Hyperglycaemia is associated with impaired muscle signalling and aerobic adaptation to exercise

Autor(es)

MacDonald, Tara L. ^{[1, 2, 3]} ; Pattamaprapanont, Pattarawan ^{[1, 2, 3]} ; Pathak, Prerana ^[2] ; Fernandez, Natalie ^[2] ; Freitas, Ellen C. ^[4] ; Hafida, Samar ^{[1, 2]} ; Mitri, Joanna ^{[1, 2]} ; Britton, Steven L. ^{[5, 6]} ; Koch, Lauren G. ^[7] ; Lessard, Sarah J. ^{[1, 2, 3]}

Afiliação do(s) autor(es)

^[1] Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 - USA

^[2] Joslin Diabet Ctr, Div Res, 1 Joslin Pl, Boston, MA 02215 - USA

^[3] Harvard Univ, Harvard Med Sch, Boston, MA 02115 - USA

^[4] Univ Sao Paulo, Sch Phys Educ & Sport, Ribeirao Preto - Brazil

^[5] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 - USA

^[6] Univ Michigan, Dept Anesthesiol, Ann Arbor, MI 48109 - USA

^[7] Univ Toledo, Dept Physiol & Pharmacol, 2801 W Bancroft St, Toledo, OH 43606 - USA

• Tipo de documento: Artigo Científico
• Fonte: NATURE METABOLISM; v. 2, n. 9, p. 902+, SEP 2020.
• Citações Web of Science: 8

Resumo

Increased aerobic exercise capacity, as a result of exercise training, has important health benefits. However, some individuals are resistant to improvements in exercise capacity, probably due to undetermined genetic and environmental factors. Here, we show that exercise-induced improvements in aerobic capacity are blunted and aerobic remodelling of skeletal muscle is impaired in several animal models associated with chronic hyperglycaemia. Our data point to chronic hyperglycaemia as a potential negative regulator of aerobic adaptation, in part, via glucose-mediated modifications of the extracellular matrix, impaired vascularization and aberrant mechanical signalling in muscle. We also observe low exercise capacity and enhanced c-Jun N-terminal kinase activation in response to exercise in humans with impaired glucose tolerance. Our work indicates that current shifts in dietary and metabolic health, associated with increasing incidence of hyperglycaemia, might impair muscular and organismal adaptations to exercise training, including aerobic capacity as one of its key health outcomes. (AU)

• Processo FAPESP: 17/21676-3 - Nocaute para acil-CoA sintase (ACSL4) no tecido adiposo e no controle do metabolismo da obesidade
• Beneficiário: Ellen Cristini de Freitas
• Modalidade de apoio: Bolsas no Exterior - Pesquisa