Potassium ions are of key importance for health and for athletic performance. The level of potassium in the blood must be regulated within fairly narrow limits: at concentrations above 12 mM there is a very high risk of sudden cardiac arrest*. Steady state levels above 6.5 mM are considered dangerous in clinical practice, while levels below 3.5 mM are associated with slow repolarization of heart muscle and risk of various disturbances of cardiac rhythm, and also with risk of additional serious disorders such as high blood pressure and stroke (reviewed by Sica and colleagues). Low blood levels are also associated with fatigue of skeletal muscles, but so too is the loss of the normal gradient of potassium ions across muscle cell membranes that arises when potassium moves out of muscle cells into the extracelular fluid.
*[As summarised in the discussion with Michael below, the highest published potassium level in a person who subsequently survived is 14 mM (possibly arising from muscle damage sustained during cardiac resuscitation.) However survival after potassium exceeds 10 mM is very rare. ]
Potassium is lost from the body via the kidneys and in sweat. But more important than the maintenance of total body levels is the distribution between the inside of cells and the extra-cellular fluids (including blood plasma). While typical concentration outside of cells is around 4.5 mM, the concentration inside nerve and muscle cells is in the vicinity of 150 mM. About 98% of the body’s potassium is contained within cells. This gradient in ion concentration across the cell membrane is essential for conduction of neural impulses and for muscular contraction. Normal neural conduction and muscle contraction entail flow of potassium though ion channels in the cell membrane, thereby depleting intracellular levels and causing extracellular concentration to rise appreciably. This reduction in the gradient across the membrane contributes to fatigue. Extracellular levels of potassium are regulated by the renin-angiotensin-aldosterone hormonal system, which promotes potassium loss when levels are high. Thus, higher extra-cellular levels promote potassium loss for the body. Molecular pumps that move potassium (K+) ions back into calls in exchange for sodium (Na+ ) ions minimise loss of potassium form cells during exercise and reducing fatigue, but continue to pump after exercise stops, resulting in a net fall of potassium below the pre-exercise levels.
The first concern of the athlete the development of effective Na/K pumping, and the second concern is ensuring that dietary intake is adequate so that total body store is not depleted. In long endurance races and even more catastrophic issue arises: damage to muscle cells during prolonged exercise can release potassium together with protein myoglobin, which damages the kidneys, and can result in potassium rising to dangerous levels. This is one of the causes of the rare sudden deaths that occur in the late stages of a marathon. Thus, it is worthwhile understanding how training can promote effective Na/K pumping and the role of both electrolyte replacement and diet in maintaining the appropriate total body level of potassium.
The role of potassium in skeletal muscle contraction
The contraction of skeletal muscles is elicited by a rapid influx of Na+ and an equivalent efflux of K+ ions across cell membranes. Skeletal muscles contain the largest pool of K+ in the body. During intense exercise, the Na/K-pumps cannot readily return K+ into the muscle cells. Therefore, the working muscles undergo a net loss of K+, while the K+ concentration in the arterial blood plasma can double in less than 1 minute. Even larger increases in K+ in interstitial tissues surrounding the muscle cells. This results in degradation in the electrical potential gradient across membranes, thereby resulting in loss of excitability and force. During continuous stimulation of isolated muscles, there is a strong correlation between the rise in extracellular K+ and the rate of force decline. These events present a major challenge for the Na/K-pumps. Excitation of the muscle itself, together with the stimulating effects of adrenaline and insulin, increases the Na/K-pumping rate. If all available pumps are engaged, the rate of pumping can increase up to 20-fold above the resting transport rate within 10 seconds. Thus in working muscles, the Na/K-pumps play a dynamic regulatory role in the maintenance of excitability and force. Down-regulation of pump capacity reduces contractile endurance in isolated muscles. The Na/K-pump capacity is a limiting factor for contractile force and endurance, especially when their capacity is reduced as a result of de-training.
The pumping capacity of Na/K-pumps is influenced by hormones, such as thyroid hormone, adrenal steroids including cortisol, insulin, and by fasting and potassium-deficiency (as reviewed by Torben Clausen from University of Aarhus in Denmark). Thus, an adequate intake of dietary potassium is important. Good sources are leafy greens, dried apricots, yoghurt, salmon, mushrooms, and bananas. Perhaps even more importantly, physical inactivity degrades pumping capacity while training enhances it. High intensity interval training is especially effective in enhancing Na/K pump capacity. For example, Bangsbo and colleagues form Copenhagen reported that six to twelve 30-s sprint runs 3-4 times/week for 9 weeks produced a 68% increase in Na/K-pump units (p<0,05) and a significant reduction of blood plasma K+ level, compared with observations in a control group who continued with endurance training (approximately 55 km/Km). The intense sprint training was associated with significant improvement in performance. In those doing the intense sprints, 3-km time was reduced by 18 seconds from 10 min 24 sec to 10 min 6sec while 10-km time improved from 37 min18 sec to 36 min18 sec.
The effect of potassium on the heart
Unlike the situation in skeletal muscle, under normal circumstances, in the heart the rise in intracellular Na+ concretion associated with activation of the muscle activate the Na/K pump adequately to completely compensate for the increased K+ release (evidence reviewed by Sejersted). Thus, whereas the K+ shifts during intense exercise can contribute substantially to fatigue in skeletal muscle in the heart, the K(+) balance is normally controlled much more effectively. This might not be the case during abnormal circumstances such as ischemia.
