Cellular hypoxia leads to reduced ATP, resulting in Na/K ATPase down regulation reducing the activity of the Na/K pump.

(Since I'm limited to two hyperlinks in a question currently, this first one is plain text since the newly added link is more relevant)

Hypoxia Leads to Na,K-ATPase Downregulation via Ca2+ Release-Activated Ca2+ Channels and AMPK Activation:


Resulting in increased cellular Na, which attract water into the cell which would lead to cellular hypertrophy.

Without sufficient supplies of ATP the plasma membrane of the cell can no longer maintain normal ionic gradients across the cell membranes and the sodium potassium pump can no longer function. This changes the ionic concentration of potassium and sodium. Potassium leaks into the extracellular space and sodium followed by water will move into the cell, causing cellular oedema and an increased intracellular osmotic pressure (Edwards, 2001). The cell may eventually burst.

The high [extracellular] potassium and low intracellular sodium and calcium concentration are maintained by active transport systems. Thus, one of the most rapid effects of hypoxia, and a shortage of ATP, is perturbation of the normal ionic gradients across the cell membrane, with a rapid efflux of potassium from the cell, and movement of sodium and calcium into the cell (Gosling, 1999).

Increased sodium in the interior of cells result in water also entering the cell, driven by osmotic forces causing cellular swelling and distortion, which may interfere with organelle function (Buckman et al, 1992).


I've always heard other explanations for the 'pump' after workout, with the most frequent explanation being along the lines of

during intense muscular contraction, this force inward momentarily occludes the vasculature, backing up blood flow through that particular muscle group. A compensatory increase of blood pressure forces plasma from the congested capillaries into the interstitial spaces of the muscle cells.


However, the above seems like it should be a significant factor that I've never heard mentioned in sports physiology texts and papers. I can't find information on the time course for reversing cellular oedema - ie would it be maintained long enough after exercise to account for the 'pump'.

  • 1
    See if you can get Darko Sarovic to chime in. He's more up to date than I am. – JohnP Jun 24 '14 at 18:01
  • Also, your first link is discussing hypoxic injury. You're pursuing something that really won't happen in an exercise session. Momentary hypoxia due to exertion won't result in the injury states that cause the hypoxia effects that are being discussed in the nursing times article. – JohnP Jun 24 '14 at 18:45
  • I'm fairly certain that exercise locally induced hypoxia is going to be the same physiological process. Also I think the nursing article is slightly wrong (Ie I don't think the author was aware of the Na/K Atapase regulation) - it isn't injury to the Na/K pump it is down regulation of the Na/K Atpase (another frequent incorrect explanation is that it is a direct shortage of ATP as if the pump were running out of fuel). – Tom M Jun 24 '14 at 19:52
  • You're missing my point, I think. It takes extended time to produce the hypoxic effects that you're describing, it won't happen (or very minimally) during exercise, and the body will pretty much correct it right away. – JohnP Jun 24 '14 at 21:13
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    Muscles can go a long time in total hypoxia before any of that happens. As ATP gets depleted, contractions stop and the ATP is used for the membrane pumps. Also, if muscle cells would burst, and since we have a fixed number of muscle cells in our bodies (with some potential for an increased number according to some sources), 400m runners would most likely run out of muscle very early in their careers. – Darko Sarovic Jun 25 '14 at 11:31

Cellular oedema would reverse rather quickly after exercise. As far as pump goes, there is one simple explanation, and one complicated one. Cellular oedema due to an influx of Na and H2O probably contribute, but not as much.

The simple one is that while exercising, there is local hypoxia and hypertension. This causes the vascular resistance to decrease, due to vasodilatory substances such as NO, leading to vascular congestion. After exercising, there is an overshoot of production of vasodilatory substances due to which the pump doesn't go away immideately.

The complicated one I can't really go into depth about, because there are many factors involved. But generally, during and after exercise there is an increased influx of nutrients, such as glucose/glycogen, amino acids etc. (also some electrolytes as you mentioned). There are also some waste products still present. All of those substances by themselves have an osmotic pressure (like sodium) which makes water enter the cells (not to the point of bursting though). That is the reason why creatine supplementation makes muscles larger (engorge with water); despite not increasing sodium, it goes into the muscles and the increased number of molecules inside the cells draws in water.

