Influence Of Water Balance On Human Organism

Water is essential for all life on earth, but too much water for some species can lead to serious health issues. Athletes consume insufficient fluid and electrolytes just before, or during training and competition. Interest in running has been growing over the past few decades, and marathon running is no exception. There are many marathon runners trying to qualify for big marathons, like the Boston Marathon. To compete in this race, runners must meet qualifying time. The race does not merely attract recreational runners but elite runners from all over the world as well. Numerous other marathons have gained the runner’s interest. Furthermore, Nutrition is a very important aspect of marathon running, for performance and safety. One of the many health threats that may arise during a marathon is hyponatremia. This condition is classified as serum sodium levels below 120 mmol/L (Davis et al., 2016). Hyponatremia causes various symptoms, ranging from vomiting, headache, seizures, and death. Studies found that approximately 13% of marathon runners in the 2002 Boston Marathon had hyponatremia (Rasmussen, et al., 2016 ). Factors that increase the possibility of hyponatremia include excess fluid absorption and slow race time. Therefore, hyponatremia may impact many runners who have insufficient experience or training, due to a lack of resources. Another way, runners may have hyponatremia is by profusely sweating. Runners sweat to sustain a low body temperature when running for 4 hours in dry heat, a lack of adverse effects from developing mild-to-moderate fluid deficits. In addition to water loss that accompanies sweating, sodium is lost as well, which leads to the problem of hyponatremia. While many athletes train in arid conditions, they tend to sweat profusely losing water to cool down. This is simply one example of exercise stress, another would be dehydration. Even though too much water absorption can cause serious medical issues, dehydration can too. Dehydration decreases blood volume, leading to a decrease in cardiac filling and output. It can further suppress the body’s cooling mechanisms, resulting in hyperthermia. The risk of these impairments increases in humid temperatures when heat diffusion through sweating is compromised (Rasmussen et al., 2001). On average each day about (2500 mL) of water leaves the human body by various routes; most of this lost water is expelled as urine(Rasmussen et al., 2001). However, our body tries to accompany the water loss, through various mechanisms. For instance, the kidneys also can regulate blood volume through mechanisms that carry water out of the filtrate and urine. It serves by balancing the water level in the body. When dehydrated, the kidney conserves water and makes the urine more dilute to expel excess water, if necessary. Another mechanism to help regulate the water concentration would be through osmoreceptors in the hypothalamus. When losing too much water your body begins to signal receptors to enable you to feel thirsty for rehydration. A nerve cell, known as the osmoreceptor in the hypothalamus of the brain monitors changes in water potential, regulating thirst and secreting ADH.

Osmoreceptor secretion and thirst are located in the anterior of the hypothalamus. They are sensory receptors that control the concentration of osmolality of the blood (Davis et al., 2016). If blood osmolality rises above its ideal content, the hypothalamus transmits signals that result in conscious recognition of thirst. The hypothalamus of a dehydrated individual also releases antidiuretic hormone (ADH) through the posterior pituitary gland. ADH signals the kidneys to retrieve water from urine, effectively decreasing the blood plasma. The antidiuretic hormone aids to manage blood pressure by acting on the kidneys and the blood vessels. Its most critical role is to maintain the fluid volume of the body by reducing the output of water passed out in the urine. It allows water in the urine to travel back to the bloodstream, allowing urine concentration to rise and water loss to reduce. When serum osmolality that increases or decreases causes vasopressin; another name for ADH, to release. The direct effect of an increase in serum osmolality is the stimulation of the Osmoreceptor. Figure 1 illustrates the process of osmoreceptors. This stimulation leads to the dissolution of vasopressin from molecules of neurophysin, to which vasopressin is readily linked within the secretory cells (Davis et al., 2016). Vasopressin is then distributed from the posterior pituitary gland, contributing to the subsequent retention of water by the kidneys.

