Robinson 2017 Cell Metabol
Robinson MM, Dasari S, Konopka AR, Johnson ML, Manjunatha S, Esponda RR, Carter RE, Lanza IR, Nair KS (2017) Enhanced protein translation underlies improved metabolic and physical adaptations to different exercise training modes in young and old humans. Cell Metab 25:581-92. |
Robinson MM, Dasari S, Konopka AR, Johnson ML, Manjunatha S, Esponda RR, Carter RE, Lanza IR, Nair KS (2017) Cell Metab
Abstract: The molecular transducers of benefits from different exercise modalities remain incompletely defined. Here we report that 12 weeks of high-intensity aerobic interval (HIIT), resistance (RT), and combined exercise training enhanced insulin sensitivity and lean mass, but only HIIT and combined training improved aerobic capacity and skeletal muscle mitochondrial respiration. HIIT revealed a more robust increase in gene transcripts than other exercise modalities, particularly in older adults, although little overlap with corresponding individual protein abundance was noted. HIIT reversed many age-related differences in the proteome, particularly of mitochondrial proteins in concert with increased mitochondrial protein synthesis. Both RT and HIIT enhanced proteins involved in translational machinery irrespective of age. Only small changes of methylation of DNA promoter regions were observed. We provide evidence for predominant exercise regulation at the translational level, enhancing translational capacity and proteome abundance to explain phenotypic gains in muscle mitochondrial function and hypertrophy in all ages.
Copyright Β© 2017 Elsevier Inc. All rights reserved. β’ Keywords: Aging, Exercise, Human, Insulin clamp, Interval, Methylation, Proteome, Skeletal muscle, Tracer, Transcriptome β’ Bioblast editor: Kandolf G β’ O2k-Network Lab: US OR Corvallis Robinson MM, US MN Rochester Nair KS
Labels: MiParea: Respiration, nDNA;cell genetics, Exercise physiology;nutrition;life style
Pathology: Aging;senescence
Organism: Human Tissue;cell: Skeletal muscle Preparation: Isolated mitochondria
Coupling state: OXPHOS
Pathway: N, NS
HRR: Oxygraph-2k