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Sodium and Bone Health

In 2004, the U.S. National Academy of Sciences Food and Nutrition Board established the adequate intake (AI) standard for sodium at 1500 mg per day.  Even this level may be much higher than what is actually necessary as experts in evolutionary nutrition report that sodium intake was historically in the range of only 500 mg per day (Eaton, Frassetto).  Presently, the average American consumes significantly more as survey data indicate typical intakes are in the order of 2-3 times this amount.  Hammer Nutrition’s Dr. Bill Misner, PhD has reported that endurance athletes ingest as much as 6000-8000 mg per day by.  While excessive sodium intake is most commonly associated with elevated blood pressure it is also directly correlated with urinary calcium excretion and bone loss.  Therefore, conscientious use of sodium may represent a lifestyle modification that endurance athletes can control that may reduce the likelihood of both hypertension and osteoporosis. 


In 1937 Aub et al. reported that sodium chloride, the most common form of dietary sodium, increased urine calcium excretion and approximately 20 years later Walser showed that sodium and calcium competed for the same resorption mechanism in the renal tubule of the kidney.  This competition between the two ions means that an increase in the filtered load of either sodium or calcium leads to increased excretion of the other or both.  The role for sodium intake in the development of osteoporosis was first reported by Goulding who showed that sodium intake could affect bone mass in both human and animals.  Additionally, several groups of researchers have demonstrated that bone remodeling, as measured by biochemical markers of bone cell activity, is inversely correlated with sodium intake (McParland, Need, Lin) and when sodium intake is reduced, markers of resorption are decreased.  The principle human study linking high sodium consumption to bone loss was by Devine and Colleagues who reported that change in bone mineral density of the total hip and an ankle location was inversely related to sodium intake.


Sodium is abundant in the human body as an average adult contains 90-130 grams of sodium.  Approximately half of this amount is located in bone while the largest remaining fraction resides in the extracellular fluid where it is involved in the regulation of a variety of metabolic and physiologic processes.  Specifically, sodium is known to be critically involved in the regulation of blood volume, the conduction of action potentials in nervous tissues, as well as the contraction of cardiac and skeletal muscle.  The body regulates sodium balance through a negative feedback loop that involves the hormone aldosterone which is produced and secreted by the adrenal cortex.  Aldosterone release is increased in response to low sodium levels.  Aldosterone’s target tissue is the renal tubule of the kidneys where its presence causes sodium to be re-absorbed back into the body’s circulatory system rather than be excreted in urine.  When sodium levels are elevated, such as during or following a salt loading regime, aldosterone levels are reduced which allows more sodium to pass through the kidneys and be excreted in urine. 


An athlete’s individual sodium requirement (and thus intake) is unique and dependent upon a variety of factors including habitual intake, fitness, and environmental acclimatization.  In general, as an athlete consumes less salt, becomes fit, and trains in the heat, the body’s sodium conservation mechanisms improve and thus sodium requirements are decreased. Research reports that well conditioned athletes that are acclimated to the heat require only 50% of the sodium required to maintain serum sodium levels as do less well prepared subjects.  As such, physiological studies have reported that sodium losses during exercise are highly variable among individuals but may range between 500-2000 mg per hour.


Defining the actual number of athletes that suffer from performance limiting hyponatremia is difficult to determine.  However, a large field study performed by Speedy and Colleagues (1999) may provide some general perspective.  In this study, 58/330 triathletes (18%) were classified as being hyponatremic following a race based upon a plasma sodium concentration of <135mmol/L.  Eleven of these athletes (11/58) had sodium concentrations <130 mmol/L and were classified as being severely hyponatremic.  Interestingly enough, only seven of these athletes were symptomatic.  The researchers noted that the subjects with the most severe cases of hyponatremia had less change in body weight during the race implying that fluid overload was the cause of the hyponatremia rather than excessive sodium loss with dehydration.  Consistent with these findings, Noakes (2002) suggests that most cases of hyponatremia are observed in the less well trained participants who take considerably longer to finish than do the top finishers.  The longer duration of exercise combined with fluid ingestion in excess of sweat loss puts these persons at greater risk of developing hyponatremia because of a dilution effect.


