisol, motor cortex, paired associative stimulation, plasticity
Nationell ämneskategori
Psykiatri Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7061 (URN)10.1016/j.bbr.2022.113926 (DOI)000816115000002 ()35568076 (PubMedID)
Forskningsfinansiär
KK-stiftelsen, 20160040, 20180151, 20210002
Anmärkning

Övriga finansiärer: ICA Gruppen, Intrum, SATS, Monark Exercise, Intrum Justitia

Tillgänglig från: 2022-05-19 Skapad: 2022-05-19 Senast uppdaterad: 2024-03-21
Moberg, M., Apro, W., Horwath, O., van Hall, G., Blackwood, S. J. & Katz, A. (2022). Acute normobaric hypoxia blunts contraction-mediated mTORC1- and JNK-signaling in human skeletal muscle.. Acta Physiologica, 234(2), Article ID e13771.
Öppna denna publikation i ny flik eller fönster >>Acute normobaric hypoxia blunts contraction-mediated mTORC1- and JNK-signaling in human skeletal muscle.
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2022 (Engelska)Ingår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 234, nr 2, artikel-id e13771Artikel i tidskrift (Refereegranskat) Published
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.

Ort, förlag, år, upplaga, sidor
John Wiley & Sons, 2022
Nyckelord
FSR, Hippo-pathway, Muscle metabolites, deuterium oxide, oxygen
Nationell ämneskategori
Fysiologi
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-6900 (URN)10.1111/apha.13771 (DOI)000744361300001 ()34984845 (PubMedID)
Forskningsfinansiär
Centrum för Idrottsforskning, D2017--0012
Tillgänglig från: 2022-01-10 Skapad: 2022-01-10 Senast uppdaterad: 2022-02-08
Blackwood, S. J., Horwath, O., Moberg, M., Pontén, M., Apro, W., Ekblom, M., . . . Katz, A. (2022). Extreme Variations in Muscle Fiber Composition Enable Detection of Insulin Resistance and Excessive Insulin Secretion.. Journal of Clinical Endocrinology and Metabolism, 107(7), e2729-e2737, Article ID dgac221.
Öppna denna publikation i ny flik eller fönster >>Extreme Variations in Muscle Fiber Composition Enable Detection of Insulin Resistance and Excessive Insulin Secretion.
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2022 (Engelska)Ingår i: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 107, nr 7, s. e2729-e2737, artikel-id dgac221Artikel i tidskrift (Refereegranskat) Published
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.

Ort, förlag, år, upplaga, sidor
Oxford University Press, 2022
Nyckelord
insulin, insulin resistance, insulin secretion, intravenous glucose tolerance test, mitochondrial respiration, muscle fiber type
Nationell ämneskategori
Endokrinologi och diabetes
Forskningsämne
Medicin/Teknik; Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7053 (URN)10.1210/clinem/dgac221 (DOI)000789019300001 ()35405014 (PubMedID)
Tillgänglig från: 2022-05-18 Skapad: 2022-05-18 Senast uppdaterad: 2022-12-06
Horwath, O., Moberg, M., Hirschberg, A. L., Ekblom, B. & Apro, W. (2022). Molecular Regulators of Muscle Mass and Mitochondrial Remodeling Are Not Influenced by Testosterone Administration in Young Women.. Frontiers in Endocrinology, 13, Article ID 874748.
Öppna denna publikation i ny flik eller fönster >>Molecular Regulators of Muscle Mass and Mitochondrial Remodeling Are Not Influenced by Testosterone Administration in Young Women.
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2022 (Engelska)Ingår i: Frontiers in Endocrinology, E-ISSN 1664-2392, Vol. 13, artikel-id 874748Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Testosterone (T) administration has previously been shown to improve muscle size and oxidative capacity. However, the molecular mechanisms underlying these adaptations in human skeletal muscle remain to be determined. Here, we examined the effect of moderate-dose T administration on molecular regulators of muscle protein turnover and mitochondrial remodeling in muscle samples collected from young women. Forty-eight healthy, physically active, young women (28 ± 4 years) were assigned in a random double-blind fashion to receive either T (10 mg/day) or placebo for 10-weeks. Muscle biopsies collected before and after the intervention period were divided into sub-cellular fractions and total protein levels of molecular regulators of muscle protein turnover and mitochondrial remodeling were analyzed using Western blotting. T administration had no effect on androgen receptor or 5α-reductase levels, nor on proteins involved in the mTORC1-signaling pathway (mTOR, S6K1, eEF2 and RPS6). Neither did it affect the abundance of proteins associated with proteasomal protein degradation (MAFbx, MuRF-1 and UBR5) and autophagy-lysosomal degradation (AMPK, ULK1 and p62). T administration also had no effect on proteins in the mitochondria enriched fraction regulating mitophagy (Beclin, BNIP3, LC3B-I, LC3B-II and LC3B-II/I ratio) and morphology (Mitofilin), and it did not alter the expression of mitochondrial fission- (FIS1 and DRP1) or fusion factors (OPA1 and MFN2). In summary, these data indicate that improvements in muscle size and oxidative capacity in young women in response to moderate-dose T administration cannot be explained by alterations in total expression of molecular factors known to regulate muscle protein turnover or mitochondrial remodeling.

