29 research outputs found

    The effects of high-intensity intermittent exercise compared with continuous exercise on voluntary water ingestion

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    Water intake occurs following a period of high intensity intermittent exercise (HIIE) due to sensations of thirst yet this does not always appear to be caused by body water losses. Thus, the aim was to assess voluntary water intake following HIIE. Ten healthy males (22±2y, 75.6±6.9kg, V˙O2peak 57.3±11.4ml.kg-1.min-1) (mean±SD) completed two trials (7-14d apart). Subjects sat for 30min then completed an exercise period involving 2min of rest followed by 1min at 100%V˙O2peak repeated for 60min (HIIE) or 60min continuously at 33%V˙O2peak (LO). Subjects then sat for 60min and were allowed ad libitum water intake. Body mass was measured at start and end of trials. Serum osmolality, blood lactate and sodium concentrations, sensations of thirst and mouth dryness were measured at baseline, post-exercise and after 5, 15, 30 and 60min of recovery. Vasopressin concentration was measured at baseline, post-exercise, 5 and 30min. Body mass loss over the whole trial was similar (HIIE: 0.77±0.50; LO: 0.85±0.55%) (p=0.124). Sweat lost during exercise (0.78±0.22 v 0.66±0.26 l) and voluntary water intake during recovery (0.416±0.299 v 0.294±0.295 l) (p<0.05) were greater in HIIE. Serum osmolality (297±3 v 288±4mOsmol.kg-1), blood lactate (8.5±2.7 v 0.7±0.4mmol.l-1), serum sodium (146±1 v 143±1mmol.l-1) and vasopressin (9.91±3.36 v 4.43±0.86pg.ml-1) concentrations were higher after HIIE (p<0.05) and thirst (84±7 v 60±21) and mouth dryness (87±7 v 64±23) also tended to be higher (p=0.060). Greater voluntary water intake after HIIE was mainly caused by increased sweat loss and the consequences of increased serum osmolality mainly resulting from higher blood lactate concentrations

    Voluntary water intake during and following moderate exercise in the cold

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    Exercising in cold environments results in water losses, yet examination of resultant voluntary water intake has focussed on warm conditions. The purpose of the study was to assess voluntary water intake during and following exercise in a cold compared to a warm environment. Ten healthy males (22±2 years, 67.8±7.0 kg, 1.77±0.06 m, V˙O2peak 60.5±8.9 ml.kg-1.min-1) completed two trials (7-8d). In each trial subjects sat for 30 minutes before cycling at 70% V˙O2peak (162±27W) for 60 minutes in 25.0±0.1°C, 50.8±1.5% relative humidity (RH) (warm) or 0.4±1.0°C, 68.8±7.5% RH (cold). Subjects then sat for 120 minutes at 22.2±1.2°C, 50.5±8.0% RH. Ad libitum drinking was allowed during the exercise and recovery periods. Urine volume, body mass, serum osmolality and sensations of thirst were measured at baseline, post-exercise and after 60 and 120 minutes of the recovery period. Sweat loss was greater in the warm trial (0.96±0.18 l v 0.48±0.15 l) (p0.05). Ad libitum water intake adjusted so that similar body mass losses occurred in both trials. In the cold there appeared to a blunted thirst response

    Assessing hydration status and reported beverage intake in the workplace

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    The aim was to examine the hydration status of adults working in different jobs at the beginning and end of a shift and their reported water intake. One hundred and fifty-six subjects (89 males, 67 females) were recruited from workplaces within the local area (students, teachers, security, office, firefighters, catering). A urine sample was obtained at the start and end of the shift and was analyzed for osmolality (Uosm), specific gravity (USG), and sodium and potassium concentrations. Euhydration was considered Uosm <700 mOsmol/kg or USG <1.020. At the end of the shift, subjects were asked to report all water intake from beverages during the shift. Females had lower Uosm than males at the start (656 [range, 85-970] vs 738 [range, 164-1090] mOsmol/kg) and end (461 [range, 105-1014] vs 642 [range, 130-1056] mOsmol/kg; P <.05) of their working day. Fifty-two percent of individuals who appeared hypohydrated at the start of the shift were also hypohydrated at the end. Reported water intake from beverages was greater in males compared with females (1.2 [range, 0.0-3.3] vs 0.7 [range, 0.0-2.0] L, respectively; P <.0001). In conclusion, a large proportion of subjects exhibited urine values indicating hypohydration, and many remained in a state of hypohydration at the end of the shift