If there is serious elevation of blood levels of potassium due to muscle damage (see the section on rhabdomyolysis below) or due to dietary excess in the presence of a disorder of the renin-angiotension –aldosterone mechanism that normally regulates potassium, there is a risk of serious reduction of the electrical gradient across the heart muscle membrane essential for conduction of the excitation signal thought the heart muscle. The consequence can be cardiac arrest, which is usually fatal.
Conversely, when blood levels of potassium are low, due to serious loss and failure of dietary replacement, the re-establishment of the electrical gradient is slower. This delayed re-polarization is, manifest as an increase in the interval between the Q wave and the T wave in the electro cardiogram. The delayed re-polarization can lead to rhythm disturbances due to alteration of the conduction pathways. The most serious of these is the rare but potentially fatal rhythm disturbance known as Torsade de Pointes. However, because of the normally tight regulation of sodium and potassium ion level by the renin-angiotensin aldosterone system, this is very unlikely in otherwise healthy individuals.
Regulation of potassium levels by the renin-angiotensin-aldosterone system
Renin is an enzyme secreted by the kidneys that acts on a substance called angiotensinogen that is produced in the liver. Renin splits angiotensinogen releasing the peptide angiotensin, which has various actions in the body directed towards retaining sodium, conserving blood volume and maintaining blood pressure. One of the important actions of angiotensin is stimulation of release of the steroid hormone, aldosterone, from the adrenal glands. Aldosterone acts on the kidney to promote retention of sodium and excretion of potassium. During exercise, aldosterone production is increased, thereby decreasing urine production and conserving fluid volume, while promoting excretion of potassium. This helps reduce the accumulation of potassium in blood due to efflux from active skeletal muscle, but contributes to the fall in potassium levels after exercise ceases. Maintenance of blood volume by moderate fluid intake is likely to minimise excessive engagement of the renin-angiotensin-aldosterone system.
On one occasion when I made an overly ambitious attempt to find a novel route across a mountain ridge for my return journey during a long run in the Sierra Nevada in southern Spain on a hot dry day with an inadequate supply of water, I became quite dehydrated. I was somewhat alarmed to experience an increase in ectopic heart beats. I suspect that the dehydration had led to excessive activity of the renin-angiotensin-aldosterone system, depletion of potassium and consequent disturbance of heart rhythm. I am now much more careful about hydration during long runs.
For runs greater than 20 Km, I generally prepare a drink containing 4 tablespoons of sugar and one quarter of a teaspoon of salt in four cups of water, together with lemon juice to make it palatable. I do not add any potassium salts to this mixture, as any added potassium might promote excessive activation of the renin-angiotensin-aldosterone system, thereby defeating the purpose. I adjust rate of intake to keep just ahead of appreciable thirst. Typically I find that consuming a mouthful of this drink per Km keeps me adequately hydrated.
Rhabdomyolysis is a condition produced by the breakdown of muscle, resulting in the release of the protein myoglobin, along with potassium in to the blood stream. The myoglobin damages the kidney with multiple adverse consequences including failure of potassium excretion. In extreme cases the increase in blood potassium can produce fatal cardiac arrest. In slightly less extreme cases, the kidney failure is nonetheless a serious medical emergency. Severe rhabdomyolysis arises rarely as a result of the muscle damage sustained during endurance events. However, some evidence indicates that mild degrees are not uncommon in males. For example a study by Maxwell and Bloor that tested for evidence of muscle damage after a 14 mile run at 8 min/mile pace in three groups of well-conditioned male athletes who had undergone training regimes differing in volume of running for a period of one months, found that the 14 mile run produced evidence of substantial muscle damage, including increases in serum myoglobin ranging from of 52-405%. The increases were most marked in those who had trained less for 8 miles/day on alternate days. Rhabdomyolysis is much less in females, possible because oestrogen stabilises muscle membranes.
It should also be noted that exercise induced rhabdomyolysis does not always lead to increased levels of potassium. In a series cases of exercise indices rhabdomyolysis reported by Sinert and colleagues there were no cases of hyperkalaemia.
Efficient regulation of potassium is essential for both good athletic performance and for health. One key issue for endurance athletes is maintaining the capacity of the Na/K-pumps that return potassium excreted by muscle cells as result of muscular activation back into the muscle cells. Inadequate pumping results in fatigue. Training, especially high intensity interval training, enhances the activity of the Na/K pumps. Potassium is lost from the body during exercise and dietary replacement of potassium is necessary though this is not generally an issue provide diet is reasonably well balanced. However, sustained potassium depletion has adverse effects including heart rhythm disturbances, increased blood pressure and risk of stroke.
The renin-angiotensin-aldosterone system acts to maintain fluid volume during exercise, but promotes potassium loss. It is important to avoid serious dehydration to minimise the risk of excessive activation of the renin-angiotensin-aldosterone system.
In rare instances, muscle damage during endurance events results in life-threatening rhabdomyolysis. This can lead to a dangerous excess of potassium in the blood. More common is moderate muscle damage that leads to accumulation of myoglobin. However, training reduces this risk.