Objective: Nitrate (NO3-)-rich beetroot juice (BR) is recognized as an ergogenic supplementation that improves exercise tolerance during submaximal to maximal intensity exercise in recreational and competitive athletes. A recent study has investigated the effectiveness of BR on exercise performance during supramaximal intensity intermittent exercise (SIE) in Olympic-level track cyclists, but studies conducted in elite endurance athletes are scarce. The present study aimed to determine whether BR supplementation enhances the tolerance to SIE in elite endurance athletes. Methods: Eleven elite endurance athletes (age: 21.7±3.7 years, maximal oxygen uptake (V̇O %&'(): 71.1±5.2 mL•kg-1 •min-1) performed a SIE test until exhaustion following either a 3-day BR supplementation (340 mg/day) or a placebo (PL) supplementation (<2,5 mg/day) in a randomized, single blind, placebo-controlled and crossover study. The exercise test consisted of 15-s cycling exercise bouts at 170% of the maximal aerobic power interspersed with 30-s passive recovery periods. Gas exchange was measured during SIE tests as local muscle O2 delivery and extraction were assessed by near infrared spectroscopy. Results: The number of repetitions completed was not significantly different between BR (13.9±4.0 reps) and PL conditions (14.2±4.5 reps). BR supplementation did not affect oxygen uptake (V̇O %) during SIE tests (BR: 3378.5±681.8 mL•min-1 , PL: 3466.1±505.3 mL•min-1). No significant change in the areas under curves was found for local muscle total hemoglobin 3 (BR: 6816.9±1463.1 arbitrary units (a.u.), PL: 6771.5±3004.5 a.u.) and deoxygenated hemoglobin (BR: 6619.7±875.8 a.u., PL: 6332.7±1336.8 a.u.) during time-matched work+recovery periods from SIE tests following BR supplementation. Conclusion: BR supplementation does not enhance the tolerance to supramaximal intensity intermittent exercise in elite endurance athletes and does affect neither V̇O % nor local muscle O2 delivery and extraction.
Background: A large yet heterogeneous body of literature exists suggesting that endothelial dysfunction appears early in type 1 diabetes, due to hyperglycemia-induced oxidative stress. The latter may also affect vascular smooth muscles (VSM) function, a layer albeit less frequently considered in that pathology. This meta-analysis aims at evaluating the extent, and the contributing risk factors, of early endothelial dysfunction, and of the possible concomitant VSM dysfunction, in type 1 diabetes. Methods: PubMed, Web of Sciences, Cochrane Library databases were screened from their respective inceptions until October 2019. We included studies comparing vasodilatory capacity depending or not on endothelium (i.e., endothelial function or VSM function, respectively) in patients with uncomplicated type 1 diabetes and healthy controls. Results: Fifty-eight articles studying endothelium-dependent function, among which 21 studies also assessed VSM, were included. Global analyses revealed an impairment of standardized mean difference (SMD) (Cohen's d) of endothelial function: −0.61 (95% CI: −0.79, −0.44) but also of VSM SMD: −0.32 (95% CI: −0.57, −0.07). The type of stimuli used (i.e., exercise, occlusion-reperfusion, pharmacological substances, heat) did not influence the impairment of the vasodilatory capacity. Endothelial dysfunction appeared more pronounced within macrovascular than microvascular beds. The latter was particularly altered in cases of poor glycemic control [HbA 1c > 67 mmol/mol (8.3%)]. Conclusions: This meta-analysis not only corroborates the presence of an early impairment of endothelial function, even in response to physiological stimuli like exercise, but also highlights a VSM dysfunction in children and adults with type 1 diabetes. Endothelial dysfunction seems to be more pronounced in large than small vessels, fostering the debate on their relative temporal appearance.
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