    Serum sodium changes in marathon participants who use NSAIDs

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    Introduction. The primary mechanism through which the development of Exercise-Associated Hyponatremia (EAH) occurs is excessive fluid intake. However, many internal and external factors have a role in the maintenance of total body water and Non-Steroidal Anti-Inflammatory medications (NSAID) have been implicated as a risk factor for the development of EAH. This study aimed to compare serum sodium concentrations ([Na]) in participants taking an NSAID before or during a marathon (NSAID group) and those not taking an NSAID (control group). Methods. Participants in a large city marathon were recruited during race registration to participate in this study. Blood samples and body mass measurements took place on the morning of the marathon and immediately post- marathon. Blood was analysed for [Na]. Data collected via questionnaires included athlete demographics, NSAID use and estimated fluid intake. Results. We obtained a full data set for 28 participants. Of these 28 participants, 16 took an NSAID on the day of the marathon. The average serum [Na] decreased by 2.1mmol/L in the NSAID group, whilst it increased by 2.3mmol/L in the control group NSAID group (p=0.0039). Estimated fluid intake was inversely correlated with both post-marathon serum [Na] and ∆ serum [Na] (r=-0.532, p=0.004 and r=-0.405 p=0.032, respectively). Conclusion. Serum [Na] levels in participants who used an NSAID decreased over the course of the marathon whilst it increased in those who did not use an NSAID. Excessive fluid intake during a marathon was associated with a lower post-marathon serum [Na]

    Electrolyte supplementation during severe energy restriction increases exercise capacity in the heat

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    PURPOSE. This study examined the effects of sodium chloride and potassium chloride supplementation during 48-h severe energy restriction on exercise capacity in the heat. METHODS. Nine males completed three 48-h trials: adequate energy intake (100 % requirement), adequate electrolyte intake (CON); restricted energy intake (33 % requirement), adequate electrolyte intake (ER-E); and restricted energy intake (33 % requirement), restricted electrolyte intake (ER-P). At 48 h, cycling exercise capacity at 60 % V˙V˙O2 peak was determined in the heat (35.2 °C; 61.5 % relative humidity). RESULTS. Body mass loss during the 48 h was greater during ER-P [2.16 (0.36) kg] than ER-E [1.43 (0.47) kg; P < 0.01] and CON [0.39 (0.68) kg; P < 0.001], as well as greater during ER-E than CON (P < 0.01). Plasma volume decreased during ER-P (P < 0.001), but not ER-E or CON. Exercise capacity was greater during CON [73.6 (13.5) min] and ER-E [67.0 (17.2) min] than ER-P [56.5 (13.1) min; P < 0.01], but was not different between CON and ER-E (P = 0.237). Heart rate during exercise was lower during CON and ER-E than ER-P (P < 0.05). CONCLUSIONS. These results demonstrate that supplementation of sodium chloride and potassium chloride during energy restriction attenuated the reduction in exercise capacity that occurred with energy restriction alone. Supplementation maintained plasma volume at pre-trial levels and consequently prevented the increased heart rate observed with energy restriction alone. These results suggest that water and electrolyte imbalances associated with dietary energy and electrolyte restriction might contribute to reduced exercise capacity in the heat

    Thirst responses following high intensity intermittent exercise when access to ad libitum water intake was permitted, not permitted or delayed

