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Exercise-associated hyponatremia
Other namesEAH

Exercise-associated hyponatremia (EAH) is a fluid-electrolyte disorder caused by a decrease in sodium levels (hyponatremia) during or up to 24 hours after prolonged physical activity.[1] This disorder can develop when marathon runners or endurance event athletes drink more fluid, usually water or sports drinks, than their kidneys can excrete.[2] This excess water can severely dilute the level of sodium in the blood needed for organs, especially the brain, to function properly.[2]

The incidence of EAH in athletes has increased in recent years, especially in the United States, as marathon races and endurance events have become more popular.[3] A recent study showed 13% of the Boston 2002 marathon runners experienced EAH; most cases were mild.[2] Eight deaths from EAH have been documented since 1985.[2]

Symptoms[edit]

Symptoms may be absent or mild for the early onset of EAH and can include impaired exercise performance, nausea, vomiting, headache, bloating, and swelling of hands, legs, and feet.[4] As water retention increases, weight gain may also occur.[1] More severe symptoms include pulmonary edema and hyponatremic encephalopathy.[5] Symptoms of hyponatremic encephalopathy are associated with an altered level of consciousness and can include sullenness, sleepiness, withdrawing from social interaction, photophobia, and seizures.[4]

Causes[edit]

The primary causes of EAH include excessive fluid retention during exercise with a significant sodium deficit and excessive fluid intake leading to an increase in total body water resulting in a reduction in blood sodium levels.[6]

Athlete-specific risk factors are being of female sex, use of non-steroidal anti-inflammatory drugs [NSAIDs], slow running, excessive fluid ingestion, low body weight, and event inexperience.[1] Event-specific risk factors are high availability of drinking fluids, duration of exercise exceeding four hours, unusually hot environmental conditions, and extreme cold temperature.[1]

Mechanism[edit]

Sodium is an important electrolyte needed for maintaining blood pressure.[7] Sodium is mainly found in the body fluids that surround the cells and is necessary for nerves, muscles, and other body tissues to function properly.[7]

Many factors may contribute to the development of EAH. Under normal conditions, sodium and water levels are regulated by the renal and hormonal systems.[3] The decrease in sodium levels can occur due to a defect in the renal and hormonal systems, an overwhelming increase in water consumption and excessive loss of sodium through sweating.[3] When the sodium levels outside of the cells decrease, water moves into the cells.[7] The cells begin to increase in size. When several cells in one area begin to increase in size, swelling occurs in the affected area. Swelling is commonly observed in hands, legs, and feet.[4]

Sodium is also important in regulating the amount of water that passes through the blood–brain barrier. Decreased sodium blood levels result in increased permeability of water across the blood–brain barrier.[8] This increased influx of water causes brain swelling which leads to severe neurological symptoms.[8]

Epidemiology[edit]

A 2012 study revealed that 26% of the athletes competing in the Triple Iron ultra-triathlon developed EAH.[9] A similar study measured the prevalence of EAH in open-water ultra-endurance swimmers and found 8% of males and 36% of females developed EAH.[10]

Diagnosis[edit]

EAH is categorized by having a blood serum or plasma sodium level below normal, which is less than 135 mmol/L.[1] Asymptomatic EAH is not normally detected unless the athlete has had a sodium blood serum or plasma test.[1] Hyponatremic encephalopathy may be detected using brain imaging studies and pulmonary edema may be confirmed by x-ray.

