A single dose of dietary nitrate supplementation protects against endothelial ischemia-reperfusion injury in early postmenopausal women.

The onset of menopause and accompanying changes to ovarian hormones often precedes endothelial dysfunction in women. In particular, accelerated impairments in macrovascular and microvascular function coincide with the loss of estrogen, as does impaired endothelial responses to ischemia-reperfusion (IR) injury. In healthy, early postmenopausal women (n = 12; 3.9 ± 1.5 years since menopause) we tested the hypothesis that acute dietary nitrate (NO3-) supplementation would improve endothelial function and attenuate the magnitude of endothelial dysfunction following whole-arm IR in comparison with placebo. In this randomized, double-blind, placebo-controlled, crossover study we tested participants before and after NO3--rich (BRnitrate) and NO3--depleted (BRplacebo) beetroot juice (BR) consumption, as well as following IR injury, and 15 min after IR to assess recovery. Analyses with repeated-measures general linear models revealed a condition × time interaction for brachial artery flow-mediated dilation (FMD; P = 0.04), and no interaction effect was found for the near-infrared spectroscopy-derived reperfusion slope (P = 0.86). Follow-up analysis showed a significant decline in FMD following IR injury with BRplacebo in comparison with all other timepoints (all, P < 0.05), while this decline was not present with BRnitrate (all, P > 0.05). Our findings demonstrate that a single dose of dietary NO3- minimizes IR-induced macrovascular endothelial dysfunction in healthy, early postmenopausal women, but does not improve resting macrovascular and microvascular function. Trial registration number: NCT03644472. Novelty: In healthy, early postmenopausal women, a single dose of NO3--rich BR can protect against IR-induced endothelial dysfunction. This protection may be due to nitric oxide bioactivity during IR rather than improved endothelial function prior to the IR protocol per se.

Allometric scaling of flow-mediated dilation: is it always helpful?

Flow-mediated dilation (FMD) is calculated as the greatest percent change in arterial diameter following an ischaemic challenge. This Traditional %FMD calculation is thought to have statistical bias towards baseline diameter (Dbase ), which is reduced by allometric scaling. This study examined whether allometric scaling FMD influenced the difference between a group of healthy young and older adults compared to the Traditional %FMD, and to determine whether a New (allometric) scaling %FMD improved the ability to obtain individually scaled FMD. Popliteal artery FMD was assessed in 18 young (26 ± 3 years) and 17 older adults (77 ± 5 years). 'Corrected' mean FMD was generated from a log-linked ANCOVA model. Individual %FMD was evaluated using three calculations: (1) Traditional %FMD calculation; (2) Atkinson (allometric) scaling %FMD (peak diameter (Dpeak)/(Dbasescalingexponent)); and (3) New scaling %FMD ((Dpeak-Dbase)/(Dbasescalingexponent)). Traditional %FMD was significantly larger in young (5·82 ± 2·58%) versus old (3·72 ± 1·26%). 'Corrected' FMD means (Y: 5·97 ± 2·12%; O: 3·98 ± 2·06%) were similar to Traditional %FMD; however, the logarithmic transformation prevents statistical interpretation of group differences. Individually scaled %FMD using the Atkinson scaling resulted in values that were corrected for variations in Dbase but that were twofold to threefold larger than those of the Traditional calculation. New scaling %FMD resulted in values that were similar to values expected (Y: 6·21 ± 2·75%; O: 3·98 ± 1·36%); however, it did not effectively correct for variation in Dbase . Recommendations regarding the advantages of allometrically scaling %FMD should be made with caution until research clearly establishes the benefits of this approach.

Effects of short-term training and detraining on VO2 kinetics: Faster VO2 kinetics response after one training session.