The kidneys operate to maintain an osmotic balance and blood pressure in the body. Blood flows into the kidney through the renal artery. This large blood vessel branches into smaller blood vessels until the blood reaches the nephrons. In the nephron, your blood is filtered by the blood vessels of the glomeruli and then it flows out of your kidney through the renal vein. The glomeruli which are a bundle of capillary blood vessels found in the kidney senses a drop in blood flow or sodium and secretes an enzyme called renin into the bloodstream. Renin moves to the liver and converts the inactive peptide angiotensinogen to angiotensin I. Then, angiotensin I travel to the lungs where another enzyme converts it to angiotensin II. After, angiotensin II makes its way to the adrenal glands at the top of the kidneys where it stimulates the production of aldosterone.

The hormone aldosterone helps the kidneys conserve sodium and water, leading to increased fluid volume and sodium levels. In comparison to ADH, which promotes the reabsorption of water to sustain appropriate water balance, aldosterone maintains proper water balance by increasing Na+ reabsorption and K+ secretion from the extracellular fluid of the cells in kidney tubules (Becchetti et al., 1995). Aldosterone is formed in the cortex of the adrenal gland and alters the concentrations of minerals Na+ and K+. It also inhibits the loss of Na+ from sweat. The reabsorption of Na+ allows for the osmotic reabsorption of water, which alters blood volume and blood pressure. In addition to the hormone, the kidney has an epithelial sodium ion channel in the epithelial cells of the distal kidney nephron. This channel helps with allowing sodium to move through the channel after an action potential is reached. The action potential is generated by depolarization of the plasma membrane that changes the membrane potential to a less negative value inside. This would open the voltage-gated Na+ channels allowing small amounts of Na+ to enter the cells down its electrochemical gradient. The influx of the positive charge would depolarize the membrane further, opening more Na+ channels, which allows more Na+ ions to enter. It’s known as a positive feedback loop that would move to rest when the membrane potential is -70 mV. Figure 3 illustrates the mechanism of the epithelial sodium ion channel in the kidney.

As mentioned in the introduction, hyponatremia causes a decrease in sodium concentration that leads to sodium in your bloodstream and wrecks the balance, reducing the ability of your kidneys to remove the water. The result is higher blood pressure due to the extra fluid and extra tension on the blood vessels leading to the kidneys. During strenuous exercise, the kidney’s excretion rates are modified. Despite a large amount of plasma lactate during strenuous exercise, renal excretion plays a limited role in lactate metabolism. After conducting experiments on mice, researchers have found that the mechanism of transcellular transport of lactate is concentrated during severe exercise (Juel et al., 1999). Lactate is produced in the cytosol by the fermentative branch of the glycolytic pathway, through the reduction of pyruvate with the concomitant oxidation of NADH to NAD+, a reaction catalyzed by lactate dehydrogenase. Lactate is used as an energy source during vigorous exercise. Aside from lactate, urine concentration plays a role in the body after exercising. Urea reabsorption is enhanced during prolonged exercise, this may limit the dehydration of an individual. Uric acid handling by the kidney is an active area of research (Johnson et al., 2013). However, uric acid is firstly eliminated into the proximal tubule by glomerular filtration or by the active uptake via OAT1 and 3; next, it is eliminated from the proximal cell by the urate channel SLC17A3; then it is reabsorbed from the proximal tubule into the cell by URAT1. The reabsorbed uric acid is returned to the blood via transporter, GLUT9 (Johnson et al., 2013). The excretion of excess protein in the urine after severe exercise appears within 30 minutes after stopping the event (Rasmussen et al., 2002).

The hypothalamus regulates the processes of ADH secretion, either by monitoring blood volume or the absorption of water in the blood. Dehydration can induce an increase of osmolarity above 300 mOsm/L, which in time, raises ADH secretion and water will be absorbed, leading to a rise in blood pressure (Bassett et al., 2010). The antidiuretic hormone travels into the bloodstream to the kidneys. Once at the kidney, ADH alters the kidneys to become more accessible to water. It does that by inserting water channels, aquaporin, into the kidney tubules, temporarily. Water flows out of the kidney tubules through the aquaporin, decreasing urine volume. It’s then reabsorbed into the capillaries, which lowers blood osmolarity back to normal. As blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus, and ADH secretion is weakened (Bassett et al., 2010). Many athletes are susceptible to have severe medical issues that occur if the different body systems are not managed. As mentioned above, excessive amounts of water intake can lead to hyponatremia, because the sodium input is too much, inhibiting the kidneys to filter water. Another example would be hypothermia and dehydration. When athletes work out in arid heat conditions and do not intake the right amount of fluid, their body begins to react harshly. The osmoreceptor is in charge of signaling the hypothalamus to secrete ADH to enable the conscious to feel thirsty and fuel up. This would help many runners stay hydrated during marathons or training.

