Exercise Physiology question about the sodium potassium pump

Fatigue is multifactorial, but Weterblad and Allan have shown great evidence that muscle fatigue is NOT due to accumulation of lactate or acidification of the blood. Btw, lactate is the molecule with the H+ released, so that the H+ is floating around in solution also ... that is the actual acid, I.e. the thing that is lowering pH.

Fatigue can derivedrom many things - lack of fuel (likely not a prob here bur def in marathon), accumulation of K+ outside the muscle cell inhibiting action potential firing, accumulation of inorganic phosphate inside the cell inhibiting contraction, or even what is referred to as central fatigue - or the inability of the motor neurons to fire correctly or even some lack of ability of higher order neural processes todunction.

Looking at these studies, what they did was taper runners. There is no mention in these studies about the long term viability if their training program. I think most anyone who knows anything about running knows that a 25% drop in mileage for a sustained period will eventually result in loss of fitness.

By the way, I think the average letsrunner under age 30 is already running faster than the subjects of this study. Having said that, the Copenhagen Muscle Research Center is extremely highly regarded and they do a lot of very good work there - not just exercise studies.

of course you can drop volume 25% and maintain or improve performance. volume is just one of many training variables.

they did not taper the athletes; they increased the training intensity.

The Stache wrote:

Fatigue is multifactorial, but Weterblad and Allan have shown great evidence that muscle fatigue is NOT due to accumulation of lactate or acidification of the blood. Btw, lactate is the molecule with the H+ released, so that the H+ is floating around in solution also ... that is the actual acid, I.e. the thing that is lowering pH.

Fatigue can derivedrom many things - lack of fuel (likely not a prob here bur def in marathon), accumulation of K+ outside the muscle cell inhibiting action potential firing, accumulation of inorganic phosphate inside the cell inhibiting contraction, or even what is referred to as central fatigue - or the inability of the motor neurons to fire correctly or even some lack of ability of higher order neural processes todunction.

So given all of this, should we re-conceptualize the "lactate threshold"? If lactate is a muscle fuel, not something causing fatigue, what's the physiological benefit of doing threshold training?

Or is my question misguided?

Well, your question is not misguided, really.

The thing is, lactate starts to accumulate when glucose being is being broken down by glycolytic enzymes faster than the resulting pyruvate can be shuttled into the mitochondria for oxidative phosphorylation.

Training just at "lactate threshold" (if such a threshold actually exists is something of great controversy, and I never saw a real threshold in any of the stress tests which I performed or in which I was a subject - yes this requires sequential blood draws from a catheter while performing a stress test) allows adaptation to occur at the mitochondrial level to allow for greater energy substrate utilization - whether through production of more shuttle proteins, Krebs cycle enzymes, or whole mitochondria altogether with all their components.

Lactate accumulation does CORRELATE with fatigue, though, in this way. As one runs/cycles/swims/etc faster and faster, you will be utilizing ATP for muscular contraction (during which ATP is broken into ADP and Pi). You can keep recycling ADP + Pi to new ATP as long as energy substrate is available. This can occur through glycolysis in the cytpolasm or oxidative phosphorylation in the mitochondria. At some point, glycolysis outpaces oxidative phosphorylation, and lactate accumulates. At some point of intensity not too much higher for most of us, ATP usage will outpace ATP production, you have an accumulation of Pi, and this accumulation has been shown as a major contributing factor to actual muscular contractile fatigue. (See reviews by Fitts and by Westerblad and Allen at pubmed.com).

All at the same time, we start seeing the Na/K pump problem arising. All excitable cells (nerve, muscle, heart, etc) utilize ATP energy to create a high Na gradient outside the cell and a high K gradient inside the cell. This unbalanced ionic milieu is the basis for action potentials. When ATP usage is so high for other processes in the cell, and when action potentials are firing so fast, eventually you start seeing K accumulation outside the cell (and of course Na accumulation inside the cell). The problem with this is that it affect voltage-gated channels responsible for action potentials, causing them to remain in refractory period for longer and preventing firing of action potentials when they're supposed to. (Action potentials are the electrical signals at the cell membrane that elicit the contractile machinery inside the cell to do its job).