Dr. Bill Misner, PhD describes the characteristics of endurance athletes reporting symptoms of severe sodium imbalance following an endurance event:

  • Consumed a diet >6000 mg sodium per day

  • Consumed >30 ounces of fluid per hour

  • Consumed >300 calories per hour

  • Did not train in the same heat or humidity as the event

  • Did not train >60% of the event distance in hyperthermic conditions   


Dr. Tim Noakes, MD generously provided his perspective on the Slowtwitch forum:

“Over a 21 year period I completed more than 70 marathon and ultra-marathon running races and a host of other standard triathlons and cycling races.  I did not ever finish a face feeling thirsty.  When I performed less well than I expected, the diagnosis was never very difficult.  Since I always drank the same amounts, changes in my drinking behaviors could not have been the cause for either my better or worse performances.  Rather the obvious cause was my preparation; when I performed well my preparation had always been ideal.  I often wonder if, when we perform poorly, we look for an easy scapegoat.  So, for example, we explain our underperformance on the basis that we must have drunk too little water or salt or whatever.  How possible could our preparation have been at fault?  This inability to be self-critical provides fertile soil for exploitation by commercial forces.”


Dr. Noakes continues by answering the following posted question: 

Is salt intake necessary during prolonged exercise like the Ironman?

“The short answer is that no one has yet provided good evidence that salt intake beyond the homeopathic amounts present in sports drinks is necessary to sustain performance during something like the Ironman.  This does not mean that the case is conclusively proven; just that there is no definitive support for this practice at present.  Interestingly our and other’s data suggests that the body probably has a reserve of sodium stored in an unionized form, perhaps in bone or skin, that can be activated in the short term should a deficit in the blood sodium content develop.  However, this is still a controversial issue. 


But more to the point is the absolutely clear evidence that subjects who drink to thirst will maintain or increase their serum sodium concentrations whether or not they ingest salt during exercise.  Only in those who drink in excess of thirst and who either maintain or increase their weight during exercise is there some evidence that the extent to which the blood sodium concentration falls will be reduced (but not prevented) by the ingestion of sodium during exercise.  (This fall can be prevented by drinking less).  Of course this finding has been seized upon by the sports drink industry as absolute evidence that sodium ingestion is essential during exercise.  What they failed to say is that if athletes just drank less during exercise (i.e. to thirst), they would not need to ingest salt in order to maintain their blood sodium concentrations.  This we have known since blood sodium concentrations were first measured in runners in the 1960’s.”


In a very interesting study published in the Medicine & Science in Sports & Exercise Journal (Bar, 1991) eight subjects (five males, three females) participated in three 6-hour exercise trials on a cycle ergometer at 55% O2 max.  Room temperature was 30 degrees C and relative humidity was 50%.  In two trials, the subjects were provided with either water (W) or saline (S) in amounts sufficient to balance sweat and urinary fluid losses, while the third trial, no fluid (NF) was provided.  Plasma sodium < 130 mmol was the predetermined criterion for trial termination.  In the NF trial, heart rate, rectal temperature, plasma sodium, plasma aldosterone, and rating of perceived exertion were all significantly higher (P<0.001) than during W or S, whereas plasma volume was lower.  On average, subjects terminated this trial 1.5 h prior to its scheduled completion, having lost 6.4% body weight.  In contrast, no significant differences between fluid replacement with W or S were detected.  Saline intake was not associated with significantly higher plasma sodium during exercise than was water intake:  plasma sodium decrease significantly during both trials (W=135.5 mmol, S=137.3 mmol).  No subject had to terminate exercise based on plasma sodium < 130 mmol.  The authors conclude by reiterating the importance of adequate fluid intake and suggest that the need for sodium replacement would not be necessary for exercise durations of < 6 hours at similar intensity levels.   


Certainly hyponatremia may be a performance limiting problem for some endurance athletes and sports medicine professionals must be watchful for individuals that demonstrate signs and symptoms of altered electrolyte status during training or racing.  For competitions that last longer than four to six hours, hyponatremia related to excessive sodium loss may be a larger concern.  Athletes of different age, gender, body size/composition, heredity, and level of fitness, create circumstances that do not fit into a one size fits all approach for sodium recommendations.  As such, the following guidelines should be considered with respect to sodium:


  • Sodium requirements are unique to an individual athlete

  • As an athlete’s level of preparedness (fitness and heat tolerance) improves, sodium losses in sweat are reduced and need for intake during races is reduced

