Nitrate-rich beetroot juice (BRJ) increases plasma nitrite concentrations, lowers the oxygen cost (V⋅O2) of steady-state exercise and improves exercise performance in sedentary and moderately-trained, but rarely in well-trained individuals exercising at sea-level. BRJ supplementation may be more effective in a hypoxic environment, where the reduction of nitrite into nitric oxide (NO) is potentiated, such that well-trained and less well-trained individuals may derive a similar ergogenic effect. We conducted a randomised, counterbalanced, double-blind placebo controlled trial to determine the effects of BRJ on treadmill running performance in moderate normobaric hypoxia (equivalent to 2500 m altitude) in participants with a range of aerobic fitness levels. Twelve healthy males (V⋅O2max ranging from 47.1 to 76.8 ml kg(-1) min(-1)) ingested 138 ml concentrated BRJ (∼15.2 mmol nitrate) or a nitrate-deplete placebo (PLA) (∼0.2 mmol nitrate). Three hours later, participants completed steady-state moderate intensity running, and a 1500 m time-trial (TT) in a normobaric hypoxic chamber (FIO2 ∼ 15%). Plasma nitrite concentration was significantly greater following BRJ versus PLA 1 h post supplementation, and remained higher in BRJ throughout the testing session (p < 0.01). Average V⋅O2 was significantly lower (BRJ: 18.4 ± 2.0, PLA: 20.4 ± 12.6 ml kg(-1) min(-1); p = 0.002), whilst arterial oxygen saturation (SpO2) was significantly greater (BRJ: 88.4 ± 2.7, PLA: 86.5 ± 3.3%; p < 0.001) following BRJ. BRJ improved TT performance in all 12 participants by an average of 3.2% (BRJ: 331.1 ± 45.3 vs. PL: 341.9 ± 46.1 s; p < 0.001). There was no apparent relationship between aerobic fitness and the improvement in performance following BRJ (r(2) = 0.05, p > 0.05). These findings suggests that a high nitrate dose in the form of a BRJ supplement may improve running performance in individuals with a range of aerobic fitness levels conducting moderate and high-intensity exercise in a normobaric hypoxic environment.

This study investigated the effect of carbohydrate (CHO) dose and composition on fuel selection during exercise, specifically exogenous and endogenous (liver and muscle) CHO oxidation. Ten trained males cycled in a double-blind randomized order on 5 occasions at 77% \dot{\mathrm{V}}{\mathrm{O}}_{2\max } for 2 h, followed by a 30-min time-trial (TT) while ingesting either 60 g·h⁻¹ (LG) or 75 g·h^{−1 13}C-glucose (HG), 90 g·h⁻¹ (LGF) or 112.5 g·h^{−1 13}C-glucose-¹³C-fructose ([2:1] HGF) or placebo. CHO doses met or exceed reported intestinal transporter saturation for glucose and fructose. Indirect calorimetry and stable mass isotope [¹³C] tracer techniques were utilized to determine fuel use. TT performance was 93% “likely/probable” to be improved with LGF compared with the other CHO doses. Exogenous CHO oxidation was higher for LGF and HGF compared with LG and HG (ES > 1.34, P < 0.01), with the relative contribution of LGF (24.5 ± 5.3%) moderately higher than HGF (20.6 ± 6.2%, ES = 0.68). Increasing CHO dose beyond intestinal saturation increased absolute (29.2 ± 28.6 g·h⁻¹, ES = 1.28, P = 0.06) and relative muscle glycogen utilization (9.2 ± 6.9%, ES = 1.68, P = 0.014) for glucose-fructose ingestion. Absolute muscle glycogen oxidation between LG and HG was not significantly different, but was moderately higher for HG (ES = 0.60). Liver glycogen oxidation was not significantly different between conditions, but absolute and relative contributions were moderately attenuated for LGF (19.3 ± 9.4 g·h⁻¹, 6.8 ± 3.1%) compared with HGF (30.5 ± 17.7 g·h⁻¹, 10.1 ± 4.0%, ES = 0.79 & 0.98). Total fat oxidation was suppressed in HGF compared with all other CHO conditions (ES > 0.90, P = 0.024–0.17). In conclusion, there was no linear dose response for CHO ingestion, with 90 g·h⁻¹ of glucose-fructose being optimal in terms of TT performance and fuel selection.