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    An increase in subjective feelings of thirst and ad libitum drinking caused by an increase in serum osmolality have been observed following high intensity intermittent exercise (HIIE) compared to continuous exercise. The increase in serum osmolality is closely linked to the rise in blood lactate and serum sodium concentrations. However, during an ensuing recovery period after HIIE when serum osmolality will decrease, the resultant effect on sensations of thirst and subsequent water intake is unclear. Therefore the aim of the study was to assess the sensations of thirst and subsequent effect on ad libitum water consumption when water intake was immediately allowed, delayed or prevented following a period of HIIE.Twelve males (26 ± 4 years, 80.1 ± 9.3 kg, 1.81 ± 0.05 m, V̇O2peak 60.1 ± 8.9 ml.kg(-1).min(-1)) participated in three randomised trials undertaken 7-14 days apart. Participants rested for 30 min then completed a 60 min HIIE exercise period (20 x 1 min at 100% V̇O2peak with 2 min rest) followed by 60 min of recovery, during which ad libitum water intake was provided immediately (W), delayed until the final 30 min (W30) or not permitted (NW). Body mass was measured at the start and end of the trial. Blood lactate and serum sodium concentrations serum osmolality and sensation of thirst were measured at baseline, immediately post-exercise and during the recovery.Body mass loss was different between all trials (W: 0.25 ± 0.45, W30: 0.49 ± 0.37, NW: 1.29 ± 0.37%; p0.05). Serum osmolality (299 ± 6 v 298 ± 5 vs. 298 ± 3 mOsmol.kg(-1)), blood lactate (7.1 ± 1.1 vs. 7.2 ± 1.1 v 7.1 ± 1.2 mmol.l(-1)) and serum sodium concentrations (142 ± 2 vs. 145 ± 2 v 145 ± 2 mmol.l(-1)) peaked post-exercise (W vs. W30 vs. NW; p0.05).Sensations of thirst were increased following HIIE and remained until satiated by water intake. This was despite the likely primary stimulus, serum osmolality, decreasing during the recovery period following a post-exercise peak. A combined effect of reduction in blood lactate and serum sodium concentrations, restoration of plasma volume and water intake contributed to the similar decrease in serum osmolality observed throughout the trials

    Does hypohydration really impair endurance performance? Methodological considerations for interpreting hydration research

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    The impact of alterations in hydration status on human physiology and performance responses during exercise is one of the oldest research topics in sport and exercise nutrition. This body of work has mainly focussed on the impact of reduced body water stores (i.e. hypohydration) on these outcomes, on the whole demonstrating that hypohydration impairs endurance performance, likely via detrimental effects on a number of physiological functions. However, an important consideration, that has received little attention, is the methods that have traditionally been used to investigate how hypohydration affects exercise outcomes, as those used may confound the results of many studies. There are two main methodological limitations in much of the published literature that perhaps make the results of studies investigating performance outcomes difficult to interpret. First, subjects involved in studies are generally not blinded to the intervention taking place (i.e. they know what their hydration status is), which may introduce expectancy effects. Second, most of the methods used to induce hypohydration are both uncomfortable and unfamiliar to the subjects, meaning that alterations in performance may be caused by this discomfort, rather than hypohydration per se. This review discusses these methodological considerations and provides an overview of the small body of recent work that has attempted to correct some of these methodological issues. On balance, these recent blinded hydration studies suggest hypohydration equivalent to 2–3% body mass decreases endurance cycling performance in the heat, at least when no/little fluid is ingested

    Blinded and unblinded hypohydration similarly impair cycling time trial performance in the heat in trained cyclists

