Interleukin-13 drives metabolic conditioning of muscle to endurance exercise.
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ABSTRACT:
SUBMITTER: Knudsen NH
PROVIDER: S-EPMC7549736 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:This study was designed to (1) investigate the effects of acute exercise under intermittent hypoxia on muscle mRNA and protein levels, and (2) clarify the mechanisms by which exercise under intermittent hypoxia improves endurance capacity. Experiment-1: Male mice were subjected to either acute endurance exercise, exercise under hypoxia (14% O2 ), exercise under intermittent hypoxia (Int, three cycles of room air [10 min] and 14% O2 [15 min]). At 3 h after exercise under intermittent hypoxia, sirtuin-6 mRNA levels and nuclear prolyl hydroxylases-2 protein levels were significantly upregulated in white gastrocnemius muscle in the Int group. Experiment-2: Mice were assigned to sedentary control (Sed), normoxic exercise-trained (ET), hypoxic exercise-trained (HYP) or exercise-trained under intermittent hypoxia (INT) groups. Exercise capacity was significantly greater in the INT group than in the ET and HYP group. Activity levels of citrate synthase were significantly greater in the INT group than in the HYP group in soleus (SOL) and red gastrocnemius muscles. In SOL, nuclear N-terminal PGC1α levels were considerably increased by the INT training (95% confidence interval [CI]: 1.09-1.79). The INT significantly increased pyruvate dehydrogenase complex activity levels in left ventricle (LV). Monocarboxylate transporter-4 protein levels were significantly increased after the INT training in LV. Capillary-to-fiber ratio values were significantly increased in SOL and were substantially increased in LV (CI: 1.10-1.22) after the INT training. These results suggest that exercise training under intermittent hypoxia represents a beneficial strategy for increasing endurance performance via improving metabolic properties and capillary profiles in several hind-leg muscles and the heart.
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Project description:PurposeThe tumor suppressor protein p53 may have regulatory roles in exercise response-adaptation processes such as mitochondrial biogenesis and autophagy, although its cellular location largely governs its biological role. We investigated the subcellular localization of p53 and selected signaling targets in human skeletal muscle following a single bout of endurance exercise.MethodsSixteen, untrained individuals were pair-matched for aerobic capacity (VO2peak) and allocated to either an exercise (EX, n = 8) or control (CON, n = 8) group. After a resting muscle biopsy, EX performed 60 min continuous cycling at ~70% of VO2peak during which time CON subjects rested. A further biopsy was obtained from both groups 3 h post-exercise (EX) or 4 h after the first biopsy (CON).ResultsNuclear p53 increased after 3 h recovery with EX only (~48%, p < 0.05) but was unchanged in the mitochondrial or cytoplasmic fractions in either group. Autophagy protein 5 (Atg-5) decreased in the mitochondrial protein fraction 3 h post-EX (~69%, P < 0.05) but remained unchanged in CON. There was an increase in cytoplasmic levels of the mitophagy marker PINK1 following 3 h of rest in CON only (~23%, P < 0.05). There were no changes in mitochondrial, nuclear, or cytoplasmic levels of PGC-1? post-exercise in either group.ConclusionsThe selective increase in nuclear p53 abundance following endurance exercise suggests a potential pro-autophagy response to remove damaged proteins and organelles prior to initiating mitochondrial biogenesis and remodeling responses in untrained individuals.
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Project description:The aim of this study was to elucidate the transcriptional signatures that distinguish the endurance-trained and the untrained muscle in healthy adult young males, both at baseline as well as in response to an acute bout of exercise.
2024-03-20 | GSE250122 | GEO