Hyper and hypokalaemia in athletes

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.

13 Responses to “Hyper and hypokalaemia in athletes”

  1. michael troup Says:

    Potassium levels above 6.5 are felt to be potentially dangerous, and this is the level at which treatment to reduce it is usually considered in hospital patients – I have never seen one anywhere near 12; an ECG is often done before treatment to see if there is evidence that the potassium level is affecting the heart – peaked T waves is the classic sign. Most people with a high potassium are on medications that push up potassium, are in renal failure, or both. Rhabdomyolysis as a cause of hyperkalemia is rare.

    The western diet of course has far too much sodium and not enough potassium – we evolved in a high potassium low sodium dietary environment, and as a result can easily survive on little salt but do need potassium to keep levels at ideal levels – between 4 and 5.5.

    There is evidence that a high potassium intake reduces blood pressure and the incidence of cardiac rhythm problems.

    Is there any evidence that training the Na/K pump separately from the muscles themselves is worthwhile – or even possible?

    • canute1 Says:


      Thanks for your comments.

      Your statement regarding a blood level of 6.5 being considered dangerous refers to steady state blood levels observed in clinical practice. Interstitial and arterial blood values rise to around 12 mM transiently during exercise. See for example table fig 2 in http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7793.2000.00849.x/full . Nonetheless I will add a phrase in the first paragraph to indicate that levels above 6.5 mM are regarded as dangerous in clinical practice.

      I agree that a high potassium diet is likely to reduce risk of arrhythmia. This is consistent with the fact that hypokalaemia increases risk rhythm disturbances . In healthy individuals high potassium diet is extremely unlikely to produce the levels of hyperkalaemia associated with cardiac arrest.

      It is true that rhabdomyolysis is a rare cause of hyperkalemia in clinical practice. The point that I am making is that in rhabdomyolysis (which is not commonly seen in clinical practice) there is a risk of hyperkalaemia. Here is a reference to an article providing an account of hyperkalaemia associated with rhabdomyolysis http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791742/
      In a review, Efstratiadis et al state: Treating rhabdomyolysis also requires to cope with subsequent electrolyte disorders. Particularly, hyperkalemia is a really dangerous complication, which can lead to life-threatening arrhythmias. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2658796/
      On the other hand, the series of cases of exercise induced rhabdomyolysis reported by Sinert et al did not observe any cases of hyperkalaemia. http://www.charlydmiller.com/LIB04/1994exerciserhabdo.html. I have added this information to my post.

  2. michael troup Says:

    I see the extremely high K+ levels – 12 or so – were measured in the muscle interstitial space – between the muscle cells – rather than in the veins draining the exercising muscle or the veins at the front of the elbow – where K+ levels are usually measured. So this is very different from ordinary clinical practice, and very different from the tests that would be done on a collapsed athlete. So to give some numbers – with focal exercise to exhaustion – say ankle flexion to exhaustion – I would expect a gastrocnemius interstitial K+ of about 12; a femoral vein K+ of 6-7; and an arm vein K+ of 4-5.

    An interesting topic!

    • canute1 Says:

      Thanks for your further comment. I agree that the interstitial values of 12 mM recorded by Green do not prove that arterial levels might reach similar levels. However, in the case report of rhabdomyolysis by Rosenberry (reference given above) plasma potassium was 8.6mM and the patient survived. In cases of fatal collapse during a marathon I understand levels around 12 mM have been recorded, but as far as I now such data has not been published. While I accept that T wave ‘tenting’ might occur above 6.5mM, and this is a sign that repolariszation is affected, the heart can continue to beat at substantially higher levels.

      Here is a reference to a case where the patient survived despite serum level of 14mM. He suffered VF and required resuscitation. The highest level was recorded during cardiac resuscitation, possibly as a consequence of rhabdomyolysis due to muscle trauma during the resuscitation. His serum level was still 9.8 mM 8 hours after the cardiac arrest. http://www.medscape.com/viewarticle/510353_2.

      Here is a detailed account of the final few hours of a boxer who died from ventricular fibrillation due to hyperkalaemia arising from rhabdomyolysis. http://www.asac.arkansas.gov/pdfs/reports/Anthony_Jones_-_Final_Investigation_Report.pdf His potassium level fluctuated. About 2 hours before the cardiac arrest, potassium level was 9.7 mM. The highest recorded value was 10.3 mM during resuscitation.

      To acknowledge the fact that survival above values of 10 mM is rare I have changed the wording in the first paragraph of my post from ‘high risk’ to ‘very high risk’ and have added a note stating: [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. ]

  3. Robert Osfield Says:

    Ouch, that gives me a few issues to think about when I do the West Highland Way Race in 11 days!

    You don’t mention ultras in your post but if muscle damage leads to increased levels of potassium in the blood in regular long runs then it’s seems very likely it’ll be higher during a 95 mile run.