Our ancestors have evolved hunting in the midday heat on the arid African savannah and generated appropriate biological adaptations that enable prolonged running in the heat ( Bassett et al., 2010). . The fitness of running in mammals and humans are relatively similar. Two of the initial purposes of running may have been to follow wounded prey while hunting and to run from predators. It enables them to capture prey by overpowering them. Humans can run long distances, the reason behind that is sweating. Our sweat allows us to cool down during vigorous exercise, that’s why it allows us to catch prey. Running can be cost-effective because we are losing too much energy, but with the help of sweat, we can re-energize. Indeed, specific features of running like speed as well as endurance were likely imperative for survival. For instance, deers are fast runners; they use their quickness to run away from predators, such as lions and cheetahs. Even though cheetahs are extremely fast, deers small legs and low body mass allows them to overcome the cheetah and escape.

The mammalian kidney is good at what it does, by maintaining equilibrated water and salt balance. In all mammals, Humans can run long distances and regulate their body temperature in the heat, but we don’t know what has been done with the evolutionary biochemistry of the hormones in humans. However, we do know the evolution of sweat and uric acid that helps regulate water concentration in the body. As mentioned before, Uric acid is the end product of purine metabolism in humans due to the lack of uricase. Researchers correlated the loss of uricase activity to the nonsense mutation of codon 33 of exon 2, which dates it to 15 million years ago ( Cade et al., 2005). The promoter region of the gene had perhaps previously been degraded in the evolutionary process by previous mutations, being more prone to a steady loss of uricase activity. Several mutations in the uricase gene occurred during the evolution of hominids as well as in monkeys of the Old and the New World (Cade et al., 2005). These mutations have been portrayed as definite evidence of significant evolutionary advantage for the first primates that had increased uric acid (Cade et al., 2005). Another evolutionary trait would be sweating, which plays a big factor when trying to conserve water concentration. Mammals have two types of sweat glands, the apocrine and eccrine. The former is found over the body surface, are linked with a hair follicle and sebaceous gland, and are not predominantly utilized in thermoregulation, except in some ungulates (Best et al., 2017). In non-primate mammals, eccrine glands are constrained to the friction pads of the hands and feet where they can be high in density and assist in frictional gripping (Adelman et al., 1999). New World monkeys have enhanced this ability to species with a prehensile tail, while in Old World monkeys eccrine glands are shared over the entire body surface and are applied in thermoregulatory sweating. Figure 4 is a phylogenetic tree of the percentage of eccrine sweat glands between species. This portrays that natural selection has favored increased thermoregulatory sweating in some nonhuman primates in hot and arid environments despite the existence of body hair. Therefore, many researchers indicate that this supports the theory that natural selection may have favored initial increases in sweating before the significant body hair reduction that arose in the hominin lineage (Best et al., 2017). Humans evolved as hot-weather runners with limited access to fluid during exercise. Marathon runners are used to running long distances in arid conditions, the only thing helping them continue for a long period is their sweat. Sweat allows the individual to cool down and helps us run long distances.

Athletic capability, effort, and exercise all display a positive impact on neural function. In athletics precisely and life more commonly, striving and succeeding is consistent throughout our lifespan. Thus, athletes, specifically slower marathon runners need only to be encouraged to drink according to the dictates of their thirst during exercise, but not to avoid the thirst. When athletes drink according to thirst, the risk that they will over-drink causing hyponatremia is minimized and there is no evidence that they are at any significant disadvantage from the scant amount of dehydration that develops as a result. There are current studies in discovering the inherited and acquired molecular factors involved in endurance capacity by genome-wide DNA sequencing and analysis of epigenetic modifications. In the future, knowledge of the discrete pathways that support endurance phenotypes may lead to novel interventions that promote optimal health.