- Jun 15, 2001
- 2,552
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I want to revisit this since recent consensus recommendations have been made by nephrologists other than myself, in case some of you think I'm a quack. We've talked briefly about this before, and I'm sure most were left without a clear answer as to how much water you should drink when working out or riding. This time, I'm going to copy and paste from my CD "Up To Date", which I get every 6 months to update me on topics from Cardiology to Heme-Onc. This is an unbiased, fair presentation of information and I trust it very much. This information confirms what I've said before.
But to preceed it, I thought you might like to know that a well known water company sponsored a marathon in San Diego about the time I was there and passed out free water. About 30 runners ended up in UCSD's ER with severe hyponatremia, several of them seizing, etc. Death is not all that rare in these scenarios. Hyponatremia is a low serum sodium concentration caused to an excess accumulation of water.
I also want to warn you of an article that was in RacerX or on their website written by an exercise 'gooroo' that has no scientific, analytical, clinical or otherwise training in human health concepts and specifically salt and water balance. The guy ought to be shot for the s**t he's spewing from his polluted traphole. And yes, I'd LOVE to debate the guy in any public forum, anywhere.
Here it is. Remember, this isn't coming from the quack. It's just the same thing I was saying before.
Exercise-induced hyponatremia — Ultramarathon and marathon runners may replace their dilute, but sodium-containing sweat losses with excessive amounts of hypotonic solutions, with the net effect being a reduction in the plasma sodium concentration [3-6]. A similar sequence can occur during military operations and desert hikes. Such individuals may also be taking NSAIDs, which can impair the excretion of free water [4]. (see "NSAIDs: Electrolyte complications", section on hyponatremia).
Excessive hypotonic fluid intake may have a greater role than sodium loss and increased ADH levels, mimicking some of the findings of primary polydipsia [5-8]. In a prospective study of 488 runners who completed the Boston marathon (approximately 42.2 kilometers), 13 and 0.6 percent had post-race plasma sodium concentrations of 135 meq/L and 120 meq/L, respectively [5]. The most important factors underlying hyponatremia were increased weight gain and race time. Of those who gained 2.0 to 2.9 kg and over 3 kg, approximately 10 and 30 percent had plasma sodium concentration 130 meq/L. Those patients with a race time greater than four hours had an odds ratio of 7.4 for hyponatremia compared to those with a race time below 3.5 hours. Theoretically, those who take longer to complete a run have a longer time to ingest hypotonic fluid [5].
In contrast, a similar study of New Zealand marathon runners reported no cases of hyponatremia [6]. As observed with the Boston marathon study, plasma sodium concentrations were directly related to changes in weight. Possible reasons for the difference in prevalence of hyponatremia in the two studies is that aggressive hydration was not promoted in New Zealand, and hydration stations were significantly fewer (one every 5 versus 1.6 km).
We can make the following general recommendations for preventing hyponatremia related to prolonged exertion: Avoid fixed, global recommendations for water intake, since there are varying rates of water and sodium loss with different body types, training regimens and climates. Athletes should rely on thirst as their guide for fluid replacement. Athletes should monitor weight before and after training sessions as a guide to appropriate fluid consumption, with the goal to avoid weight gain. Medical personnel should avoid hypotonic intravenous solutions in individuals with exertion-related collapse, especially if the serum sodium concentration is not known.
In 2005, a consensus conference published guidelines concerning the evaluation and management of exercise-induced hyponatremia [8]. The following recommendations were made: Onsite analysis of serum or plasma sodium should be performed at medical facilities at endurance events. if the medical staff is experienced in treating hyponatremia in the field, any patient with exercise-induced hyponatremia and respiratory insufficiency, confusion, obtundation, nausea, and vomiting can be administered 100 mL of 3 percent sodium chloride over ten minutes. This maneuver should raise the plasma sodium concentration an average of 2 to 3 meq/L and should not pose a substantial danger.
This initial strategy is intended to stabilize the athlete prior to transfer to the hospital. Further treatment of symptomatic patients is the same as for any cause of symptomatic hyponatremia [8]. (See "Treatment of hyponatremia").
But to preceed it, I thought you might like to know that a well known water company sponsored a marathon in San Diego about the time I was there and passed out free water. About 30 runners ended up in UCSD's ER with severe hyponatremia, several of them seizing, etc. Death is not all that rare in these scenarios. Hyponatremia is a low serum sodium concentration caused to an excess accumulation of water.
I also want to warn you of an article that was in RacerX or on their website written by an exercise 'gooroo' that has no scientific, analytical, clinical or otherwise training in human health concepts and specifically salt and water balance. The guy ought to be shot for the s**t he's spewing from his polluted traphole. And yes, I'd LOVE to debate the guy in any public forum, anywhere.
Here it is. Remember, this isn't coming from the quack. It's just the same thing I was saying before.
Exercise-induced hyponatremia — Ultramarathon and marathon runners may replace their dilute, but sodium-containing sweat losses with excessive amounts of hypotonic solutions, with the net effect being a reduction in the plasma sodium concentration [3-6]. A similar sequence can occur during military operations and desert hikes. Such individuals may also be taking NSAIDs, which can impair the excretion of free water [4]. (see "NSAIDs: Electrolyte complications", section on hyponatremia).
Excessive hypotonic fluid intake may have a greater role than sodium loss and increased ADH levels, mimicking some of the findings of primary polydipsia [5-8]. In a prospective study of 488 runners who completed the Boston marathon (approximately 42.2 kilometers), 13 and 0.6 percent had post-race plasma sodium concentrations of 135 meq/L and 120 meq/L, respectively [5]. The most important factors underlying hyponatremia were increased weight gain and race time. Of those who gained 2.0 to 2.9 kg and over 3 kg, approximately 10 and 30 percent had plasma sodium concentration 130 meq/L. Those patients with a race time greater than four hours had an odds ratio of 7.4 for hyponatremia compared to those with a race time below 3.5 hours. Theoretically, those who take longer to complete a run have a longer time to ingest hypotonic fluid [5].
In contrast, a similar study of New Zealand marathon runners reported no cases of hyponatremia [6]. As observed with the Boston marathon study, plasma sodium concentrations were directly related to changes in weight. Possible reasons for the difference in prevalence of hyponatremia in the two studies is that aggressive hydration was not promoted in New Zealand, and hydration stations were significantly fewer (one every 5 versus 1.6 km).
We can make the following general recommendations for preventing hyponatremia related to prolonged exertion: Avoid fixed, global recommendations for water intake, since there are varying rates of water and sodium loss with different body types, training regimens and climates. Athletes should rely on thirst as their guide for fluid replacement. Athletes should monitor weight before and after training sessions as a guide to appropriate fluid consumption, with the goal to avoid weight gain. Medical personnel should avoid hypotonic intravenous solutions in individuals with exertion-related collapse, especially if the serum sodium concentration is not known.
In 2005, a consensus conference published guidelines concerning the evaluation and management of exercise-induced hyponatremia [8]. The following recommendations were made: Onsite analysis of serum or plasma sodium should be performed at medical facilities at endurance events. if the medical staff is experienced in treating hyponatremia in the field, any patient with exercise-induced hyponatremia and respiratory insufficiency, confusion, obtundation, nausea, and vomiting can be administered 100 mL of 3 percent sodium chloride over ten minutes. This maneuver should raise the plasma sodium concentration an average of 2 to 3 meq/L and should not pose a substantial danger.
This initial strategy is intended to stabilize the athlete prior to transfer to the hospital. Further treatment of symptomatic patients is the same as for any cause of symptomatic hyponatremia [8]. (See "Treatment of hyponatremia").