    It’s interesting that you are just using salt as an electrolyte rather than a standard shop bought electrolyte, it certainly makes sense. Typically electrolytes have potassium added – for instance the S!caps that I have used in the past contain 241mg of Sodium and 21mg of Potassium, the label also suggests the % Daily Value are 13.6% and 0.5% respectively. The 0.5% looks reassuring low of Potassium so perhaps having one of these an hour won’t be an issue.

    Should I just go with salt added to water, liquid and solid foods? Thoughts on amount of salt that it would be sensible to aim for during a 20+hr run?

    Another are that I’m wondering about is spotting whether my bodies homeostatis is being upset by excessive amounts of potassium in the blood. Are there particular symptoms to watch out for? Are they strategies to employ to help the body get back into balance before too much damage is done?

    • canute1 Says:


      I do not think you need to worry too much though there is need for some prudence.

      I am not aware of studies of potassium levels during an ultra but I suspect they are usually no higher than during a marathon. The degree of increase in extra-cellular K+ during exercise is dependent on the vigour of the exercise. Eccentric muscle contraction is more harmful than concentric contraction. Eccentric contraction is inevitable during running though I suspect that the impact forces are generally less at ultra pace. Mild degrees of rhabdomyolysis are nonetheless relatively common during ultras –simply due to the duration of running, but rhabdomyolysis does not always produce hyperkalaemia. I suspect that serious dehydration is likely to be major a risk factor, though the body’s primary response to dehydration is conserving fluid volume and sodium. The medical examiner in the case of the boxer, Anthony Jones, considered dehydration, and substantial dietary intake of potassium, together with high level of muscle tension were all contributory to the rhabdomyolysis and hyperkalaemia in that case. Jones died after a knock-down at the end of the second round – quite different from the trauma of an ultra-marathon.

      With regard to adding potassium to the electrolyte mix during an ultra, this is probably OK as the intensity of exercise is unlikely to cause a major efflux of K+ from muscle cells, yet over the long duration of an ultra, there will be loss though sweat. I suspect that if you stop for 15 minutes at a check point late in an ultra, you might suffer appreciate hypokalaemia as K+ is pumped back into your cells, if you have not taken in any K+ during the event.

      Although I think that endurance athletes should be aware of rhabdomyolysis and of hyperkalaemia, I think that the risks are small provided sensible precautions are taken.

      Most important is training adequately for the event. Most forms of training improve Na/K pumping. Some evidence suggests that HIT is the most effective, but aerobic training does also improve Na/K pumping. Efficient Na/K pumping should minimise fatigue while minimising the large swings in extra-cellular K+ levels. Furthermore, adequate training conditions the muscles to cope with the pounding thereby reducing the risk of rhabdomyolysis. It is a challenge to find time for fully adequate training for extremely long event such as the WHWR, and therefore in such races one should take sensible note of how well your body is coping. I would regard unstable heart rate as a warning that should not be ignored.

      Second most important is adequate hydration – but take care to avoid over-hydration. I aim to keep just a little ahead of the level of overt thirst at which my mouth feels dry. During a run of several hours duration, I often lose between one and two Kg in weight. During very long runs I add sodium chloride. As descried above, during an ultra, I would probably also add some K+. In addition, it is useful to monitor urine output and colour. Urine output will be decreased, but I would be concerned if it ceased entirely or if the urine become dark.

      I suspect that the fact that you have adjusted you diet in a way that minimises gut upset is also likely to protect you against electrolyte disturbance.

      The role of stimulants such as caffeine and of anti-inflammatories is uncertain. I would not consume these drugs because of uncertainty about their effects and also because I think they are on the borderline of unethical drug use. However I am aware that many ultra runners consume caffeine with little evidence of adverse effects.

      The WHW will probably present a major challenge to your physiology, but I think you are well prepared. Good luck

  4. michael troup Says:

    It is important to differentiate between a high potassium causing a cardiac arrest, and a high potassium measured during a cardiac arrest – during an arrest there is usually severe hypoxia and therefore acidosis and this can result in very high potassium levels – the treatment is that of the underlying cause – cardioversion if in VF for example – and the potassium will usually return to normal as the circulation is restored and the hypoxia/acidosis resolve. There will of course be the occasional case where ongoing poor circulation results in persistent acidosis and a high potassium that needs specific treatment. Most people with a high potassium measured during a cardiac arrest will have had a normal – or even low – potassium before the arrest.

    As to electrolyte disturbances during prolonged exertion the commonest potentially serious problem is of course hyponatremia from excess water intake – a high potassium is way down the list – indeed any attempt to restrict potassium intake is likely to result in a low potassium which predisposes to cardiac rhythm problems and can result in a feeling of generalised weakness and muscle cramps.

