Thread: New Findings on Lactic acid

Heck yeah, but this isn't exactly a new revelation in physiology.

An Italian group did some rock solid, old thyme biochemistry (bread and butter shit we used to do, before molecular biology techniques came along), back in 2002.

This is elegant science: full paper

"In the present study we investigated whether isolated rat liver mitochondria can take up and metabolize D-lactate.

We found the following: (1) externally added D-lactate causes oxygen uptake by mitochondria [P/O ratio (the ratio of mol of ATP synthesized to mol of oxygen atoms reduced to water during oxidative phosphorylation) = 2] and membrane potential (Dy) generation in processes that are rotenone-insensitive, but inhibited by antimycin A and cyanide, and proton release from coupled mitochondria inhibited by a-cyanocinnamate, but not by phenylsuccinate; (2) the activity of the putative flavoprotein ( D-lactate dehydrogenase) was detected in inside-out submitochondrial particles, but not in mitochondria and mitoplasts, as it is localized in the matrix phase of the mitochondrial inner membrane; (3) *three novel separate translocators* exist to mediate D-lactate traffic across the mitochondrial inner membrane: the D-lactate/H+ symporter, which was investigated by measuring fluorimetrically the rate of endogenous flavin reduction, the D- lactate/oxoacid antiporter (which mediates both the D-lactate/pyruvate and D-lactate/oxaloacetate exchanges) and D-lactate/malate antiporter studied by monitoring photometrically the appearance of the D-lactate counteranions outside mitochondria.

The D-lactate translocators, in the light of their different inhibition profiles separate from the monocarboxylate carrier, were found to differ from each other in the V max values and in the inhibition and pH profiles and were shown to regulate mitochondrial D-lactate metabolism in vitro.

--->The D-lactate translocators and the D-lactate dehydrogenase could account for the removal of the toxic methylglyoxal from cytosol, as well as for D-lactate-dependent gluconeogenesis."


Kinda complex, and really interesting that you got 3 translocators for lactate.

My guess - they get differentially used ...sorta stacked in activity...when the rate of respiration jumps up under exertion load (increases in intensity).

Sweet. How well it works is probably determined by your glucose metabolic efficiency. Insulin sensitivity mediated effect.

And that ultimately...drives androgen receptor turnover, this coupling with enhanced glucose driven ATP in mito, in liver and muscle cells - at synaptic junctions (via P2Y / ACh activation).

I don't get how this is a new finding? I always though this was a know fact....

Ditto, H+ ions are what most attribute the burn and resulting inability to contract to.

And those excess protons in the trans-membrane environment...precisely why you want handy dandy reducing equivalents present.

Three cheers for glutathione and NAC.

Got creatine nonresponder issues?

Ahhhh. Now you know why.

What are your thoughts on sodium bicarbonate supplementation, Trouble? Aside from GI issues.

Originally Posted by P-funk

I don't get how this is a new finding? I always though this was a know fact....

I guess its a new thing for me. I'v never studied human anotomy and i'v read some bodybuilding books stating that lactic acid was bad for the muscle and you should do some aerobic excercises, like a cool down phase after heavy lifting to reduce the amount of lactic acid in your body after a workout.

"A cool-down of 10 to 25 minutes consist of activities tht facilitate faster recovery and regeneration. After a tough workout, the muscles are exhausted, tense, and rigid. To overcome this, you must allow for muscle recovery. Hitting the showers immediately after exercise, thought tempting is not the best activity.
Removal of lactic acid from the blood and muscles is necessary if the effect of fatigue are to be eliminated quickly. The best way to achieve this is by performing 20 to 25 minutes of light, continous aerobic activityy, such as jogging, cycling, or rowing, which will cause the body to continue perspirinbg. This will remove about half of the lactic acid from the system and help you recover more quickly between training sessions. Remember, the faster you recover, the greater the amount of work you can perform the following session." Tudor O. Bompa, Phd, Mauro Di Pasquale, Phd, MD, Lorenzo J. Cornacchia SERIOUS STRENGTH TRAINING. SECOND EDITION, pg 42-43

Originally Posted by BillsFan4life

I guess its a new thing for me. I'v never studied human anotomy and i'v read some bodybuilding books stating that lactic acid was bad for the muscle and you should do some aerobic excercises, like a cool down phase after heavy lifting to reduce the amount of lactic acid in your body after a workout.

That is absurd...everyone knows you cool down so that you can talk to the hot chick on the elliptical trainer.

The lactic acid does need to get out of there, and facilitating it with a cool down just allows you to recover more quickly.

What if the chick is waiting to use your station - at the same resistance load?
She still hot?

Answer: transport of bicarbonate for pH regulation (offseting lactate/H+ buildup) is iffy in muscle

Active regulator: sodium bicarbonate cotransporter aka biocarbonate symporter

Biological process: mediates the coupled movement of sodium and bicarbonate ions across the plasma membranes; mportant role in Na+ dependent HCO3- flux in renal basolateral membranes (kidney, primary bicarbonate flux effector site).

Expression: expression not affected in chronic metabolic acidosis; widely expressed in organs like brain,liver, cornea,heart and lung; higher levels found in outer medulla and cortex of kidneys than inner medulla; predominant distribution in the thick ascending limb of Henles loop in renal medulla and cortex; expressed in spinal chord,cerebellum, cortex, olfactory bulb, and subcortical structures.

Isoform 1 is expressed in skeletal muscle.

Coupled transporters: Coupled transporters (Na+‑glucose, Na+/H+‑antiporter, Na+‑K+‑2Cl‑‑symporter, Na+‑phosphate symporter, Na+‑Cl‑‑symporter, Na+‑HCO3‑‑symporter, Cl‑/HCO3‑‑antiporter)

Now, you note that sodium is a featured ion in this coupled pumping for ion and pH regulation in many cells.

Now there is a symporter (isoform 1) that operates to relocalize Na+ across membranes, a controller of the rise in Ca+2 (calcium pump protein is coupled with Na+/K+ ATPase activity) during skeletal muscle fiber contraction.

In fact, this sodium pump action is upregulated as a result of chronic muscle training (most of you probably haven't heard of this benefit of exercise).

Thats a celullar adaptation, and pumping of sodium and potassium thru membrane channels is a key feature of skeletal muscle contactile action (Nobel prize in chemistry was awarded in 1996 to Skou for his discoveries in 1957 of this mechanism).

Its not so much a action of bicarbonate as of sodium pumping --and carbonate concentration is regulated by kidney tubule (Loop of Henle). So, I wouldn't count on it for a pH regulation in sarcoplasm or mitochrondria.

By the way, active cool down is really all about reperfusion of the tissue, to move ions out and oxygen in, to stave off hypoxic damage and begin the process of oxidative damage control.