Blood flow changes in response to exercise have been attributed, among other factors, to the effect of vasodilators factors on the microvasculature, suggesting a close relationship between small blood vessels and conducting arteries. The main purpose of this study was to determine the relationship between the changes in near infrared spectroscopy (NIRS)-derived total haemoglobin ([tHb]) and muscle oxygen saturation (SmO₂) signals and femoral artery blood flow in response to resistance exercise at fast- and slow-velocity muscle contraction. The study randomised crossover design included twelve participants. NIRS and blood flow measurements were continuously monitored before, during, and 5 min after the exercise protocol. There was a significant correlation between [tHb] reperfusion slope ([tHb]_slope) and peak blood flow (BF_peak) after slow- and fast-velocity muscle contraction (r = 0.83, p = 0.0008 and r = 0.72, p = 0.0080, respectively). No significant correlation existed between the SmO₂ reperfusion slope (SmO_{2_slope}) and BF_peak after both slow- and fast-velocity muscle contraction exercise (r = −0.46, p = 0.1253 and r = 0.33, p = 0.2841, respectively). This study demonstrated a strong relationship between the NIRS-derived [tHb] and Doppler ultrasound BF during the recovery period of dynamic resistance exercise at both slow- and fast-velocity contraction.

Key points: It is unknown whether excessive reactive oxygen species (ROS) production drives the isocapnic hyperoxia (IH)‐induced decline in human cerebral blood flow (CBF) via reduced nitric oxide (NO) bioavailability and leads to disruption of the blood–brain barrier (BBB) or neural‐parenchymal damage. Cerebral metabolic rate for oxygen (CMR) and transcerebral exchanges of NO end‐products, oxidants, antioxidants and neural‐parenchymal damage markers were simultaneously quantified under IH with intravenous saline and ascorbic acid infusion. CBF and were reduced during IH, responses that were followed by increased oxidative stress and reduced NO bioavailability when saline was infused. No indication of neural‐parenchymal damage or disruption of the BBB was observed during IH. Antioxidant defences were increased during ascorbic acid infusion, while CBF, , oxidant and NO bioavailability markers remained unchanged. ROS play a role in the regulation of CBF and metabolism during IH without evidence of BBB disruption or neural‐parenchymal damage. To test the hypothesis that isocapnic hyperoxia (IH) affects cerebral blood flow (CBF) and metabolism through exaggerated reactive oxygen species (ROS) production, reduced nitric oxide (NO) bioavailability, disturbances in the blood–brain barrier (BBB) and neural‐parenchymal homeostasis, 10 men (24 ± 1 years) were exposed to a 10 min IH trial (100% O₂) while receiving intravenous saline and ascorbic acid (AA, 3 g) infusion. Internal carotid artery blood flow (ICABF), vertebral artery blood flow (VABF) and total CBF (tCBF, Doppler ultrasound) were determined. Arterial and right internal jugular venous blood was sampled to quantify the cerebral metabolic rate of oxygen (CMR), transcerebral exchanges (TCE) of NO end‐products (plasma nitrite), antioxidants (AA and AA plus dehydroascorbic acid (AA+DA)) and oxidant biomarkers (thiobarbituric acid‐reactive substances (TBARS) and 8‐isoprostane), and an index of BBB disruption and neuronal‐parenchymal damage (neuron‐specific enolase; NSE). IH reduced ICABF, tCBF and , while VABF remained unchanged. Arterial 8‐isoprostane and nitrite TCE increased, indicating that CBF decline was related to ROS production and reduced NO bioavailability. AA, AA+DA and NSE TCE did not change during IH. AA infusion did not change the resting haemodynamic and metabolic parameters but raised antioxidant defences, as indicated by increased AA/AA+DA concentrations. Negative AA+DA TCE, unchanged nitrite, reductions in arterial and venous 8‐isoprostane, and TBARS TCE indicated that AA infusion effectively inhibited ROS production and preserved NO bioavailability. Similarly, AA infusion prevented IH‐induced decline in regional and total CBF and re‐established . These findings indicate that ROS play a role in CBF regulation and metabolism during IH without evidence of BBB disruption or neural‐parenchymal damage.

