Journal
NATURE METABOLISM
Volume 2, Issue 9, Pages 902-+Publisher
NATURE RESEARCH
DOI: 10.1038/s42255-020-0240-7
Keywords
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Categories
Funding
- Pilot and Feasibility award
- NIH (NIDDK) [P30DK036836]
- American Heart Association [15SDG25560057, 19POST34381036]
- Boston Nutrition and Obesity Research Center (BNORC) Pilot Program [P30DK046200, 7513]
- Mary K. Iacocca Senior Visiting Fellowship
- Sao Paulo Research Foundation [FAPESP 2017/21676-3]
- NCI Cancer Center Support grant [NIH 5 P30 CA06516]
- NINDS P30 Core Center grant [NS072030]
- Office of Infrastructure Programs from the NIH [P40ODO21331]
- Joslin Clinical Research Center
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [17/21676-3] Funding Source: FAPESP
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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.
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