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Hydration, Sports and Training

Dehydration Impairs Physical Performance

Dehydration is not simply an issue for the sick and elderly.  Athletes who are dehydrated are well-known to suffer from impaired performances, which has resulted in the development of guidelines for fluid replacement in physically demanding sports professions.1

The physiologic mechanisms by which dehydration impairs athletic performance are complex, involving different levels of exercise intensity, cardiovascular strain, heat strain, altered metabolic function, and altered neurologic function.  Exercise-induced dehydration and hyperthermia decreases the plasma volume due to fluid shifts and subsequent reductions in myocardial stroke volume.2  This decreased stroke volume is accompanied by an accelerated heart rate. The degree of dehydration has been shown to be closely correlated with these physiological changes.3

Consequences of a Closed Circulatory System

The human circulatory system behaves as a closed fluid system where the viscosity or thickness of the blood circulating directly influences the mechanical and physical demands of the heart and vessels.  When fluid shifts occur during acute exercise, a process called hemoconcentration occurs, increasing hematocrit and concentrating the plasma, both of which contribute to a reversible elevation in blood viscosity.

A clinical study of 20 healthy adults showed an increase of blood viscosity after just 15 minutes of submaximal exercise, with the most significant changes occurring at the lowest shear rates.4 When blood becomes thicker and stickier, peripheral vascular resistance increases, causing the heart to work harder to provide the same level of perfusion.

Endurance Training Reduces Blood Viscosity

The human body is able to adapt to exercise-induced hemoconcentration as with most homeostatic shifts. Endurance-trained athletes mitigate hemoconcentration by increasing their plasma volumes which reduces resting hematocrit.  This is an important change that takes place in all highly trained athletes.  Such people have been shown to have lower baseline resting blood viscosity levels.5

The adaptations seen with endurance training enable the athlete to respond to hyperthermic states and respond to dehydration more effectively.  Clinical evidence shows that overall fitness is associated with a lower blood viscosity and lower hematocrit state rather than a more viscous state rich with red blood cells.5

Overtraining reverses these benefits.  In a study of 47 healthy endurance-trained and untrained females, all 47 women experienced a 12.6% elevation in whole blood viscosity after 1 hour of maximal intensity exercise.6  The elevation in viscosity was greater than what could be attributed to hematocrit, which increased on average by 8.9%.  There was no apparent adaptive advantage in endurance-trained females, which was likely due to the intensity of the exercise regimen used in this study and overtraining.6  The bottom line is that, regardless of the type of training program that an athlete uses, it is hemodynamically beneficial to avoid overtraining.

The Hematocrit Paradox

Despite the commonly held belief in the athletic community that more red blood cells equal better fitness, clinical evidence suggests the opposite is true.  Greater number of red blood cells (or hematocrit) makes blood thicker and more viscous.  Thicker blood cannot deliver oxygen as effectively or efficiently as thinner, free-flowing blood, especially in the capillaries at the tissue and organ level.  While a healthy individual's endothelium can adapt to surges in blood viscosity through the release of the vasodilator nitric oxide, those with stiff vessels or underlying vascular disease may not.

Exercise Induced Dehydration Increases Blood Viscosity

Dehydration is a direct contributor to exercise-induced changes in blood viscosity.  A clinical study of 10 healthy adults who performed two endurance training exercises--the first which did not allow drinking and the second which allowed rehydration with a hypo-osmolar beverage of equal volume to the amount of sweat lost in the first exercise--showed blood viscosity increased significantly only after exercise without rehydration.7 The researchers attributed this increase to hemoconcentration which was attenuated after oral rehydration.

A crossover study of 12 healthy men who, prior to 4 hours of sitting in a dry environment, were either hydrated with an electrolyte-glucose beverage, water, or no pre-hydration, showed a time-dependent and graded increase in blood viscosity.8  After the 4 hours, mean systolic blood viscosity increased by 9.3% and mean diastolic blood viscosity increased by 12.5% in the control group who did not receive pre-hydration.  Pre-hydration with water or the carbohydrate-electrolyte beverage was reported to attenuate blood viscosity surges caused by dehydration.