The amino acid L-arginine is crucial for nitric oxide (NO) synthesis, an important molecule regulating vascular tone. Considering that vascular dysfunction precedes cardiovascular disease, supplementation with precursors of NO synthesis (e.g., L-arginine) is warranted. However, supplementation of L-citrulline is recommended instead of L-arginine since most L-arginine is catabolized during its course to the endothelium. Given that L-citrulline, found mainly in watermelon, can be converted to L-arginine, watermelon supplementation seems to be effective in increasing plasma L-arginine and improving vascular function. Nonetheless, there are divergent findings when investigating the effect of watermelon supplementation on vascular function, which may be explained by the L-citrulline dose in watermelon products. In some instances, offering a sufficient amount of L-citrulline can be impaired by the greater volume (>700 mL) of watermelon needed to reach a proper dose of L-citrulline. Thus, food technology can be applied to reduce the watermelon volume and make supplementation more convenient. Therefore, this narrative review aims to discuss the current evidence showing the effects of watermelon ingestion on vascular health parameters, exploring the critical relevance of food technology for acceptable L-citrulline content in these products. Watermelon-derived L-citrulline appears as a supplementation that can improve vascular function, including arterial stiffness and blood pressure. Applying food technologies to concentrate bioactive compounds in a reduced volume is warranted so that its ingestion can be more convenient, improving the adherence of those who want to ingest watermelon products daily.

Beetroot juice (BJ) consumption has been associated with improved cardiovascular health owing to an increase in NO bioconversion. This study evaluates the effect of BJ consumption on macrovascular endothelial function (flow-mediated dilation (FMD)) and muscle oxygen saturation (StO₂) parameters in pregnant women within a randomised, crossover, double-blind design in which twelve pregnant women consumed a single dose (140 ml) of BJ or placebo (PLA). Urinary nitrate was assessed before (T0) and 150 min after BJ/PLA consumption. FMD was used to evaluate macrovascular endothelial function, and near-IR spectroscopy was used to evaluate muscle StO₂ parameters during the occlusion and reperfusion phases, which were taken at baseline (PRE) and 120 and 140 min after BJ/PLA consumption, respectively. A significant increase in urinary nitrate was observed at 150 min after BJ consumption when compared with T0 (BJ: 0·20 (sd 0·13) v. T0: 0·02 (sd 0·00), P=0·000) and PLA intervention (PLA: 0·02 (sd 0·00), P=0·001). FMD improved after BJ consumption when compared with PRE (BJ: 11·00 (sd 1·67) v. PRE: 5·53 (sd 1·17), P=0·000) and PLA (5·34 (sd 1·31), P=0·000). No significant difference between PLA and PRE in FMD (P=1·000) was observed. In StO₂ parameters, a difference was not observed after BJ consumption compared with PRE and PLA intervention. The data demonstrate that a single dose of 140 ml of BJ consumption improves macrovascular endothelial function, but not StO₂ parameters.

The ergogenic effect of beetroot on the exercise performance of trained cyclists, runners, kayakers, and swimmers has been demonstrated. However, whether or not beetroot supplementation presents a beneficial effect on the exercise performance of jiu-jitsu athletes remains inconclusive. Therefore, the present study assessed the effect of beetroot-based gel (BG) supplementation on maximal voluntary contraction (MVC), exercise time until fatigue (ETF), muscle O₂ saturation (SmO₂), blood volume (tHb), and plasma nitrate and lactate in response to handgrip isotonic exercise (HIE) in jiu-jitsu athletes. In a randomized, crossover, double-blind design, 12 jiu-jitsu athletes performed 3 sets of HIE at 40% of the MVC until fatigue after 8 days (the eighth dose was offered 120 min previous exercise) of BG supplementation or a nitrate-depleted gel (PLA), and forearm SmO₂ and tHb were continuously monitored by using near-infrared spectroscopy. Blood samples were taken before, immediately after exercise, and 20 min after exercise recovery in the PLA and BG conditions. MVC was evaluated at baseline and 20 min after HIE. There was a significant reduction in ΔMVC decline after HIE in the BG condition. Forearm SmO₂ during exercise recovery was significantly greater only after BG supplementation. No significant difference in ETF and tHb were observed between both BG and PLA in response to HIE. Plasma nitrate increased only after BG, whereas the exercise-induced increase in plasma lactate was significantly lower in BG when compared with PLA. In conclusion, BG supplementation may be a good nutritional strategy to improve forearm SmO₂ and prevent force decline in response to exercise in jiu-jitsu athletes.