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• W2963626659 abstract "As modern-day humans, we still bear the genetic heritage of our ancestors who evolved under conditions very different from today and who were selected for a great amount of daily physical exercise.1 We should be aware of this 2-million-year-old heritage2 and include physical exercise in our everyday lives to prevent civilization-induced disorders, as for example metabolic syndrome and cardiovascular diseases,3 and to stay physically and mentally fit.4 Indeed, regular endurance training has many beneficial consequences such as improved cardiovascular function, lower morbidity, and mortality rates and overall improved physical fitness.5-7 Moreover, exercise training may even reverse pathological changes associated with diseases of civilization.3, 8-11 Endurance performance, that is, physical exertion of longer than 5 minutes at around 65%-100% of the maximal oxygen uptake ,12 is mainly because of oxygen availability and its use by skeletal muscle cells to sustain continuous ATP-synthesis through aerobic processes in a steady state. The duration and intensity under which such a performance can be maintained are dependent on genetic potential, age, gender and endurance training status12 and are thus highly individual. Endurance performance depends on the oxygen uptake capacity (environmental pO2, lung's diffusion rate, Haldane-effect),13 the oxygen transport capacity of the blood (haemoglobin concentration, total blood volume), the maximum cardiac output, the ability to release oxygen (oxygen affinity to haemoglobin, Bohr effect), the oxygen usage by the musculature (capillarization, density of mitochondria, oxidative enzymes and mitochondrial electron transport chain),14, 15 and availability of fuels (carbohydrates and lipids), as well as body temperature, neurophysiological factors (muscle-fibre-type recruitment) and psychological aspects (motivation). Therefore, the assessment of represents a standardized test, specific to exercise modality (eg cycling, running, rowing etc), to determine individual aerobic fitness levels. The varies between 30 and 40 mL kg−1 min−1 for healthy untrained adults and up to 90 mL kg−1 min−1 for highly trained endurance athletes.16 Regular endurance training can thus more than double the through changes in its various determinants, but there has been less focus on the fluid shift and its role in the oxygen diffusion rate towards the working muscle. Indeed, anamnestic assessment of the rehydration status in athletes to undergo -measurement frequently yielded: “just one or two cups of coffee.” Thus, the hydration status is often neglected, also from athletes undergoing an exhaustion test. So, why is hydration critical to physical exercise and what occurs during the fluid shift? Physical exercise leads to many physiological short- and long-term changes, among them a fluid shift in plasma volume from intravascular to extravascular space and back again, which is influenced by posture,17 temperature, hydration status, as well as amount and characteristics of physical exertion and recovery. These fluid shifts are based on alterations in the microcirculation and its processes of filtration and absorption, leading to changes in hydrostatic, oncotic and osmotic pressure. The ratio of these pressures in intravasal and extravasal space determines the direction and amount of the net flow.18, 19 In the working muscle, the higher capillary pressure, resulting from increased systolic and mean arterial pressure,18, 19 leads to greater capillary filtration18, 20 with a net outward fluid shift (from intravasal to extravasal compartment). Furthermore, there is a buildup of osmotically active compounds in working muscle such as lactate, potassium ions and phosphate with an increase in extravasal osmolarity,20, 21 thus further increasing outward flow of hypotonic plasma.18, 22 The increased cardiac output during physical exercise also increases capillary permeability for proteins. Since 1 g of protein binds about 15 mL water,23 this protein flow to extravasal space increases oncotic pressure there and fosters the plasmatic filtration and the fluid shift. Thus, because of the increases in hydrostatic pressure as well as the osmotic and oncotic gradients, there is initially a net outward fluid shift. This outward fluid shifts results in haemoconcentration of about 1 g haemoglobin per 100 mL blood,21, 24 which corresponds to an increase in blood oxygen content of about 67 mL for a total blood volume of 5 L. In other words, the haemoconcentration as an effect of the fluid shift leads to an elevation of the oxygen-carrying capacity of the blood by 7%. The initial outward flow of plasma water, in turn, leads to an increased blood osmolarity from 283 to 299 mmol L−1,22 and eventually an increase in intravasal total protein content from 7 g per 100 mL to 8.1 g per 100 mL blood, corresponding to an increase in oncotic pressure from 25 to 31 mm Hg.22 These consequences of the fluid shift cause a self-limitation of plasma loss to a maximum of 18% at a performance rate of 65% .22 Further limitations to the fluid shift are higher lymphatic reflux including proteins from the interstitial reservoir to intravasal space,25 as well a higher hydrostatic pressure within the contracting muscle, eventually resulting in a balance state between outward and inward plasma flow, thus limiting the net fluid shift. Of note, even short-term exercise of 10 minutes at high intensity may cause a sufficient fluid shift into working muscle, which is not more pronounced at longer duration.18, 26 A decrease in 7%-20% in plasma volume corresponds to the amount of shifted volume into the musculature of about 700 mL.20 Apart from hydration status, exercise intensity exerts a great influence,27 as the fluid shift is proportional to the increased metabolic and thermoregulatory demands.23 Following the first two phases of the fluid shift from plasma to the working muscle causing haemoconcentration in the blood and the limitation of the fluid shift, there is the final third phase during the recovery period, which is marked by an increase in plasma volume. This mechanism is triggered by renal functions such as activation of