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    Knowledge of hydration status may contribute to hypohydration-induced exercise performance decrements, therefore, this study compared blinded and unblinded hypohydration on cycling performance. Fourteen trained, non-heat acclimated cyclists (age 25 ± 5 y; V̇O2peak 63.3 ± 4.7 mL∙kg-1∙min-1; cycling experience 6 ± 3 y) were pair-matched to blinded (B) or unblinded (UB) groups. After familiarisation, subjects completed euhydrated (B-EUH; UB-EUH) and hypohydrated (B-HYP; UB-HYP) trials in the heat (31˚C); 120 min cycling preload (50% Wpeak) and a time trial (~15 min). During the preload of all trials, 0.2 mL water∙kg body mass-1 was ingested every 10 min, with additional water provided during EUH trials to match sweat losses. To blind the B group, a nasogastric tube was inserted in both trials and used to provide water in B-EUH. The preload induced similar ( P=0.895) changes in body mass between groups (B-EUH -0.6 ± 0.5%; B-HYP -3.0 ± 0.5%; UB-EUH -0.5 ± 0.3%; UB-HYP -3.0 ± 0.3%). All variables responded similarly between B and UB groups ( P≥0.558), except thirst ( P=0.004). Changes typical of hypohydration (increased heart rate, RPE, gastrointestinal temperature, serum osmolality and thirst, decreased plasma volume; P≤0.017) were apparent in HYP by 120 min. Time trial performance was similar between groups ( P=0.710) and slower ( P≤0.013) with HYP for B (B-EUH 903 ± 89 s; B-HYP 1008 ± 121 s; -11.4%) and UB (UB-EUH 874 ± 108 s; UB-HYP 967 ± 170 s; -10.1%). Hypohydration of ~3% body mass impairs time trial performance in the heat, regardless of knowledge of hydration status

    Hypohydration impairs endurance performance: a blinded study

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    The general scientific consensus is that starting exercise with hypohydration >2% body mass impairs endurance performance/capacity, but most previous studies might be confounded by a lack of subject blinding. This study examined the effect of hypohydration in a single blind manner using combined oral and intragastric rehydration to manipulate hydration status. After familiarization, seven active males (mean ±SD: age 25± 2 years, height 1.79±0.07, body mass 78.6±6.2, VO2peak 48 ±7 mL.kg.min -1) completed two randomized trials at 34°C. Trials involved an intermittent exercise preload (8x15 min exercise/5 min rest), followed by a 15-min all-out performance test on a cycle ergometer. During the preload, water was ingested orally every 10 min (0.2 mL.kg body mass -1). Additional water was infused into the stomach via a gastric feeding tube to replace sweat loss (EU) or induce hypohydration of ~2.5% body mass (HYP). Blood samples were drawn and thirst sensation rated before, during, and after exercise. Body mass loss during the preload was greater (2.4 ±0.2% vs. 0.1± 0.1%; P < 0.001), while work completed during the performance test was lower (152± 24 kJ vs. 165 ±22 kJ; P < 0.05) during HYP. At the end of the preload, heart rate, RPE, serum osmolality, and thirst were greater and plasma volume lower during HYP (P < 0.05). These results provide novel data demonstrating that exercise performance in the heat is impaired by hypohydration, even when subjects are blinded to the intervention

    Addition of sodium alginate and pectin to a carbohydrate-electrolyte solution does not influence substrate oxidation, gastrointestinal comfort, or cycling performance

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    Eight well-trained cyclists ingested 68 g·h-1 of a carbohydrate-electrolyte solution with sodium alginate and pectin (CHO-ALG) or a taste and carbohydrate-type matched carbohydrate-electrolyte solution (CHO) during 120 min cycling at 55% Wmax followed by a ~20 min time trial. V̇O2, V̇CO2 blood glucose concentration, substrate oxidation, gastrointestinal symptoms and time trial performance (CHO-ALG: 1219 ± 84 s, CHO: 1267 ± 102 s; P = 0.185) were not different between trials. Novelty bullet: • Inclusion of sodium alginate and pectin in a carbohydrate drink does not influence blood glucose, substrate oxidation, gastrointestinal comfort or performance in cyclists
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