Ort, förlag, år, upplaga, sidor
Frontiers Media S.A., 2022
Nyckelord
androgen receptor, fission, fusion, mTORC1-signaling, ubiquitin-proteasome system
Nationell ämneskategori
Fysiologi
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7055 (URN)10.3389/fendo.2022.874748 (DOI)000795475000001 ()35498440 (PubMedID)
Tillgänglig från: 2022-05-18 Skapad: 2022-05-18 Senast uppdaterad: 2024-01-17
Horwath, O., Nordström, F., Apro, W. & Moberg, M. (2022). Satellite cell pool expansion induced by resistance exercise is not altered by acute normobaric hypoxia. In: Svensk idrottsmedicin 2022:2: . Paper presented at SFAIMs vårmöte 2022. Tillsammans för framtidens fysiska aktivitet och idrottsmedicin. Stockholm 19-20 maj 2022. (pp. 30). Svensk förening för fysisk aktivitet och idrottsmedicin, 41
Öppna denna publikation i ny flik eller fönster >>Satellite cell pool expansion induced by resistance exercise is not altered by acute normobaric hypoxia
2022 (Engelska)Ingår i: Svensk idrottsmedicin 2022:2, Svensk förening för fysisk aktivitet och idrottsmedicin , 2022, Vol. 41, s. 30-Konferensbidrag, Muntlig presentation med publicerat abstract (Övrigt vetenskapligt)
Ort, förlag, år, upplaga, sidor
Svensk förening för fysisk aktivitet och idrottsmedicin, 2022
Nationell ämneskategori
Idrottsvetenskap
Forskningsämne
Medicin/Teknik
Identifikatorer
urn:nbn:se:gih:diva-7430 (URN)
Konferens
SFAIMs vårmöte 2022. Tillsammans för framtidens fysiska aktivitet och idrottsmedicin. Stockholm 19-20 maj 2022.
Tillgänglig från: 2022-12-05 Skapad: 2022-12-05 Senast uppdaterad: 2023-01-11
Projekt
E-PABS - ett excellenscenter inom fysisk aktivitet, hälsosamma hjärnfunktioner och hållbarhet [20210002 01 H]; Gymnastik- och idrottshögskolan, GIH; Publikationer
Projektet Fysisk aktivetet för hälsosamma hjärnfunktioner bland skolungdomar, ., Helgadóttir, B. & Kjellenberg, K. (2024). Balansen mellan skärmtid, rörelse och hjärnhälsa hos unga. Stockholm: Gymnastik- och idrottshögskolan, GIHWiklund, C. A., Ekblom, Ö., Paulsson, S., Lindwall, M. & Ekblom Bak, E. (2024). Cardiorespiratory fitness in midlife and subsequent incident depression, long-term sickness absence, and disability pension due to depression in 330,247 men and women.. Preventive Medicine, 181, Article ID 107916. Hoy, S., Larsson, H., Kjellenberg, K., Nyberg, G., Ekblom, Ö. & Helgadóttir, B. (2024). Gendered relations? Associations between Swedish parents, siblings, and adolescents' time spent sedentary and physically active. Frontiers in Sports and Active Living, 6, Article ID 1236848. Projektet Fysisk aktivetet för hälsosamma hjärnfunktioner bland skolungdomar, ., Helgadóttir, B. & Kjellenberg, K. (2024). Vikten av sunda matvanor för hjärnhälsa bland ungdomar. Stockholm: Gymnastik- och