Blood Doping in Cyclists

Surges in blood viscosity and overall cardiovascular risk may be substantially exacerbated in blood doping athletes, notably cyclists.  Recombinant erythropoietin (EPO) has been used by athletes to gain competitive advantage since the late 1980s.  EPO, a drug indicated for various types of anemia, stimulates the body to produce red blood cells and therefore boost oxygen-carrying capacity.  

Rapid elevation of hematocrit and subsequent thickening of the blood may have contributed to the sudden death of five Dutch cyclists in 1987, the year which EPO was released in Europe.9  Eighteen other cyclists met a similar fate, dying from stroke, pulmonary embolism, or myocardial infarction between 1997 and 2000.9  Combine that hematocrit with high blood pressure, and the study found a nine fold increase in overall stroke risk.  Dehydration is yet another important factor that contributes to a state of hyperviscosity.

Blood viscosity increases exponentially as a result of hematocrit increases.  Some blood doping cyclists in the 1990s and 2000s had blood thick and sticky enough to cause them to collapse prior to races, according to 2011 featured news article published in Nature.10  It was not uncommon for cyclists to show up to races with hematocrits exceeding 60%.

One study of 7,735 men aged 40-59 showed a significantly elevated risk of stroke (relative risk = 2.5) in men with hematocrit greater than 51%, even after adjusting for other stroke risk factors.11  As demonstrated by the hematocrit paradox, those who dope with EPO may experience immediate gains in athletic performance but are placing a potentially catastrophic burden on the cardiovascular system.  In those without anemia and those with underlying cardiovascular insufficiencies, EPO can induce polycythemia and hyperviscosity syndrome, increasing the risk for venous thromboembolism.12

The late Allan J. Erslev, M.D., the pioneering Jefferson hematologist who discovered erythropoietin while he was a member of the Yale faculty, spoke strongly of the benefits of EPO for anemic patients.  He was concerned, however, with athletes using EPO for doping purposes, stating:  "It seems likely that an erythropoietin-induced rise in the hematocrit, aggravated by the dehydration that occurs during exhausting performances, would increase blood viscosity and be not only detrimental to muscular action but also the cause of possible life-threatening thromboses."13


1.  Sawka MN, Burke LM, Eichner ER, Maughan RJ, Montain SJ, Stachenfeld NS. American College of Sports Medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc. 2007;39(2):377.

2.  Coyle E. Cardiovascular drift during prolonged exercise and the effects of dehydration. Int J Sports Med. 2007;19(S 2):S121-S124.

3.  Montain SJ, Coyle EF. Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise. J Appl Physiol. 1992;73(4):1340-1350.

4.  Nageswari K, Banerjee R, Gupte RV, Puniyani RR. Effects of exercise on rheological and microcirculatory parameters. Clin Hemorheol Microcirc. 2000;23(2-4):243-247.

5.  Brun JF, Varlet-Marie E, Connes P, Aloulou I. Hemorheological alterations related to training and overtraining. Biorheology. Jan 1 2010;47(2):95-115.

6.  Martin DG, Ferguson EW, Wigutoff S, Gawne T, Schoomaker EB. Blood viscosity responses to maximal exercise in endurance-trained and sedentary female subjects. J Appl Physiol. Aug 1985;59(2):348-353.

7.  Vandewalle H, Lacombe C, Lelievre J, Poirot C. Blood viscosity after a 1-h submaximal exercise with and without drinking. Int J Sports Med. 2008;9(02):104-107.

8.  Doi T, Sakurai M, Hamada K, et al. Plasma volume and blood viscosity during 4 h sitting in a dry environment: effect of prehydration. Aviat Space Environ Med. Jun 2004;75(6):500-504.

9.  Tokish JM, Kocher MS, Hawkins RJ. Ergogenic aids: a review of basic science, performance, side effects, and status in sports. Am J Sports Med. 2004;32(6):1543-1553.

10.  Callaway E. Sports doping: Racing just to keep up. Nature. Jul 21 2011;475(7356):283-285.

11.  Wannamethee G, Perry I, Shaper A. Haematocrit, hypertension and risk of stroke. J Intern Med. 1994;235(2):163-168.

12.  Lippi G, Franchini M, Favaloro EJ. Thrombotic complications of erythropoiesis-stimulating agents. Semin Thromb Hemost. Jul 2010;36(5):537-549.

13.  Erslev AJ. Erythropoietin. N Engl J Med. 1991;324(19):1339-1344.


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