Hydration and Exercise: Hypohydration and Exercise-Induced Hyponatremia

Changes in cell hydration are critically important for the signaling towards metabolic responses to hormones, substrates and reactive oxygen intermediates (1).

Hypohydration and exercise

Hypohydration during exercise strongly rises the catabolic hormonal response to resistance exercise, and increase circulating concentrations of metabolic substrates. Hydration status during exercise changes the endocrine and metabolic adaptive responses to resistance exercise and also changes the postexercise internal environment. Specifically, there’s increase in cortisol, epinephrine, and norepinephrine (2).

Hypohydration stimulates the catabolic hormones by increasing core temperature (3,4) and increases cardiovascular demand due to decreased plasma volume (5,6,7).

A 3% to 4% loss of body weight (water) reduces strength by about 2% and power by about 3% (8).

Competitive athletes competing in multi-day, ultraendurance events have been observed with over 2.5% body mass loss per stage of road race (60). Likewise, industrial workers are not only subject to dehydration on the job, but could also start the workday with a fluid deficit (61).

As noted before, a decrease in cell volume caused by hypohydration promotes insulin resistance (1,9,10).

Resistance exercise might exacerbate the effects of hypohydration on insulin resistance, because muscle damage is also related with insulin resistance (11,12,13,14).   

There’s decreased GLUT-4 protein content (15,16), and impaired insulin signal transduction at the level of IRS-1, PI 3-kinase, and Akt-kinase (12). 

Downhill treadmill running and resistance exercise result in transient insulin resistance (17,18,19), and the reductions in glucose uptake in muscle damage models may be of the order of 20–30% (15,17).


Extreme exercise conditions (equal or above three hours continuously), such as the marathon or triathlon, without the intake of electrolytes increase the risk dehydration or hyponatremia (20). 

Symptomatic hyponatremia is typically observed with greater than 6 hours of prolonged exercise. Acute water toxicity happens due to rapid consumption of large quantities of water that greatly exceeded the kidney’s maximal excretion rate (from 0.7 to 1.0 L/hour) (1).

Severe exercise-associated hyponatremia (EAH) starts as significant mental status changes resulting from cerebral edema, at times associated with noncardiogenic pulmonary edema (19,20). The osmotic imbalance results in fluid movement into the brain, causes swelling, which then leads to disorientation, confusion, general weakness, grand mal seizures, coma, and possibly death (8,21,22,23).

Exercise-associated hyponatremia (EAH) typically occurs during or up to 24 hours after prolonged physical activity, and is defined by a serum or plasma sodium concentration below the normal reference range of 135 mEq/L (24,25).

Usually only less than 1% of marathons athletes present signs of EAH (26,27), however it was as high as 23% in an Ironman Triathlon (28) and 38% in runners participating in a marathon and ultramarathon in Asia (29). There’s also now a trend for symptomatic EAH for shorter distance events, such as a half marathon (30) and sprint triathlon taking approximately 90 minutes to complete (31). There’s also no statistical significance for the incidence of symptomatic between genders (32), though women may be at greater risk than men (32).

The estimated incidence rate for Grand Canyon hikers from May 31 to September 31 in 1993, was 16% with an estimated incidence rate between 2.0 and 4.0 per 100,000 persons (33,34). The US marine corps and army infantry are also experiencing an increase, between 1999 and 2011 the incidence was 12.6 per 100,000 personyears (35), compared to 1.0 to 3.0 per 100,000 personyears between 1997 and 2005 (36); 4 deaths from EAH have been reported (37,38).

We have seen that the major risk factor for developing EAH is excessive water intake beyond the capacity for renal water excretion (1,39,40) largely as a result of persistent secretion of arginine vasopressin (41,42). Elevations in brain natriuretic peptide (NT-BNP) may lead to excessive losses of urine sodium and raise the risk of hyponatremia (43).

Another concern is the inability to mobilize body sodium bound in bone. Sodium can be released from internal stores such as bone (44,45,46), 25% of body sodium is bound in bone (osmotically inactive) and is potentially recruitable. Inability to recruit sodium from that pool may increase the risk of hyponatremia.

Individuals under normal conditions are able to excrete between 500 and 1000 mL/h of water (47), plus the non-renal losses of water as sweat, so athletes should be able to consume as much as 1000 to 1500 ml/h before developing water retention and dilutional hyponatremia, therefore it seems likely that excessive water intake (>1500 mL/h) is the main cause.

The combination of excessive water intake and inappropriate AVP secretion will clearly lead to hyponatremia (24).

Arginine vasopressin (AVP) must be suppressed appropriately with water loading, otherwise the ability to produce dilute urine is markedly impaired (48).

Water can also be absorbed from the gastrointestinal tract at the end of a race causing an acute drop in serum sodium concentration (49), with clinical signs of EAHE after 30 minutes. During exercise, breakdown of glycogen into lactate increases cellular osmolality and rises serum sodium, but some minutes after exercise this is reversed and serum sodium levels drop (50,51). 
The risk also rises if the degree of fluid loss through sweet is sufficient to produce significant volume depletion (stimulating AVP release and impairing urine excretion of water), coupled with ingestion of hypotonic fluids (24).

Although not conclusive, nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated as a risk factor in the development of EAH by potentiating the water retention effects of AVP at the kidney (24).

At least two strategies can be used to present EAH: avoid overdrinking (real time sensation of thirst) and limiting the availability of fluids during events. Supplementation with sodium may delay of even prevent the decline in blood sodium concentration (52,53) however drinking beyond thirst (overdrinking) will not prevent hyponatremia (54), the amount of fluid ingested is more important than the amount of sodium ingested for blood sodium concentrations (55).

EAH has a complex pathogenesis and multifactorial etiology:


An athlete should consume approximately 500 to 600 mL (17 to 20 fl oz) of water 2 to 3 hours before exercise (56). By hydrating several hours prior to the exercise, there is sufficient time for urine output to return toward normal before starting the event (30).

For normal athletic events in moderate temperatures (and altitudes), it should be enough to hydrate slowly over several hours. If the body needs water urgently it can absorb some water right through the walls of the stomach. A 1% to 2% decrease in your body weight (due to water loss) will affect performance.

The threshold for reduced performance appears to be 2% body water loss of total body mass (57,58). Dehydration equivalent to 1.5% to 2% of total body mass may decrease performance up to 15% (59). 

We’ve seen before that 3% to 4% losses impairs muscular strength by 2% and muscular power by 3% (8), and also reduces high-intensity endurance performance (e.g., distance running) by approximately 10% (60). 

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