title: Dietary nitrate markedly improves voluntary running in mice.
abstract: Nitrate supplementation is shown to increase submaximal force in human and mouse skeletal muscles. In this study, we test the hypothesis that the increased submaximal force induced by nitrate supplementation reduces the effort of submaximal voluntary running, resulting in increased running speed and distance. C57Bl/6N male mice were fed nitrate in the drinking water and housed with or without access to an in-cage running wheel. Nitrate supplementation in sedentary mice had no effect on endurance in a treadmill test, nor did it enhance mitochondrial function. However, after three weeks with in-cage running wheel, mice fed nitrate ran on average 20% faster and 30% further than controls (p<0.01). Compared to running controls, this resulted in ~13% improved endurance on a subsequent treadmill test (p<0.05) and increased mitochondrial oxidative capacity, as judged from a mean increase in citrate synthase activity of 14% (p<0.05). After six weeks with nitrate, the mice were running 58% longer distances per night. When nitrate supplementation was removed from the diet, the running distance and speed decreased to the control level, despite the improved endurance achieved during nitrate supplementation. In conclusion, low-frequency force improvement due to nitrate supplementation facilitates submaximal exercise such as voluntary running.
authors: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. Electronic address: Niklas.ivarsson@ki.se.
authors: Niklas
authors: N
authors: Ivarsson
authors: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors: Tomas A
authors: TA
authors: Schiffer
authors: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors: Andrés
authors: A
authors: Hernández
authors: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors: Johanna T
authors: JT
authors: Lanner
authors: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors: Eddie
authors: E
authors: Weitzberg
authors: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors: Jon O
authors: JO
authors: Lundberg
authors: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors: Håkan
authors: H
authors: Westerblad
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002155:Calsequestrin; D019587:Dietary Supplements; D003576:Electron Transport Complex IV / Q000378:metabolism; D005080:Exercise Test; D008124:Locomotion / Q000502:physiology; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000378:metabolism; D018482:Muscle, Skeletal / Q000502:physiology* / Q000648:ultrastructure; D009566:Nitrates / Q000008:administration & dosage*; D012420:Running / Q000502:physiology*; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D018709:Statistics, Nonparametric
chemical_list: D002135:Calcium-Binding Proteins; D002155:Calsequestrin; C503130:Casq1 protein, mouse; D009566:Nitrates; D019837:Ryanodine Receptor Calcium Release Channel; C000592747:ryanodine receptor 1, mouse; D000255:Adenosine Triphosphate; D003576:Electron Transport Complex IV
keywords: Endurance; Excitation-contraction coupling; Exercise; Oxidative capacity