Gymnastik- och idrottshögskolan, GIH

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Acute normobaric hypoxia blunts contraction-mediated mTORC1- and JNK-signaling in human skeletal muscle.
Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Physiology and Pharmacology, Karolinska Institute, Sweden.ORCID iD: 0000-0003-3747-0148
Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics. Department of Clinical Science, Intervention and Technology, Karolinska Institute, Sweden.ORCID iD: 0000-0003-1942-2919
Swedish School of Sport and Health Sciences, GIH, Department of Physiology, Nutrition and Biomechanics.ORCID iD: 0000-0002-3500-2896
University of Copenhagen, Denmark.; Rigshospitalet, Copenhagen, Denmark..
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2022 (English)In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 234, no 2, article id e13771Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
John Wiley & Sons, 2022. Vol. 234, no 2, article id e13771
Keywords [en]
FSR, Hippo-pathway, Muscle metabolites, deuterium oxide, oxygen
National Category
Physiology
Research subject
Medicine/Technology
Identifiers
URN: urn:nbn:se:gih:diva-6900DOI: 10.1111/apha.13771ISI: 000744361300001PubMedID: 34984845OAI: oai:DiVA.org:gih-6900DiVA, id: diva2:1626116
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Swedish National Centre for Research in Sports, D2017--0012Available from: 2022-01-10 Created: 2022-01-10 Last updated: 2022-02-08

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Moberg, MarcusApro, WilliamHorwath, OscarBlackwood, Sarah JKatz, Abram

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