We conducted a systematic review and meta-analysis of randomized clinical trials examining the effect of inorganic nitrate or nitrite supplementation on cognitive function (CF) and cerebral blood flow (CBF). Two databases (PubMed, Embase) were searched for articles from inception until May 2017. Inclusion criteria were: randomized clinical trials; participants >18 years old; trials comparing a nitrate/nitrite intervention with a control. Thirteen and nine trials were included in the meta-analysis to assess CF and CBF, respectively. Random-effects models were used and the effect size described as standardized mean differences (SMDs). A total of 297 participants (median of 23 per trial) were included for CF; 163 participants (median of 16 per trial) were included for CBF. Nitrate/nitrite supplementation did not influence CF (SMD +0.06, 95% CI: -0.06, 0.18, P = 0.32) or CBF under resting (SMD +0.14, 95% CI: -0.13, 0.41, P = 0.31), or stimulated conditions (SMD + 0.23, 95% CI: -0.11, 0.56, P = 0.19). The meta-regression showed an inverse association between duration of the intervention and CBF (P = 0.02) but no influence of age, BMI or dose (P < 0.05). Nitrate and nitrite supplementation did not modify CBF or CF. Further trials employing larger samples sizes and interventions with longer duration are warranted.

New Findings: What is the central question of this study? Splenic contractions occur in response to apnoea‐induced hypoxia with and without face immersion in water. However, the splenic responses to a series of static or dynamic apnoeas with whole‐body water immersion in non‐divers and elite breath‐hold divers are unknown. What is the main finding and its importance? Static and dynamic apnoeas were equally effective in stimulating splenic contractions across non‐divers and elite breath‐hold divers. These findings demonstrate that the magnitude of the splenic response is largely dictated by the degree of the hypoxemic stress encountered during voluntary apnoeic epochs. Splenic contractions occur in response to apnoea‐induced hypoxia with and without facial water immersion. However, the splenic responses to a series of static (STA) or dynamic (DYN) apnoeas with whole‐body water immersion in non‐divers (NDs) and elite breath‐hold divers (EBHDs) are unknown. EBHD (n = 8), ND (n = 10) and control participants (n = 8) were recruited. EBHD and ND performed a series of five maximal DYN or STA on separate occasions. Control performed a static eupnoeic (STE) protocol to control against any effects of water immersion and diurnal variation on splenic volume and haematology. Heart rate (HR) and peripheral oxygen saturation (SpO₂) were monitored for 30 s after each apnoea. Pre‐ and post‐apnoeic splenic volumes were quantified ultrasonically, and blood samples were drawn for haematology. For EBHD and ND end‐apnoeic HR was higher (P < 0.001) and SpO₂ was lower in DYN (P = 0.024) versus STA. EBHD attained lower end‐apnoeic SpO₂ during DYN and STA than NDs (P < 0.001). Splenic contractions occurred following DYN (EBHD, −47 ± 6%; ND, −37 ± 4%; P < 0.001) and STA (EBHD, −26 ± 4%; ND, −26 ± 8%; P < 0.01). DYN‐associated splenic contractions were greater than STA in EBHD only (P = 0.042). Haemoglobin concentrations were higher following DYN only (EBHD, +5 ± 8g/L , +4 ± 2%; ND, +8 ± 3 g/L , +4.9 ± 3%; P = 0.019). Haematocrit remained unchanged after each protocol. There were no between group differences in post‐apnoeic splenic volume or haematology. In both groups, splenic contractions occurred in response to STA and DYN when combined with whole‐body immersion. DYN apnoeas, were effective at increasing haemoglobin concentrations but not STA apnoeas. Thus, the magnitude of the splenic response relates to the hypoxemic stress encountered during apnoeic epochs.

