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Competitive swimmers complete 50‐m front crawl swimming without breathing or with a limited number of breaths. Breath holding during exercise can trigger diving reflex including bradycardia and diminished active muscle blood flow, whereas oxygen supply to vital organ such as brain is maintained. We hypothesized that swimmers achieving faster time in 50‐m front crawl with limited number of breaths demonstrate a blunted diving reflex of cardiac and active muscle blood flow responses with elevated cerebral perfusion to counteract peripheral and central fatigues. Twenty‐eight competitive swimmers (12 females) underwent a 50‐m front crawl swimming time trial with minimum respiratory interruptions, following which they were categorized into two groups: Fast (n = 13) and Slow (n = 15). Additionally, they performed knee extension exercises with maximal voluntary breath‐ holding, wherein leg blood flow (Doppler ultrasound), cardiac output (Modelflow), heart rate (electrocardiogram), and middle cerebral artery mean blood velocity (transcranial Doppler ultrasound) were evaluated. The pattern of leg blood flow response differed between the two groups (p = 0.031) with the Fast group experiencing a delayed onset of reductions in leg blood flow (p = 0.035). The onset of bradycardia was also delayed in the Fast group (p = 0.014), with this group demonstrating a higher value of the lowest heart rate (between‐trial difference in average: 15.9 [3.73, 28.2] beats/min) and cardiac output (between‐trial difference in median: 2.84 L/min) (both, p ≤ 0.013). Middle cerebral artery mean blood velocity was similar between the groups (all p ≥ 0.112). We show that swimmers with superior performance in 50‐m front crawl swim with limited breaths display a diminished diving reflex. [ABSTRACT FROM AUTHOR]

Hyperthermia stimulates ventilation in humans. This hyperthermia-induced hyperventilation may be mediated by the activation of peripheral chemoreceptors implicated in the regulation of respiration in reaction to various chemical stimuli, including reductions in arterial pH. Here, we investigated the hypothesis that during passive heating at rest, the increases in arterial pH achieved with sodium bicarbonate ingestion, which could attenuate peripheral chemoreceptor activity, mitigate hyperthermia-induced hyperventilation. We also assessed the effect of sodium bicarbonate ingestion on cerebral blood flow responses, which are associated with hyperthermia-induced hyperventilation. Twelve healthy men ingested sodium bicarbonate (0.3 g/kg body weight) or sodium chloride (0.208 g/kg). One hundred minutes after the ingestion, the participants were passively heated using hot-water immersion (42°C) combined with a water-perfused suit. Increases in esophageal temperature (an index of core temperature) and minute ventilation (V̇E) during the heating were similar in the two trials. Moreover, when V̇E is expressed as a function of esophageal temperature, there were no between-trial differences in the core temperature threshold for hyperventilation (38.0 ± 0.3 vs. 38.0 ± 0.4°C, P = 0.469) and sensitivity of hyperthermia-induced hyperventilation as assessed by the slope of the core temperature-V̇E relation (13.5 ± 14.2 vs. 15.8 ± 15.5 L/min/°C, P = 0.831). Furthermore, middle cerebral artery mean blood velocity (an index of cerebral blood flow) decreased similarly with heating duration in both trials. These results suggest that sodium bicarbonate ingestion does not mitigate hyperthermia-induced hyperventilation and the reductions in cerebral blood flow index in resting heated humans. NEW & NOTEWORTHY: Hyperthermia leads to hyperventilation and associated cerebral hypoperfusion, both of which may impair heat tolerance. This hyperthermia-induced hyperventilation may be mediated by peripheral chemoreceptors, which can be activated by reductions in arterial pH. However, our results suggest that sodium bicarbonate ingestion, which can increase arterial pH, is not an effective intervention in alleviating hyperthermia-induced hyperventilation and cerebral hypoperfusion in resting heated humans. [ABSTRACT FROM AUTHOR]