Prevention[edit]

Traditional prevention of EAH focuses on reducing fluid consumption to avoid fluid retention before, during, and after exercise.[1]

However, since this can risk dehydration, an alternative approach is possible of consuming a substantial amount of salt prior to exercise.[11] It is still important not to overconsume water to the extent of requiring urination, because urination would cause the extra salt to be excreted.[1]

Role of thirst[edit]

In a published statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, researchers concluded that drinking in accordance with the sensation of thirst is sufficient for preventing both dehydration and hyponatremia.[2] This advice is contradicted by the American College of Sports Medicine, which has previously recommended athletes drink "as much as tolerable."[12][13] In October 2015, ACSM President W. Larry Kenney stated that “[T]he clear and important health message should be that thirst alone is not the best indicator of dehydration or the body’s fluid needs.”[14]

In a letter to the editors of The Journal of Wilderness and Environmental Medicine, Brad L. Bennett, PhD claimed "perpetuation of the myth that one needs to drink beyond the dictates of thirst can be deadly."[15] Similarly, authors of the Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference claim this advice has "facilitated inadvertent overdrinking and pathological dilutional EAH."[2]

Critics of the ACSM's view have questioned their motives, pointing out that Gatorade is one of the organizations "platinum sponsors."[16][17][18]

Treatment[edit]

Treatments are focused on the underlying cause of hyponatremia and include fluid restriction and saline. When EAH is treated early, complete recovery is expected.[5]

Data from one study suggests that immediate administration of 100 mL intravenous bolus of 3% hypertonic saline was more effective at normalizing blood sodium levels than oral administration for asymptomatic EAH.[19]

Athletes experiencing EAH encephalopathy may also receive high-flow oxygen and a rapid infusion of 100 mL of 3% NaCl to reduce brain edema.[1]

References[edit]