idrottshögskolan, GIHHeiland, E. G., Kjellenberg, K., Tarassova, O., Nyberg, G., Ekblom, M., Ekblom, Ö. & Helgadóttir, B. (2023). Acute effects of nitrate and breakfast on working memory and cerebral blood flow in adolescents: a randomized crossover trial. In: : . Paper presented at The International Society of Behavioral Nutrition and Physical Activity (ISBNPA), Uppsala, Sweden, June 15-18, 2023. Regan, C., Heiland, E. G., Ekblom, Ö., Tarassova, O., Kjellenberg, K., Larsen, F. J., . . . Helgadóttir, B. (2023). Acute effects of nitrate and breakfast on working memory, cerebral blood flow, arterial stiffness, and psychological factors in adolescents: Study protocol for a randomised crossover trial.. PLOS ONE, 18(5), Article ID e0285581. Farias, L., Nyberg, G., Helgadóttir, B. & Andermo, S. (2023). Adolescents' experiences of a school-based health promotion intervention in socioeconomically advantaged and disadvantaged areas in Sweden: a qualitative process evaluation study.. BMC Public Health, 23(1), Article ID 1631. Larsson, L. E., Wang, R., Cederholm, T., Wiggenraad, F., Rydén, M., Hagman, G., . . . Thunborg, C. (2023). Association of Sarcopenia and Its Defining Components with the Degree of Cognitive Impairment in a Memory Clinic Population.. Journal of Alzheimer's Disease, 96(2), 777-788Yman, J., Helgadóttir, B., Kjellenberg, K. & Nyberg, G. (2023). Associations between organised sports participation, general health, stress, screen-time and sleep duration in adolescents.. Acta Paediatrica, 112(3), 452-459Wu, J., Xiong, Y., Xia, X., Orsini, N., Qiu, C., Kivipelto, M., . . . Wang, R. (2023). Can dementia risk be reduced by following the American Heart Association's Life's Simple 7?: A systematic review and dose-response meta-analysis.. Ageing Research Reviews, 83, Article ID 101788.
Plasmamarkörer för neurodegeneration, kognition och fysisk aktivitet hos friska äldre; Gymnastik- och idrottshögskolan, GIHSamspel mellan muskler och hjärnan för molekylär reglering av neuroplasticitet [M21-0134_Åke Wiberg]; Gymnastik- och idrottshögskolan, GIHAnvändning av xenotransfusion för att klargöra hur träning påverkar neurofunktion [CIF 2023-0083]; Gymnastik- och idrottshögskolan, GIHLactate – a regulator of human adipose tissue metabolic function [M22-0107]; Gymnastik- och idrottshögskolan, GIHRörelsepauser för hjärnhälsa hos rullstolsanvändare; Gymnastik- och idrottshögskolan, GIHLactate – a regulator of human adipose tissue metabolic function [M22-0107]; Gymnastik- och idrottshögskolan, GIHExStress-studien - Intensitetens betydelse för träningens effekter på hjärnhälsa vid stress; Gymnastik- och idrottshögskolan, GIH
Organisationer
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ORCID-id: ORCID iD iconorcid.org/0000-0003-3747-0148

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