The objective was to assess if post‐exercise ingestion of carbonated water in a hot environment ameliorates hypotension, enhances cerebral blood flow and heat loss responses, and positively modulates perceptions and mood states. Twelve healthy, habitually active young adults (five women) performed 60 min of cycling at 45% peak oxygen uptake in a hot climate (35°C). Subsequently, participants consumed 4°C carbonated or non‐carbonated (control) water (150 and 100 mL for males and females regardless of drink type) at 20 and 40 min into post‐exercise periods. Mean arterial pressure decreased post‐exercise at 20 min only (P = 0.032) compared to the pre‐exercise baseline. Both beverages transiently (∼1 min) increased mean arterial pressure and middle cerebral artery mean blood velocity (cerebral blood flow index) regardless of post‐exercise periods (all P ≤ 0.015). Notably, carbonated water ingestion led to greater increases in mean arterial pressure (2.3 ± 2.8 mmHg vs. 6.6 ± 4.4 mmHg, P < 0.001) and middle cerebral artery mean blood velocity (1.6 ± 2.5 cm/s vs. 3.8 ± 4.1 cm/s, P = 0.046) at 20 min post‐exercise period compared to non‐carbonated water ingestion. Both beverages increased mouth exhilaration and reduced sleepiness regardless of post‐exercise periods, but these responses were more pronounced with carbonated water ingestion at 40 min post‐exercise (mouth exhilaration: 3.1 ± 1.4 vs. 4.7 ± 1.7, P = 0.001; sleepiness: −0.7 ± 0.91 vs. −1.9 ± 1.6, P = 0.014). Heat loss responses and other perceptions were similar between the two conditions throughout (all P ≥ 0.054). We show that carbonated water ingestion temporarily ameliorates hypotension and increases the cerebral blood flow index during the early post‐exercise phase in a hot environment, whereas it enhances mouth exhilaration and reduces sleepiness during the late post‐exercise phase. What is the central question of this study?Post‐exercise hypotension can cause syncope, and an established practical countermeasure to mitigate this response is currently lacking: does ingestion of carbonated water restore post‐exercise hypotension and positively modulate mood states?What is the main finding and its importance?Carbonated water ingestion transiently increased blood pressure and cerebral blood flow index post‐exercise in the heat. Additionally, carbonated water ingestion increased exhilaration for the mouth and decreased sleepiness post‐exercise. Thus, carbonated water ingestion may mitigate post‐exercise hypotension, increase cerebral perfusion and improve mood states. [ABSTRACT FROM AUTHOR]

Seasonal heat acclimatization is known to enhance autonomic thermoeffector responses, whereas the behavioural response following seasonal heat acclimatization remains unknown. We investigated whether seasonal heat acclimatization would alter autonomic and behavioural thermoregulatory responses. Sixteen healthy participants (eight males and eight females) underwent two trials involving 50 min of lower‐leg passive heating (lower‐leg submersion in 42°C water) with (Fan trial) and without (No fan trial) the voluntary use of a fan in a moderate thermal environment (27°C, 50% relative humidity) across winter and summer months. In Fan trials, participants were allowed to use a fan to maintain thermal comfort, but this was not allowed in the No fan trials. Cool‐seeking behaviour was initiated at a lower change in rectal temperature [mean (SD): 0.21 (0.18)°C vs. 0.11 (0.13)°C, P = 0.0327] and change in mean skin temperature [2.34 (0.56)°C vs. 1.81 (0.32)°C, P < 0.0001], and cooling time was longer [16.46 (5.62) vs. 20.40 (4.87) min, P = 0.0224] in summer compared with winter. However, thermal perception was not modified by season during lower‐leg passive heating (all P > 0.0864). Furthermore, rectal temperature was higher in summer (P = 0.0433), whereas mean body temperature and skin temperature were not different (all P > 0.0631) between the two seasons in Fan trials. In conclusion, seasonal heat acclimatization enhanced the cool‐seeking behaviour from winter to summer. [ABSTRACT FROM AUTHOR]

Dietary nitrate (NO 3 - ) supplementation can offer health benefit and improve exercise performance by increasing nitric oxide (NO) through NO 3 - -nitrite (NO 2 - )-NO pathway. Individuals may benefit from dietary NO 3 - supplementation by monitoring blood [NO 3 - ] and [NO 2 - ], although a simple and practical method for assessing blood [NO 3 - ] and [NO 2 - ] has not been established. We examined whether fingertip serum samples could substitute for venous plasma samples in assessing [NO 3 - ] and [NO 2 - ]. Ten young adults consumed 140 mL of nitrate-rich beetroot juice. Fingertip serum and venous plasma samples were collected at baseline and every hour for up to 4 h after ingestion. [NO 3 - ] and [NO 2 - ] were similar between samples at baseline, whereas they were higher in fingertip serum throughout the post-ingestion periods. Significant correlations existed between fingertip serum vs. venous plasma for both [NO 3 - ] and [NO 2 - ] throughout post-drink periods, except [NO 3 - ] assessed at 2 and 4 h after ingestion of beetroot juice. We show that although fingertip serum [NO 3 - ] and [NO 2 - ] overestimate those measured by venous plasma after dietary NO 3 - intake (125-141% and 156-183% of venous values), [NO 3 - ] and [NO 2 - ] in fingertip serum samples may be utilized for assessing blood [NO 3 - ] and [NO 2 - ] levels, although [NO 3 - ] assessment may lack precision compared to [NO 2 - ].