Acute normobaric hypoxia blunts contraction-mediated mTORC1- and JNK-signaling in human skeletal muscle
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Acute normobaric hypoxia blunts contraction-mediated mTORC1- and JNK-signaling in human skeletal muscle. / Moberg, Marcus; Apró, William; Horwath, Oscar; van Hall, Gerrit; Blackwood, Sarah Joan; Katz, Abram.
I: Acta Physiologica, Bind 234, Nr. 2, e13771, 2022.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Acute normobaric hypoxia blunts contraction-mediated mTORC1- and JNK-signaling in human skeletal muscle
AU - Moberg, Marcus
AU - Apró, William
AU - Horwath, Oscar
AU - van Hall, Gerrit
AU - Blackwood, Sarah Joan
AU - Katz, Abram
N1 - Publisher Copyright: © 2022 The Authors. Acta Physiologica published by John Wiley & Sons Ltd on behalf of Scandinavian Physiological Society.
PY - 2022
Y1 - 2022
N2 - 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 signalling pathways involved in the 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 0, 90,180 minutes after exercise. Muscle analyses included levels of signalling 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- to 40-fold immediately after the exercise in normoxia, but hypoxia blocked almost 70% of the activation. Throughout recovery, phosphorylation of JNK and SMAD2 remained elevated following the exercise in normoxia, but the effect of hypoxia was lost at 90-180 minutes post-exercise. Hypoxia had no effect on exercise-induced Hippo or autophagy signalling 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 signalling in human skeletal muscle, effects that do not appear to be mediated by changes in the degree of metabolic stress in the muscle.
AB - 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 signalling pathways involved in the 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 0, 90,180 minutes after exercise. Muscle analyses included levels of signalling 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- to 40-fold immediately after the exercise in normoxia, but hypoxia blocked almost 70% of the activation. Throughout recovery, phosphorylation of JNK and SMAD2 remained elevated following the exercise in normoxia, but the effect of hypoxia was lost at 90-180 minutes post-exercise. Hypoxia had no effect on exercise-induced Hippo or autophagy signalling 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 signalling in human skeletal muscle, effects that do not appear to be mediated by changes in the degree of metabolic stress in the muscle.
U2 - 10.1111/apha.13771
DO - 10.1111/apha.13771
M3 - Journal article
C2 - 34984845
AN - SCOPUS:85122083204
VL - 234
JO - Acta Physiologica
JF - Acta Physiologica
SN - 0370-839X
IS - 2
M1 - e13771
ER -
ID: 291227108