Increased oxidative stress and anaerobic energy release, but blunted Thr172-AMPKα phosphorylation, in response to sprint exercise in severe acute hypoxia in humans

التفاصيل البيبلوغرافية
العنوان: Increased oxidative stress and anaerobic energy release, but blunted Thr172-AMPKα phosphorylation, in response to sprint exercise in severe acute hypoxia in humans
المؤلفون: David Morales-Alamo, Lorena Rodríguez-García, Borja Guerra, Alfredo Santana, Mario Guerrero, Amelia Guadalupe-Grau, Jose A. L. Calbet, Maria Roser Cusso, Jesús Gustavo Ponce-González, Cecilia Dorado
المصدر: Journal of Applied Physiology. 113:917-928
بيانات النشر: American Physiological Society, 2012.
سنة النشر: 2012
مصطلحات موضوعية: Adult, Blood Glucose, Male, Threonine, medicine.medical_specialty, Time Factors, Anaerobic Threshold, Physiology, Biopsy, AMP-Activated Protein Kinases, Protein Serine-Threonine Kinases, medicine.disease_cause, Severity of Illness Index, Quadriceps Muscle, Running, Protein Carbonylation, Young Adult, Oxygen Consumption, Mediator, AMP-Activated Protein Kinase Kinases, Sirtuin 1, AMP-activated protein kinase, Physiology (medical), Internal medicine, medicine, Humans, Insulin, Lactic Acid, Muscle Strength, Phosphorylation, Hypoxia, Protein kinase A, Exercise, biology, GTPase-Activating Proteins, AMPK, Blood Proteins, Metabolism, NAD, Oxidative Stress, Endocrinology, Acute Disease, Exercise Test, biology.protein, Energy Metabolism, Anaerobic exercise, Oxidative stress, Muscle Contraction
الوصف: AMP-activated protein kinase (AMPK) is a major mediator of the exercise response and a molecular target to improve insulin sensitivity. To determine if the anaerobic component of the exercise response, which is exaggerated when sprint is performed in severe acute hypoxia, influences sprint exercise-elicited Thr172-AMPKα phosphorylation, 10 volunteers performed a single 30-s sprint (Wingate test) in normoxia and in severe acute hypoxia (inspired Po2: 75 mmHg). Vastus lateralis muscle biopsies were obtained before and immediately after 30 and 120 min postsprint. Mean power output and O2 consumption were 6% and 37%, respectively, lower in hypoxia than in normoxia. O2 deficit and muscle lactate accumulation were greater in hypoxia than in normoxia. Carbonylated skeletal muscle and plasma proteins were increased after the sprint in hypoxia. Thr172-AMPKα phosphorylation was increased by 3.1-fold 30 min after the sprint in normoxia. This effect was prevented by hypoxia. The NAD+-to-NADH.H+ ratio was reduced (by 24-fold) after the sprints, with a greater reduction in hypoxia than in normoxia ( P < 0.05), concomitant with 53% lower sirtuin 1 (SIRT1) protein levels after the sprint in hypoxia ( P < 0.05). This could have led to lower liver kinase B1 (LKB1) activation by SIRT1 and, hence, blunted Thr172-AMPKα phosphorylation. Ser485-AMPKα1/Ser491-AMPKα2 phosphorylation, a known negative regulating mechanism of Thr172-AMPKα phosphorylation, was increased by 60% immediately after the sprint in hypoxia, coincident with increased Thr308-Akt phosphorylation. Collectively, our results indicate that the signaling response to sprint exercise in human skeletal muscle is altered in severe acute hypoxia, which abrogated Thr172-AMPKα phosphorylation, likely due to lower LKB1 activation by SIRT1.
تدمد: 1522-1601
8750-7587
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::018e65507362919e78fa539706cd23eaTest
https://doi.org/10.1152/japplphysiol.00415.2012Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....018e65507362919e78fa539706cd23ea
قاعدة البيانات: OpenAIRE