"Beet-ing" the Mountain: A Review of the Physiological and Performance Effects of Dietary Nitrate Supplementation at Simulated and Terrestrial Altitude

Abstract

Exposure to altitude results in multiple physiological consequences. These include, but are not limited to, a reduced maximal oxygen consumption, drop in arterial oxygen saturation, and increase in muscle metabolic perturbations at a fixed sub-maximal work rate. Exercise capacity during fixed work rate or incremental exercise and time-trial performance are also impaired at altitude relative to sea level. Recently, dietary nitrate (NO₃^-) supplementation has attracted considerable interest as a nutritional aid during altitude exposure. In this review, we summarise and critically evaluate the physiological and performance effects of dietary NO₃^- supplementation during exposure to simulated and terrestrial altitude. Previous investigations at simulated altitude indicate that NO₃^- supplementation may reduce the oxygen cost of exercise, elevate arterial and tissue oxygen saturation, improve muscle metabolic function, and enhance exercise capacity/performance. Conversely, current evidence suggests that NO₃^- supplementation does not augment the training response at simulated altitude. Few studies have evaluated the effects of NO₃^- at terrestrial altitude. Current evidence indicates potential improvements in endothelial function at terrestrial altitude following NO₃^- supplementation. No effects of NO₃^- supplementation have been observed on oxygen consumption or arterial oxygen saturation at terrestrial altitude, although further research is warranted. Limitations of the present body of literature are discussed, and directions for future research are provided.

Fig. 1

A schematic representation of the metabolic pathways for nitric oxide (NO) generation in the human body (adapted from Jones [32], with permission). The ‘traditional’ pathway for NO generation involves oxidation of the semi-essential amino acid l-arginine, in a reaction which requires the availability of O₂ and is catalysed via the NO synthase (NOS) enzymes. This O₂-dependent reaction is suppressed in hypoxia. Alternatively, NO can be generated via the nitrate (NO₃ ⁻)–nitrite (NO₂ ⁻)–NO pathway. Here, NO₃ ⁻ from dietary sources or produced as an oxidation product of the l-arginine pathway is reduced into NO₂ ⁻ via oral bacteria (a rapid pathway) or via the enzyme xanthine oxidoreductase (XOR) (a slower pathway). NO₂ ⁻ can subsequently be reduced into NO via multiple catalysts, particularly under conditions of low O₂ availability. This second pathway may serve to maintain or enhance NO signalling under conditions of hypoxia, such as that experienced at an altitude