by Jeff Rocco MD

If you are reading this you are probably an endurance athlete looking to improve your training and performance.  You may recall from high school science class that electrolytes are dissolved mineral salts contained in our body fluid–both inside and outside our cells.  It is not our focus here to review in depth all of the cellular biology related to electrolyte homeostasis.  The enlightened athlete needs to know where electrolytes go when they are lost, what the symptoms are when electrolytes are deficient, and how to maintain electrolyte levels to achieve optimum performance.  The five key electrolytes for endurance athletes are Sodium (Na+), Potassium (K+), Chloride (Cl-), Calcium (Ca++), and Magnesium (Mg++)

In our bodies, hydration is linked intimately with electrolyte concentrations.  For athletes, electrolyte losses occur primarily through sweating.  Early experience with endurance athletes recognized dehydration as a significant problem.  Fluid losses as little as 1-2% of body weight can cause a drop in performance, while losses exceeding 4% of body weight can cause critical failure.  Realizing this, athletes drank.  Things got worse for those athletes when they drank primarily or exclusively water.  Consuming water without electrolytes replaces fluid losses, but dilutes electrolytes. In Ironman medical tents, electrolyte deficiencies are now found more commonly than dehydration.  Hydration before and during longer events should contain electrolytes.

Sodium (Na+) and Chloride (Cl-)

Sodium is the most abundant and perhaps the most important of the electrolytes.  Na+ is found in higher concentrations outside of cells in our bodies.  All cells depend on sodium and potassium to bring nutrients inside the cell and to remove waste.  Nerve conduction–a process important for thinking and for activation of muscles—is also heavily dependent on sodium and potassium.    Sodium Chloride (NaCl) is table salt and often referred to simply as “salt.”  Many foods contain sodium. Deficiency of sodium is called hyponatremia.  Hyponatremia is the most common electrolyte disorder in the U.S.  Hyponatremia in athletes is usually due to sodium lost in sweat.  Other disease processes may cause hyponatremia, but the symptoms of hyponatremia are the same for athletes and non-athletes.  These include fatigue, muscle weakness, muscle spasms or cramps, convulsions, nausea, vomiting, confusion, or decreased consciousness.  Vomiting due hyponatremia can cause Na+ levels to drop even further.

A good discussion of sodium and possible benefits of sodium loading can be found here http://team.firstendurance.com/page/sodium-loading-2

Chloride is a negatively charged ion which binds readily to Sodium and Potassium.  When sodium or potassium is consumed chloride is usually present.  Don’t look for supplements containing only chloride- they don’t exist!

Potassium (K+)

Potassium is the primary electrolyte found inside of cells.  It works closely with Sodium and Chloride in maintaining fluid balance, cellular homeostasis, and conducting nerve impulses.  K+ is lost from contracting muscles with consumption of muscle glycogen during exercise.  K+ is then further excreted in urine or sweat.  Low potassium is called hypokalemia.  Symptoms of hypokalemia may be similar hyponatremia and include muscle fatigue, weakness, drowsiness, confusion, or irregular heartbeat.

Calcium (Ca++)

Many people think of bones when they think of calcium. Bones are the largest reservoir of Ca++ in the body. However, soluble calcium in body fluid is also necessary for neuromuscular conduction, muscular contraction, inter- and intracellular messaging, and plays a key regulatory role in glycogen metabolism.  Significant quantities of Ca++ can be lost in sweat.  Studies in college basketball players have found decreased bone mineral densities and stress fractures to correlate with calcium losses in sweat.  Treatment with a Ca++ rich sports drink and supplements lead to increased bone densities (Klesges 1996).  While chronic calcium deficiency may lead to depletion of bone mineral density, acute symptoms of hypocalcemia during exercise may manifest as muscle spasms or cramps, intestinal distress, confusion, tingling in fingers and toes.

Magnesium (Mg+)

Magnesium is perhaps the most underappreciated electrolyte. Because many athletes recognize the importance of sodium and potassium supplementation, low Mg+ is often the reason for sub-optimal performance. Mg+ is important for proper transmission of nerve impulses, muscular contraction, and energy production associated with ATP.  More than 300 enzymatic reactions in your body depend on magnesium as a co-factor.  Magnesium can have direct effects on sodium, potassium, and calcium channels located in cell walls.  Longer and more intense exercise depletes magnesium levels.  Mg+ is excreted in sweat and urine.  Symptoms of magnesium depletion include weakness, muscle cramps, confusion and irregular heartbeat.

The Bottom Line __________________________________________________

Weakness, confusion, muscle cramps and nausea do not make for a good day on the racecourse.  By now you may begin to recognize a theme:  depletion of any of these five essential electrolytes may result in similar symptoms.  It may be difficult to identify an isolated electrolyte deficiency without a laboratory analysis.  All five of these electrolytes are lost in sweat and can be depleted with exercise.  Endurance athletes need all five electrolytes before, during and after exercise.  Nutrition strategies that ignore some of these electrolytes will fail in more extreme circumstances.  Hotter temperatures, longer or more intense exercise results in greater electrolyte losses, which need to be replaced to train and race effectively.

Next month we will look at recommendations for energy and electrolyte beverages, including recommended quantities of electrolytes.

Changes in bone mineral content in male athletes. Mechanisms of action and intervention effects.

Klesges RC, Ward KD, Shelton ML, Applegate WB, Cantler ED, Palmieri GM, Harmon K, Davis J.

JAMA. 1996 Jul 17;276(3):226-30. Erratum in: JAMA 1997 Jan 1;277(1):24.