All these processes leading to actual fatigue occur NEAR the same level of perceived intensity, but come on at various time points of elevating muscular fatigue.

I hope this helps. I could go on for days about this stuff. Ask more specific questions if you want.

And to dsrunner - OK, maybe this is not a true taper, but this is what occurs later in a racing season: One moves from more mileage based training with moderate intensity to interval/sprint training with higher intensity. Sometimes the volume drops, sometimes it does not. Either way, what is described in the article is preparation for the "racing season" by some runners.

Sodium depletion is certainly one of the many causes of fatigue. It most likely coincides with dehyration obviously.

In terms of putting together a training plan, you want adequate hydration, glycogen storage and dietary salt before hard training. And the ability to continue to train hard when those fuels are becoming depleted.

Lactate comes from muscle and liver glycogen, but there is no exact lacate level that is more beneficial in training, rather a big variety of paces and lactate levels, and the ability to hold the paces you experience in races for longer.

1.Associating anything to a “Lactate Threshold” is not going to help you understand the anatomy and physiology of human performance.

a.Google McArdle’s Disease and you’ll understand why

b.The concept of association of performance via lactate threshold should further mean that any race distance would have a LT associated.

c.Lactic acid is a strong acid, it dissociates into lactate and H+. Research is done on single muscle fibers outside the body (in vitro) and do not occur in the same relation in vivo (inside the whole body).

d. Understand that there is not one site of fatigue. Many areas.. central, peripherial, local etc. Some research is leaning towards an increase in inorganic phosphate during high intensity exercise as a mechanism of depressed contraction. Increase in inorganic phosphate may directly act on the myofibrils and decrease cross-bridge force production and myofibrillar calcium sensitivity.

> c.Lactic acid is a strong acid, it dissociates into lactate > and H+.

>

In acid/base chemistry, "strong" means 100% ionization when in dilute aqueous solution. That is, no detectable reverse reaction in the equilibrium. Quantitatively, this requires a *VERY* small pKa. Wikipedia indicates that the pKa's of strong acids must be less than -1.7, which seems about right to me. The pKa of lactic acid is +3.9. Clearly it is not a "strong" acid.

Nevertheless, even "weak" acids can be 100% ionized when the pH >> pKa (here "weak" simply means acids that do not satisfy the above requirement). Let's assume that muscular pH at exercise is 6.7, which is in the ballpark of reality. Thus, using Henderson-Hasselbalch, this means that 100% of the lactic acid is ionized (lactate) at this pH (rounded due to sig-figs).

My understanding is that Lactate Threshold refers to blood lactate inflection point (LIP), an exercise intensity beyond which lactic acid is being produced faster than it can be removed.

Lactate in fact is an indicator of Hydrogen Ions that disassociate from lactic acid (H+ is the acid component) within the muscle. The accumulating H+ cause acidosis within the muscle, and in this environment glycolytic enzymes are inhibited. Therefore a runner experiences a slowing in the breakdown of glycogen and hence a slowing in the resynthesis of ATP (the muscles source of energy for muscular contraction) = fatigue.

With sufficient oxygen lactic acid can be a source of energy as it can be converted back to glycogen or redirected through the aerobic pathway for more complete breakdown (once returning to pyruvic acid).

Lactic acid accumulates when the exercise intensity is such that the aerobic system can not provide sufficient ATP. Aerobic training is one way to delay LIP, or delay an increased reliance on the anaerobic glycolysis energy system (formerly known as the lactic acid system).

An aerobically trained athlete may experience LIP at 90% of MHR as opposed to 85% (closer to what the average person would experience). Higher intensity training can increase our ability to tolerate H+ accumulation and or become better at buffering the H+ (acid) - but exercising at intensities above LIP is not sustainable due to the fatiguing affect outlined above.

Good luck with your training. (Percentages from Australia).

Your understanding of how muscle contraction works normally is WAAAAAAAAY to simplistic to even begin contemplating how fatigue works.

Pretty much everything in this thread confirms my bias that most exercise physiology is done by dumb jocks.