    • canute1 Says:

      Thanks for your continuing comments. While it is important to distinguish between high potassium during a cardiac arrest and high potassium causing an arrest, my blog post was concerned with the latter. There is little doubt that high potassium can cause an arrest. Indeed you first comment implied that arrest was likely at values lower than the 12 mM that I mentioned in my blog. I am well aware that many doctors consider that 10 mM is the usual level beyond which there is a very high risk of arrest, and that levels above 6.5 warrant attention. I think that 10 mM is a reasonable estimate of the critical level in most circumstances. I quoted the somewhat higher value of 12 mM because I was aware of several cases where values around 10 mM did not lead to immediate arrest, together with evidence from the case reported by Tran (http://www.ncbi.nlm.nih.gov/pubmed/?term=Tran+HA+Southern+Medcial+Journal ) in whom levels came down from 14 mM to 9.8 mM during about 8 hours of stable cardiac state following resuscitation. It is probable that anti-arrhythmic medication administered during this period helped stabilise the myocardium in that case. The question of whether 10 mM or 12 mM is the level at which risk of arrest is very high is of little relevance to the point that I made: namely in rare instances rhabdomyolysis results in very dangerous levels of hyperkalaemia that can cause cardiac arrest. It is probable that multiple factors combine to determine when this occurs since rhabdomyolysis does not always cause hyperkalaemia. The detailed description of the case of Anthony Jones, the boxer who died of cardiac arrest attributed to hyperkaemia associated with rhabdomyolysis provides a good illustration of the complexity of the situation.

      I agree that hyponatraemia due to excessive water intake is probably the most common serious electrolyte disturbance suffered by recreational runners, possibly due to overemphasis on the need to be well hydrated during exercise. I myself take substantially less fluid than required for full replacement during a long run. In addition, during very long runs, I add sodium chloride to the fluid that I carry. I do not add potassium salts because blood levels of potassium are usually elevated during vigorous exercise due to transport of K+ out of muscle cells. There is good evidence that the resulting decrease in the potassium ion gradient across the cell membrane contributes to muscle fatigue. There is of course a risk that potassium levels might fall too low after I stop running, due to the continued pumping of potassium back into cells, but I believe that substantial post-exertional hypokalaemia is best averted by a diet that is fairly rich in potassium (including the foods listed in my blog post). One certainly should start a long race with adequate intracellular potassium levels.

  5. David Fogelson Says:

    I believe lisinopril is causing a degradation in my athletic performance. My potassium is within normal limits but slightly higher on lisinopril than without. My wattage output is down 20%. The challenge is that it works better than other meds in controlling my BP. Thanks for your time.

    • canute1 Says:

      Thanks. That is interesting. I wonder whether the reduction in baseline BP is associated with diminution of the normal transient increase of BP during exercise. If so, this might be a factor in your reduced power output. But clearly for the sake of health, you need to keep your resting BP down, and it appears that the lisinopril is having the required effect.
      In addition, the mild elevation of potassium might be contributing to decreased potassium gradient across the muscle cell membrane and thereby contributing to loss of power. If so, it is important to ensure that your Na/K pump efficiency is good. As mentioned in my post, any aerobic training helps keep the pumps working well, but HIT is appears to be especially effective.

      • David Fogelson Says:

        What is HIT? I am an endurance cyclist and ride 130 miles per week, 6,000 pluses per year. I am going to get a repeat potassium level. Thanks for the kindness of your reply.

  6. Ron George Says:

    I’m showing an extended downward ST curve in my ECGs taken from a chest strap reading. Someone else looked at it and pointed towards ‘Hypokalemia’ while also advising that towards a 12 lead ECG reading done in a clinic. While the later advice makes sense, I was wondering whether it is not feasble to use chest strap style electrodes (500Hz sampling) to detect such trends. Certainly for athletes who want to monitor every day condition, a hospital visit in impactical. What’s your opinion? If you share your email address, I’d be happy to share some ECG traces with you. Thanks.


  7. canute1 Says:

    Dear Ron

    Sorry for the tardy response.

    I presume that by down-sloping ST curve, you are referring to T wave inversion. T wave inversion can occur in various cardiac and non-cardiac conditions, and indeed inverted T waves can occur normally in several of the leads of a 12 lead ECG. The T wave is usually inverted in aVR (in association with normal inversion of the R wave in that lead).

    I am not familiar with the EEG trace derived from a chest strap. I presume it would be most similar to lead 1, but it might in fact represent a mixture of characteristics seen in several of the 12 leads. The interpretation of an inverted T wave in such a trace is likely to be difficult to interpret because one cannot be sure of which combination of the 12 leads that it corresponds to.

    Therefore in my non-expert opinion, I would recommend a full 12 lead recording (and perhaps also a blood test for potassium level) to establish the most likely diagnosis.

    I accept that daily 12 lead ECG is likely to be impractical. If the clinical testing does confirm low potassium, you should discuss the likely cause with a clinician. If it is a recurrent condition that requires monitoring, discuss the best strategy for regular testing and ask the clinician about the credibility of the evidence from a chest strap. But I suspect that most clinicians would be unlikely to recommend use of a chest strap.

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