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ETA: I've now changed the title of the thread to the title of the paper, originally it had the title of the newspaper article.
If, and how, this might apply to us I have no idea but thought it was interesting.
The article is based on this study - http://www.cell.com/cell-metabolism/fulltext/S1550-4131(17)30211-5
If, and how, this might apply to us I have no idea but thought it was interesting.
https://www.theguardian.com/science...ld-deliver-benefits-of-fitness-in-tablet-formFor those who cannot exercise, it could be the answer: rather than spending hours in the gym, the benefits of fitness training could be delivered in a tablet.
The prospect of an “exercise pill” might be music to the ears of couch potatoes, long-distance truck drivers and stressed-out office workers, but researchers believe it could transform the lives of people who are unable to exercise because of obesity or serious physical disabilities.
Hopes for such a pill emerged on Tuesday from scientists who found that an experimental drug allowed mice to run on a treadmill for 270 minutes before exhaustion set in. Mice that went without the drug lasted only 160 minutes before reaching their physical limit.
The endurance boost was accompanied by other apparent health benefits, scientists found, leading mice who had the drug for eight weeks to put on less weight and better control their blood sugar levels, suggesting a pill might also help people with diabetes.
Scientists led by Ronald Evans at the Salk Institute in San Diego made the discovery after they set out to explore what endurance meant on the molecular level. “If we really understand the science, can we replace training with a drug?” he said.
The article is based on this study - http://www.cell.com/cell-metabolism/fulltext/S1550-4131(17)30211-5
PPARδ Promotes Running Endurance by Preserving Glucose
Highlights
Summary
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Exhaustion of systemic glucose limits endurance exercise
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PPARδ regulates substrate utilization without mitochondrial biogenesis
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PPARδ represses glycolytic genes in muscle to slow glucose consumption
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Glucose sparing by PPARδ dramatically extends running time
Management of energy stores is critical during endurance exercise; a shift in substrate utilization from glucose toward fat is a hallmark of trained muscle. Here we show that this key metabolic adaptation is both dependent on muscle PPARδ and stimulated by PPARδ ligand. Furthermore, we find that muscle PPARδ expression positively correlates with endurance performance in BXD mouse reference populations. In addition to stimulating fatty acid metabolism in sedentary mice, PPARδ activation potently suppresses glucose catabolism and does so without affecting either muscle fiber type or mitochondrial content. By preserving systemic glucose levels, PPARδ acts to delay the onset of hypoglycemia and extends running time by ∼100 min in treated mice. Collectively, these results identify a bifurcated PPARδ program that underlies glucose sparing and highlight the potential of PPARδ-targeted exercise mimetics in the treatment of metabolic disease, dystrophies, and, unavoidably, the enhancement of athletic performance.
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