Incubation with sodium nitrite attenuates fatigue development in intact single mouse fibres at physiological Po2
Stephen J. Bailey J Physiol 2020 Jan
Dietary nitrate supplementation increases plasma nitrite concentration, which provides an oxygen‐independent source of nitric oxide and can delay skeletal muscle fatigue.
Nitrate supplementation has been shown to increase myofibre calcium release and force production in mouse skeletal muscle during contractions at a supra‐physiological oxygen tension, but it is unclear whether nitrite exposure can delay fatigue development and improve myofibre calcium handling at a near‐physiological oxygen tension.
Single mouse muscle fibres acutely treated with nitrite had a lower force and cytosolic calcium concentration during single non‐fatiguing contractions at a near‐physiological oxygen tension.
Nitrite treatment delayed fatigue development during repeated fatiguing isometric contractions at near‐physiological, but not at supra‐physiological, oxygen tension in combination with better maintenance of myofilament calcium sensitivity and sarcoplasmic reticulum calcium pumping.
These findings improve understanding of the mechanisms by which increased skeletal muscle nitrite exposure might be ergogenic and imply that this is related to improved calcium handling.
Abstract
Dietary nitrate (NO3−) supplementation, which increases plasma nitrite (NO2−) concentration, has been reported to attenuate skeletal muscle fatigue development. Sarcoplasmic reticulum (SR) calcium (Ca2+) release is enhanced in isolated single skeletal muscle fibres following NO3− supplementation or NO2− incubation at a supra‐physiological Po2 but it is unclear whether NO2− incubation can alter Ca2+ handling and fatigue development at a near‐physiological Po2.
These findings extend our understanding of the mechanisms by which increased NO2− exposure can mitigate skeletal muscle fatigue development.