This study examined the time course of short-term training and detraining-induced changes in oxygen uptake ( V ˙ O 2 ) kinetics. Twelve men (24 ± 3 years) were assigned to either a 50% or a 70% of V ˙ O 2 m a x training intensity (n = 6 per group). V ˙ O 2 was measured breath-by-breath. Changes in deoxygenated-hemoglobin concentration (Δ[HHb]) were measured by near-infrared spectroscopy. Moderate-intensity exercise on-transient V ˙ O 2 and Δ[HHb] were modeled with a mono-exponential and normalized (0-100% of response) and the [ H H b ] / V ˙ O 2 ratio was calculated. Similar changes in time constant of V ˙ O 2 ( t V ˙ O 2 ) were observed in both groups. The combined group mean for t V ˙ O 2 decreased ∼14% (32.3 to 27.9 s, P < 0.05) after one training session with a further ∼11% decrease (27.9 to 24.8 s, P < 0.05) following two training sessions. The t V ˙ O 2 p remained unchanged throughout the remaining of training and detraining. A significant "overshoot" in the [ H H b ] / V ˙ O 2 ratio was decreased (albeit not significant) after one training session, and abolished (P < 0.05) after the second one, with no overshoot observed thereafter. Speeding of V ˙ O 2 kinetics was remarkably quick with no further changes being observed with continuous training or during detraining. Improve matching of local O2 delivery to O2 utilization is a mechanism proposed to influence this response.

Laboratory 20-km cycle time trial reproducibility.

This study evaluated the reproducibility of laboratory based 20-km time trials in well trained versus recreational cyclists. Eighteen cyclists (age = 34 +/- 8 yrs; body mass index = 23.1 +/- 2.2 kg/m (2); VO(2max) = 4.19 +/- 0.65 L/min) completed three 20-km time trials over a month on a Velotron cycle ergometer. Average power output (PO) (W), speed, and heart rate (HR) were significantly lower in the first time trial compared to the second and third time trial. The coefficients of variation (CV) between the second and third trial of the top eight performers for average PO, time to completion, and speed were 1.2 %, 0.6 %, 0.5 %, respectively, compared to 4.8 %, 2.0 %, and 2.3 % for the bottom ten. In addition, the average HR, VO(2), and percentage of VO(2max) were similar between trials. This study demonstrated that (1) a familiarization session improves the reliability of the measurements (i.e., average PO, time to completion and speed), and (2) the CV was much smaller for the best performers.

A small amount of inhaled nitric oxide does not increase lung diffusing capacity.

The aim of the present study was to determine: 1) whether 40-50 ppm nitric oxide (NO) increases diffusing capacity of the lung for NO (D(L,NO)) and carbon monoxide (D(L,CO)), membrane diffusing capacity for CO (D(m,CO)) and pulmonary capillary blood volume (V(c)); 2) the actual number of tests required to provide a reasonable estimate of D(L,NO), D(L,CO), D(m,CO) and V(c); and 3) repeatability of these parameters using the single-breath D(L,NO)-D(L,CO) method. In total, 31 subjects performed five single-breath hold manoeuvres at rest, inhaling 43+/-3 ppm NO together with a standard diffusion mixture. D(L,NO) (D(m,CO)) remained unchanged from the first to fifth trial. However, compared with the first trial, D(L,CO) and V(c) had decreased by the fourth (-4+/-5%; 95% confidence interval (CI) = -5- -2%) and third trial (-5+/-7%; 95% CI = -7- -2%), respectively. Repeatability over five trials was 17, 3 and 7 mL.min(-1).mmHg(-1) for D(L,NO), D(L,CO) and D(m,CO), respectively, and 13 mL for V(c) when D(m,CO) = D(L,NO)/2.42. In conclusion, nitric oxide inhaled during sequential single-breath manoeuvres has no effect on diffusing capacity of the lung for nitric oxide and, thus, membrane diffusing capacity for carbon monoxide. Since more than two and three trials will lower pulmonary capillary blood volume and diffusing capacity of the lung for carbon monoxide, respectively, the average value of only two properly performed trials is suggested.