  1. ^ a b c d e f g h i Hew-Butler, Tamara; Ayus, J Carlos; Kipps, Courtney; Maughan, Ronald J; Mettler, Samuel; Meeuwisse, Willem H; Page, Anthony J; Reid, Stephen A; Rehrer, Nancy J; Roberts, William O; Rogers, Ian R; Rosner, Mitchell H; Siegel, Arthur J; Speedy, Dale B; Stuempfle, Kristin J; Verbalis, Joseph G; Weschler, Louise B; Wharam, Paul (2008). "Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007" (PDF). Clinical Journal of Sport Medicine. 18 (2): 111–21. doi:10.1097/JSM.0b013e318168ff31. PMID 18332684. S2CID 205731476.
  2. ^ a b c d e f Hew-Butler, Tamara; Rosner, Mitchell H.; Fowkes-Godek, Sandra; Dugas, Jonathan P.; Hoffman, Martin D.; Lewis, Douglas P.; Maughan, Ronald J.; Miller, Kevin C.; Montain, Scott J.; Rehrer, Nancy J.; Roberts, William O.; Rogers, Ian R.; Siegel, Arthur J.; Stuempfle, Kristin J.; Winger, James M.; Verbalis, Joseph G. (2015). "Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015". Clinical Journal of Sport Medicine. 25 (4): 303–20. doi:10.1097/JSM.0000000000000221. PMID 26102445. S2CID 1943832.
  3. ^ a b c Rosner, Mitchell H.; Bennett, Brad; Hew-Butler, Tamara; Hoffman, Martin D. (2013). "Exercise-Associated Hyponatremia". In Simon, Eric E. (ed.). Hyponatremia. pp. 175–92. doi:10.1007/978-1-4614-6645-1_10. ISBN 978-1-4614-6645-1. S2CID 202569531.
  4. ^ a b c Noakes, T. Waterlogged: The Serious Problem of Overhydration in Endurance Sports. Human Kinetics, 2012.
  5. ^ a b Goudie, AM; Tunstall-Pedoe, DS; Kerins, M; Terris, J (2006). "Exercise-associated hyponatraemia after a marathon: case series". Journal of the Royal Society of Medicine. 99 (7): 363–67. doi:10.1177/014107680609900720. PMC 1484555. PMID 16816267.
  6. ^ Noakes, T. D.; et al. (2005). "Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances". Proceedings of the National Academy of Sciences of the United States of America. 102 (51): 18550–18555. Bibcode:2005PNAS..10218550N. doi:10.1073/pnas.0509096102. PMC 1311740. PMID 16344476.
  7. ^ a b c MedlinePlus Encyclopedia: Hyponatremia
  8. ^ a b Murray, B., Stofan, J., and Eichner, R. "SSE #88: Hyponatremia in Athletes." Gatorade Sports Science Institute. (2003).
  9. ^ Rüst, Christoph Alexander (2012). "Higher Prevalence of Exercise-Associated Hyponatremia in Triple Iron Ultra-Triathletes Than Reported for Ironman Triathletes". The Chinese Journal of Physiology. 55 (3): 147–55. CiteSeerX 10.1.1.453.798. doi:10.4077/CJP.2012.BAA010. PMID 22784278.
  10. ^ Wagner, Sandra; Knechtle, Beat; Knechtle, Patrizia; Rüst, Christoph Alexander; Rosemann, Thomas (2012). "Higher prevalence of exercise-associated hyponatremia in female than in male open-water ultra-endurance swimmers: the 'Marathon-Swim' in Lake Zurich". European Journal of Applied Physiology. 112 (3): 1095–106. doi:10.1007/s00421-011-2070-5. PMID 21748367. S2CID 15950689.
  11. ^ DiNicolantonio, James (2017). The Salt Fix: Why the Experts Got it All Wrong and How Eating More Might Save Your Life. Little, Brown Book Group. ISBN 978-0349417387.
  12. ^ Convertino, V. A.; Armstrong, L. E.; Coyle, E. F.; Mack, G. W.; Sawka, M. N.; Senay, L. C.; Sherman, W. M. (1996-01-01). "American College of Sports Medicine position stand. Exercise and fluid replacement". Medicine and Science in Sports and Exercise. 28 (1): i–vii. doi:10.1097/00005768-199610000-00045. ISSN 0195-9131. PMID 9303999.
  13. ^ Noakes, T. D. (2007-05-01). "Drinking guidelines for exercise: what evidence is there that athletes should drink "as much as tolerable", "to replace the weight lost during exercise" or "ad libitum"?". Journal of Sports Sciences. 25 (7): 781–96. doi:10.1080/02640410600875036. ISSN 0264-0414. PMID 17454546. S2CID 21582407.
  14. ^ "Do You Know When and How Much To Drink for Exercise?". About.com Health. Archived from the original on 2016-01-06. Retrieved 2016-01-15.
  15. ^ Bennett, Brad L.; Hew-Butler, Tamara; Hoffman, Martin D.; Rogers, Ian R.; Rosner, Mitchell H. (2014). "Reply to: Is drinking to thirst a prudent guideline to avoid hyponatremia?". Wilderness & Environmental Medicine. 25 (4): 493–494. doi:10.1016/j.wem.2014.09.035. PMID 25498754. Retrieved 2016-01-13.
  16. ^ Noakes, Timothy David; Speedy, Dale B (2007-02-01). "Lobbyists for the sports drink industry: an example of the rise of "contrarianism" in modern scientific debate". British Journal of Sports Medicine. 41 (2): 107–09. ISSN 0306-3674. PMC 2658915.
  17. ^ "The ACSM Let Gatorade Distort Science". THE RUSSELLS. 2014-02-20. Retrieved 2016-01-13.
  18. ^ "Exposing the truth about sports drinks". MinnPost. 2012-07-24. Retrieved 2016-01-13.
  19. ^ Rogers, Ian R; Hook, Ginger; Stuempfle, Kristin J; Hoffman, Martin D; Hew-Butler, Tamara (2011). "An Intervention Study of Oral Versus Intravenous Hypertonic Saline Administration in Ultramarathon Runners With Exercise-Associated Hyponatremia: A Preliminary Randomized Trial". Clinical Journal of Sport Medicine. 21 (3): 200–3. doi:10.1097/JSM.0b013e31821a6450. PMID 21519296. S2CID 32466825.
source: https://en.wikipedia.org/wiki/Exercise-associated_hyponatremia

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