buffering lactic

[ASheaff]

@QUIKAZHELL

Thanks for the references.
In the first study it appears an “oral solution” (wonder what that tasted like lol) was ingested. Wouldn’t this be much different than your body actually “working” to acumulate lactate/hydrogen ions? On top of that the higest concentration of lactate recorded in that study was a measly 3-5 mmols! As many people on this forum have mentioned before during a 400m race or even a 400 meter race or even training for one (4x250m @ 90% with 6’ rest) blood lactate level reach upwards of 20 mmols. So perhaps we need to find a study (if it even exists) that tests blood lactate after such a race or training session and tries to find a corelation with GH levels.

Regarding study #2…Forgive me for only reading the abstract and notes you have given but you said “the conditions with higher lactate levels actually had lower GH concentrations.” When and for how long? Perhaps they drop initially and then supercompensate hours later?

Study #3 seems a bit more interesting and I will take a look at the full paper when I get a chance. You mentioned “The GH response to exercise is probably not significant enough to meaningfully influence fat loss. GH can mobilize fatty acids, but that doesn’t mean they will be oxidized (‘burned’).” My question is what levels of GH actually influence fat loss then? I’m assuming its something very high. Is this something that can actually be induced by exercises? (I’m thinking in terms of levels that would constitute actually putting more into your body by artificial means however that is all I will mention about that since it would be in violation of this forum).

#1 The oral solution was sodium bicarbonate, not lactate. This served to prevent the drop in pH during intense exercise and was compared to exercise in normal conditions. Conclusion could then be drawn as to whether changes in GH result from acidosis/lactate accumulation or simply intense exercise. Lactate infusion was only 3-5 mmol/liter, which is probably insufficient. However, in the other aspect of the study, there were no differences in GH concentration between the bicarbonate and control conditions, so I feel the conclusions are still valid. Does that make sense? Correlations between lactate levels and GH have been found, correlation does not equal CAUSATION, as this study demonstrates.

#2 I believe across all time points. There is a delay in GH release following exercise, but blood concentrations are not elevated for long. I don’t believe that ‘supercompensation’ would occur. Perhaps an augmented GH release at night, but this would be the result of the intense exercise, and not the lactate/pH, as these changes would have been reversed hours ago. Remember intense exercise, such as the 4*250m you mentioned, does elevate GH levels. However, it is not necessarily caused by lactate.

#3 GH functions to liberate triglycerides from fat cells and dump them into the blood in order to provide energy. However, if there is no energy demand or caloric deficit, these triglycerides will not be used, and simply to return be redeposited by adipocytes in time. This is where the confusion comes in, as people do not understand what GH actually does. Even if GH is through the roof (exogenous means), if you don’t burn the fatty acids in your blood, there is no effect. Does that make sense?