the renin-angiotensin-aldosterone-system (RAAS), antidiuretic hormone (ADH, alias vasopressin) and inactivation of the atrial natriuretic peptide.28 These hormonal adaptations lead to increased water consumption (activation of thirst), decreased urine excretion (20% less within 24 hours) as well as decreased sweat production.23, 25 Renal sodium- and water retention are based on increased aldosterone-receptor-sensitivity leading to a decrease in sodium clearance of 50%.25 Additional de novo synthesis of albumin increases intravasal oncotic pressure, keeping plasma volume in intravasal space.25, 29 Thus, the initial adaptation during recovery is marked by an increase in plasma volume, causing haemodilution.30 Oxygen desaturation during endurance exercise31 as well as the reduced haematocrit through haemodilution during recovery lead to lower oxygen availability in renal cells. This lower oxygen availability activates the transcription rate of erythropoietin through the hypoxia-inducible factor-2 (HIF-2), resulting in higher erythropoiesis. The following increase in haemoglobin concentration leads to a normalization of haematocrit level and reaches the pre-training ratio after about 4 weeks.23 Thus, long-term adaptation to endurance exercise finally leads to an increase in total blood volume of up to 25% with averaged haemoglobin concentration23, 25 that proportionally correlates with an increase in .25 It should be noted that the increase in total blood volume does not increase the blood pressure; to the contrary, since blood pressure decreases as a beneficial effect of endurance training, which can be attributed to increased production of nitric oxide32 and lower activity of the RAAS.33 The improved aerobic capacity, as expressed as is based on higher oxygen content through increased blood volume, as well as higher cardiac output but also to a greater peripheral capacity for oxygen consumption, that is, augmented muscle capillarization and mitochondrial content leading to an increased arteriovenous oxygen difference (a-vO2diff)12; adaptations that take place simultaneously and complement each other. Hypervolaemia, as a result of regular endurance exercise, enhances thermoregulatory capabilities (higher cutaneous blood flow, evaporation rate, and thus increased radiation and convective heat loss). Furthermore, hypervolemia supports cardiovascular function to maintain an increased cardiac output up to the maximum cardiac output, which varies between 20 and 30 L min−1 for well-trained recreational athletes and up to over 35 L min−1 for highly trained endurance athletes.23, 34, 35 This is necessary to support the increased muscular blood flow (up to 80% of the increased cardiac output) to maintain muscular performance as well as the concurrent demand for increased cutaneous blood flow (up to 20%) for thermoregulation.36 In addition, an endurance-trained heart with greater stroke volume can maintain a lower heart rate at any given workload since a lower heart rate corresponds to longer diastolic duration and, thus, promotes a better oxygen supply to cardiac myocytes.23, 25, 31 Interestingly, the exertion of the upper extremities represents a greater stimulus for fluid shift than of the lower extremities. It was shown that arm-exercise intensity at 66% of attained by leg exercise, was sufficient to cause the same haemoconcentration.19, 37 Thermoregulation by heat stress also influences the fluid shift,19, 23, 38 however, physical exercise has a greater impact, especially with respect to long-term consequences. In contrast, the cessation of regular exercise causes a decrease. Ten days of bed rest may reduce blood volume by 10%, stroke volume by 12% and by 6%.23 So why does hydration matter? Physical exercise, especially long-duration endurance training in combination with external heat and humidity, can lead to significant dehydration with hyperosmolar hypovolaemia,39 which in turn increases intravasal osmolarity and oncotic pressure resulting in activation of the RAAS system and ADH.19, 39 Furthermore, hypohydration decreases the fluid shift, as well as sweat production and stroke volume, leading to an increased heart rate and accelerated the rise in body core temperature at any given workload. A lower shift volume, as a result of a greater plasma protein concentration with higher oncotic pressure, keeps the plasma volume within intravascular space and maintains blood pressure, while hyperhydration allows a greater fluid shift capacity even in the presence of cutaneous vasodilation and maintains a lower heart rate through higher stroke volume.18 The initial hydration status and rehydration during exercise can significantly influence these reactions and may counteract the hyperosmolar hypovolaemia—athletes should, therefore, strive to be well hydrated. Taken together, a “Western” sedentary lifestyle with little exercise, may lead to a decreased blood volume involving further risk factors such as increases in cholesterol and sympathetic activation, which are associated with high blood pressure.23 It is therefore recommendable to maintain an active lifestyle with regular physical exercise to benefit from an increased blood volume, known to have consequences for improved health and performance. There are much more reasons for being well hydrated, however, be aware of the fluid shift! The authors declare that there are no conflict of interest. MS, JL and MAM contributed to the manuscript. MF contributed to and confirmed the final draft of the manuscript." @default.
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• W2963626659 title "A fluid shift for endurance exercise—Why hydration matters" @default.
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• W2963626659 cites W2167498879 @default.
• W2963626659 cites W2270359433 @default.
• W2963626659 cites W2314391470 @default.
• W2963626659 cites W2323071171 @default.
• W2963626659 cites W2536411415 @default.
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• W2963626659 cites W2590214643 @default.
• W2963626659 cites W2593494545 @default.
• W2963626659 cites W2600181102 @default.
• W2963626659 cites W2623804275 @default.
• W2963626659 cites W2742015761 @default.
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