  • Reduction in daily habitual salt intake may improve physiologic mechanisms to conserve sodium during exercise

  • Athletes should avoid drinking fluids in excess of sweat rates; especially fluids that contain little or no sodium

  • Consider your level of preparedness, heat adaptation, and pacing strategies more important than supplemental sodium concerns with respect to race performances


Because there appears to be no performance benefits by consuming dietary sodium in amounts above current recommendations, and perhaps a risk of losing bone mass, consider the following suggestions:

  • Avoid adding salt to meals

  • Eliminate most boxed or prepared foods

  • Attempt to purchase canned foods that contain no added salt

  • Drain or rinse canned foods that do contain added salt


Suggested Reading List:
Aub J, Tibbets D, McLean R (1937) The influence of parathyroid hormone, urea, sodium chloride, fat and of intestinal activity upon calcium balance.  J Nutr 113:635-655.


Bar S, Costil D, Fink W (1991) Fluid replacement during prolonged exercise:  effects of water, saline, or no fluid.  Med Sci Sport Exerc 23(7):811-817.


Burtis W, Gay L, Insogna K, Ellison A, Broadus A (1994) Dietary hypercalciuria in patients with calcium oxalate kidney stones.  Am J Clin Nutr 60:424-429.  


Cappuccio F, Meilahn E, Zmuda J, Cauley J (1999) High blood pressure and bone mineral loss in elderly white women:  a prospective study.  Study of Osteoporotic Fractures Research Group.  Lancet 354:971-975.


Devine A, Criddle R, Dick I, Kerr D, Prince R (1995) A longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal women.  Am J Clin Nutr 62:740-745.


Eaton S, Konner M (1985) Paleolithic nutrition.  A consideration of its nature and current implications.  N Engl J Med 312:283-289.


Frassetto L, Morris R, Sellmeyer D, Todd K, Sebastian A (2001) Diet, evolution, and aging.  Eur J Nutr 40:200-213.


Food and Nutrition Board, Institute of Medicine of the National Academy of Sciences (2004) Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate.  Washington, DC:  National Academies Press.


Goulding A (1980) Effects of dietary NaCl supplements on parathyroid function, bone turnover and bone composition in rats taking restricted amounts of calcium.  Miner Electrolyte Metab 4:203-208.


Goulding A, Lim P (1983) Effects of varying dietary salt intake on the fasting excretion of sodium, calcium, and hydroxyproline in young women.  NZ Med J 96:853-854. 

Goulding A (1990) Osteoporosis:  why consuming less sodium chloride helps to conserve bone.  NZ Med J 18:120-122.

Heaney R (2006) Role of Dietary Sodium in Osteoporosis J Am Col Nutr 25:271S-276S.

Kirby C, Convertino V (1986) Plasma aldosterone and sweat sodium concentration after exercise and heat acclimation.  J Appl Phys 61:967-970.

Lin P, Ginty F, Appel L, Aickin M, Bohannon A, Garnero P, Barclay D, Svetkey L (2003) The DASH diet and sodium reduction improve markers of bone turnover and calcium metabolism in adults.  J Nutr 133:3130-3136.

McParland B, Goulding A, Campbell A (1989) Dietary salt affects biochemical markers of resorption and formation of bone in elderly women.  BMJ 299:834-835.

Misner B (2010) Does A High Sodium Diet Inhibit Endurance Performance and Health? (

Noakes T (2002) Hyponatremia in distance runners:  fluid and sodium balance during exercise.  Curr Sports Med Rep 1:197-207.

Oliver W, Cohen E, Neel J (1975) Blood pressure, sodium intake, and sodium related hormones, a “no-salt” culture.  Circulation 52:146-151.

Shepherd R, Kavanaugh T (1978) Fluid and Mineral Needs of Middle Aged and Post Coronary Distance Runners.  Phys and Sports Med.  May:90-102.

Speedy D, Noakes T, Rogers I, et al. (1999).  Hyponatremia in ultradistance athletes.  Med Sci Sports Exerc 31:809-815.

Verde T, et al. (1982) Sweat Composition in Exercise and Heat.  J Appl Phys 53(6):1541-1543.

Walser M (1961) Calcium clearance as a function of sodium clearance in the dog.  Am J Physiol 200:769-773.

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