This study compared the effects of coingesting glucose and fructose on exogenous and endogenous substrate oxidation during prolonged exercise at altitude and sea level, in men. Seven male British military personnel completed two bouts of cycling at the same relative workload (55% W max) for 120 min on acute exposure to altitude (3375 m) and at sea level (~113 m). In each trial, participants ingested 1.2 g·min−1 of glucose (enriched with 13C glucose) and 0.6 g·min−1 of fructose (enriched with 13C fructose) directly before and every 15 min during exercise. Indirect calorimetry and isotope ratio mass spectrometry were used to calculate fat oxidation, total and exogenous carbohydrate oxidation, plasma glucose oxidation, and endogenous glucose oxidation derived from liver and muscle glycogen. Total carbohydrate oxidation during the exercise period was lower at altitude (157.7 ± 56.3 g) than sea level (286.5 ± 56.2 g, P = 0.006, ES = 2.28), whereas fat oxidation was higher at altitude (75.5 ± 26.8 g) than sea level (42.5 ± 21.3 g, P = 0.024, ES = 1.23). Peak exogenous carbohydrate oxidation was lower at altitude (1.13 ± 0.2 g·min−1) than sea level (1.42 ± 0.16 g·min−1, P = 0.034, ES = 1.33). There were no differences in rates, or absolute and relative contributions of plasma or liver glucose oxidation between conditions during the second hour of exercise. However, absolute and relative contributions of muscle glycogen during the second hour were lower at altitude (29.3 ± 28.9 g, 16.6 ± 15.2%) than sea level (78.7 ± 5.2 g ( P = 0.008, ES = 1.71), 37.7 ± 13.0% ( P = 0.016, ES = 1.45). Acute exposure to altitude reduces the reliance on muscle glycogen and increases fat oxidation during prolonged cycling in men compared with sea level.

Purpose This study investigated the effect of small manipulations in carbohydrate (CHO) dose on exogenous and endogenous (liver and muscle) fuel selection during exercise. Method Eleven trained males cycled in a double-blind randomised order on 4 occasions at 60% \(\dot {V}{{\text{O}}_{2\;\hbox{max} }}\) for 3 h, followed by a 30-min time-trial whilst ingesting either 80 g h⁻¹ or 90 g h⁻¹ or 100 g h^{−1 13}C-glucose-¹³C-fructose [2:1] or placebo. CHO doses met, were marginally lower, or above previously reported intestinal saturation for glucose–fructose (90 g h⁻¹). Indirect calorimetry and stable mass isotope [¹³C] techniques were utilised to determine fuel use. Result Time-trial performance was 86.5 to 93%, ‘likely, probable’ improved with 90 g h⁻¹ compared 80 and 100 g h⁻¹. Exogenous CHO oxidation in the final hour was 9.8–10.0% higher with 100 g h⁻¹ compared with 80 and 90 g h⁻¹ (ES = 0.64–0.70, 95% CI 9.6, 1.4 to 17.7 and 8.2, 2.1 to 18.6). However, increasing CHO dose (100 g h⁻¹) increased muscle glycogen use (101.6 ± 16.6 g, ES = 0.60, 16.1, 0.9 to 31.4) and its relative contribution to energy expenditure (5.6 ± 8.4%, ES = 0.72, 5.6, 1.5 to 9.8 g) compared with 90 g h⁻¹. Absolute and relative muscle glycogen oxidation between 80 and 90 g h⁻¹ were similar (ES = 0.23 and 0.38) though a small absolute (85.4 ± 29.3 g, 6.2, − 23.5 to 11.1) and relative (34.9 ± 9.1 g, − 3.5, − 9.6 to 2.6) reduction was seen in 90 g h⁻¹ compared with 100 g h⁻¹. Liver glycogen oxidation was not significantly different between conditions (ES < 0.42). Total fat oxidation during the 3-h ride was similar in CHO conditions (ES < 0.28) but suppressed compared with placebo (ES = 1.05–1.51). Conclusion ‘Overdosing’ intestinal transport for glucose–fructose appears to increase muscle glycogen reliance and negatively impact subsequent TT performance.