So to sum up, I personally think that the vasogenic effects are the main actors in "pump". More so than the osmotic due to how pump behaves (how long it lasts and why it occurs). It is hard to find anything on the topic because it is extremely hard to study. The vasogenic and osmotic effects go hand in hand after training. We can't really test their individual effects in humans on particular muscles. From what i've heard and read, people who use NO supplements get an increased pump that lasts longer, speaking in favor of blood engorgement being the cause. But people who use creatine get a similar effect, speaking in favor of an osmotic effect and water engorgement.

Personally I see this question as a mere curiosity. I'm still to think of anything we could use the knowledge about "pump" for. Mostly because it is a byproduct of training (that is, the "pump" is not what causes sarcoplasmic or myofibrillar hypertrophy in the long run. However, it could be an actor in the acute phase, which initiates the anabolism that occurs after). If anyone can think of any way we could use the knowledge about the etiology of "pump" for (assuming it has a benefitial effect in training, other than the psychological one when you look in the mirror), please write it in the comments :)

  • I've found a good review article on the current best understanding of 'pump'. journals.lww.com/nsca-scj/Abstract/publishahead/… lookgreatnaked.com/articles/the_muscle_pump.pdf Regarding its applicability, see the above article. – Tom M Jun 27 '14 at 20:13
  • As to why I asked the question - was doing some studying on hypoxia and it mentioned that a classic symptom of hypoxia was cellular edema due to Na/K pumps starving for ATP (which from further research appears to be a slightly incorrect explanation). Since I knew that exercise induces local hypoxia - it made me curious if it was a contributory mechanism to the pump. – Tom M Jun 27 '14 at 20:19

You probably won't see this addressed in the texts and papers as it is a somewhat rare occurrence that doesn't affect the general sporting population. In this study, they address alveolar hypoxia due to lung injury and/or climbing at high altitudes (Everest type altitudes) that causes pulmonary edema. Both of these would impair the gas exchange at the alveolar level (Lungs) which in turn deprives the tissues since you are delivering less than O2 saturated blood.

The net effect of this, however, isn't an accumulation of more plasma (Blood wouldn't get trapped in a cell), it results in more Ca++ (Calcium ions) being trapped in the cell. Basically the Na+ gradient decreases across the sarcolemma, so there is less movement, and the Ca++ ions don't get transported out.

The net effect would be to increase lactate production, as you are increasingly working in an anaerobic environment, and the resulting acidosis would eventually start inhibit muscular contraction.

  • Added a bit more on the cellular oedema. Are you sure that the time course for the correction of the oedema would be fast enough that it wouldn't be a significant contributor to the 'pump'? – Tom M Jun 24 '14 at 19:37
  • @TomM - Certain? No. Fairly sure? Yes. Most exercise sessions will produce momentary ischemia, but not enough to produce an extended hypoxia state. Where I might see it happening in an otherwise healthy individual is in swimmers doing hypoxic sets (Which in itself doesn't do anything for you), or other activities where you are forced to hold your breath for extended periods, but even that reverses once oxygen is re-introduced. – JohnP Jun 24 '14 at 21:16
  • I'm talking local tissue hypoxia, not global hypoxia. You can create local hypoxia trivially - any contraction, especially extended contractions do so - see Occlssion/Kaatsu for a way to deliberate induce tissue hypoxia for accelerated muscle mass gains. en.wikipedia.org/wiki/Kaatsu or stretch induced hypoxia muscleevo.net/where-muscles-grow-faster – Tom M Jun 24 '14 at 21:37
  • @TomM - Muscle evo quote-"For one, these are the results from just one study. As I mentioned in The Sherlock Holmes Guide to Separating Fitness Fact from Fiction, one study is not really news. It’s only when you get several studies showing the same thing, ideally from different research groups, that it’s worth sitting up and paying attention." For the Kaatsu method, the originator almost killed himself doing it, and the only other link is a hockey player that got hospitalized trying it. It may be a great thing, but I'm not holding my breath on it. :p – JohnP Jun 24 '14 at 21:51

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