Ferri 2018 Eur J Appl Physiol
|Ferri A, Panariti A, Miserocchi G, Rocchetti M, Buoli Comani G, Rivolta I, Bishop DJ (2018) Tissue specificity of mitochondrial adaptations in rats after 4 weeks of normobaric hypoxia. Eur J Appl Physiol 118:1641-52.|
Abstract: Exposure to hypoxia has been suggested to activate multiple adaptive pathways so that muscles are better able to maintain cellular energy homeostasis. However, there is limited research regarding the tissue specificity of this response. The aim of this study was to investigate the influence of tissue specificity on mitochondrial adaptations of rat skeletal and heart muscles after 4 weeks of normobaric hypoxia (FiO2: 0.10).
Twenty male Wistar rats were randomly assigned to either normobaric hypoxia or normoxia. Mitochondrial respiration was determined in permeabilised muscle fibres from left and right ventricles, soleus and extensorum digitorum longus (EDL). Citrate synthase activity and the relative abundance of proteins associated with mitochondrial biogenesis were also analysed.
After hypoxia exposure, only the soleus and left ventricle (both predominantly oxidative) presented a greater maximal mass-specific respiration (+48 and +25%, p < 0.05) and mitochondrial-specific respiration (+75 and +28%, p < 0.05). Citrate synthase activity was higher in the EDL (0.63 ± 0.08 vs 0.41 ± 0.10 µmol min- 1 µg- 1) and lower in the soleus (0.65 ± 0.17 vs 0.87 ± 0.20 µmol min- 1 µg- 1) in hypoxia with respect to normoxia. There was a lower relative protein abundance of PGC-1α (-25%, p < 0.05) in the right ventricle and a higher relative protein abundance of PGC-1β (+43%, p < 0.05) in the left ventricle of rats exposed to hypoxia, with few differences for protein abundance in the other muscles. • Keywords: Heart, Hypoxia, Mitochondrial respiration, Skeletal muscles • Bioblast editor: Kandolf G • O2k-Network Lab: AU Melbourne Stepto NK
Labels: MiParea: Respiration, mt-Biogenesis;mt-density
Stress:Hypoxia Organism: Rat Tissue;cell: Heart, Skeletal muscle Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS Pathway: N HRR: Oxygraph-2k