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Overconsumption of fluids by athletes

BMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7407.113 (Published 17 July 2003) Cite this as: BMJ 2003;327:113

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Evidence base for fluid overload causing hyponatraemia

Dr Shephard's understanding of basic electrolyte and fluid balance
during exercise appears to be in error. Almost all the body's sodium is
distributed essentially in the extracellular fluid (ECF) volume which has
a volume of approximately 17 litres and not in the total body water of
approximately 40 litres. Thus it takes a relatively small increase in the
volume of ECF to drop the serum sodium concentration as we have repeatedly
stressed (1). For example without any sodium loss at all, an increase in
the ECF volume from 17 to 19.5 litres will drop the serum sodium
concentration to 125mmol per litre, sufficient to cause significant mental
impairment and perhaps coma in some athletes. This theoretical
calculation fits exactly the findings in our clinical studies (2) as noted
by Dr Shephard.

I am not certain why Dr Shephard believes that I have stated that a
female marathon runners needs to gain 12-15kg to become significantly
hyponatraemic; this is clearly not in line with either our clinical
findings (2)or our theoretical calculations (1). That a self-reported
fluid intake of 15 litres has been described in one female marathon runner
in the United States is correct (3) but Dr Shephard incorrectly credits me
with that finding. This lady's post-race serum sodium concentration was
however 118mmol per litre (3). This suggests that her ECF volume
increased by about 3.7 litres. Given that the ECF volume is about 42% of
the total body water, this would represent a body weight increase during
the race of approximately 8.8 kg, not the 12-15kg that his calculations
require. Presumably if this athlete did indeed ingest 15 litres she also
lost a substantial amount (3-5 litres) of fluid in urine and sweat during
the marathon. Such a loss is not inconceivable during 5 hours of exercise.

We have indeed measured increases in body weight of up to 6kg (2) in
South African ultramarathon runners; that these increases are not greater
is because, unlike the situation in the United States, South African
runners have never been encouraged to "drink as much as tolerable" during
exercise. If they had, the probability is that hundreds if not thousands
of runners in our very popular 90km Comrades ultramarathon, which annually
attracts 10 000 or more runners, would have succumbed to this condition.
Instead we have had relatively few such cases (2).

Perhaps Dr Shephard's more subtle point is that the injudicious use
of intravenous fluids might very rapidly turn a moderate case of exercise-
related hyponatraemia into a potentially fatal condition. Indeed I have
often wondered how fatalities occur in this condition since the assumption
would seem to be that a self-inflicted condition should begin to reverse
itself immediately the athlete falls unconscious and is unable to continue
the causative mechanism - overdrinking.

That there have been no fatalities from this condition in South
Africa may indeed result from our absolute rule that collapsed athletes
may not receive intravenous fluids unless their is an evidence-based
reason for such treatment.

1. Noakes TD. Hyponatremia in distance runners: Fluid and sodium
balance during exercise. Curr Sports Med Rep 2002; 4: 197-207.

2. Irving RA, Noakes TD, Buck R, van Zyl Smit R, Raine E, Godlonton J, et
al. Evaluation of renal function and fluid homeostasis during recovery
from exercise induced hyponatremia. J Appl Physiol 1991; 70: 342-348.

3. Hew TD, Chorley JN, Cianca JC, Divine JG. The incidence, risk factors
and clinical manifestations of hyponatremia in marathon runners. Clin J
Sports Med 2003; 13: 41-47.

Competing interests:  
Receives research funding from Bromor Foods, manufacturer of sports drinks in South Africa

Competing interests: No competing interests

19 August 2003
Timothy D Noakes
Professor
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University of Cape Town, Cape Town, South Africa, 7700