You are reporting the following post to the moderators for review and possible removal from the forum
RE: LYDIARD OR DANIELS?
I'll fully admit that I have been defensive in the past on letsrun. I definitely appologize for that. In some cases it was provoked (by attack), but in other cases I was up late and should not have been debating with others who werre being aggressive in their assertions. I have, at times, mistook heated debated for personal attack, and I was wrong in those cases. Again, I am sorry for that.
Let's move forward and work on the merits of our discussion, if you don't mind.
Now, about lactic acid:
If one is inexperienced or unaware of the many sources of information available it would be easy to draw (erroneous) conclusions about lactic acid. A flaw in debate would be to focus on just one authors point of view and think is is the only truth. Dr. Robergs is a brilliant man, no doubt, but reading just his articles on lactic acid / lactate and looking no further would cause one to miss some valuable counter-points.
Lactic acid may not exist for lengthy time frames in working muscle, experts now agree to an extent. It still doesn't mean that lactate - which exists when pyruvate is not assimilated into the mitochondria for aerobic glycolysis(oxidative pholphorylation)- isn't "free" of causation. And, even if it lactate wasn't a causation factor of fatigue, it is still highly associated with local muscle fatigue.
In ISOLATION one may erroneous conclude that lactate accumulation is not a harm at all, but that may be wrong; according some very bright scientists. Read the quotes below!
From Dr. Graham D. Lamb and Dr George Stephenson of the Lo Trobe University of Victoria, Australia. They cite many reserach articles to support their point.
"In humans, the negative consequence of lactic acid accumulation far exceed any postive effects."
"It has been observed that the lactate ion per se reduces muscle force independent of any PH changes."
"It has been reported that lactate and H+ induce an impairment of sarcoplasmic reticulum Ca2+ release channels (Ma j, et al, 1988), depresses Ca2+ activation of thin filaments (Metzger JM and Fitts RH, 1987), and H+ induces a reduction of the Ca2+ reloading into sarcopasmic reticulum (Fabiato And Fabiato F, 1978)."
"There is merit in providing a useful summary of the underlying biochemical reactions involved in energy production within muscle and in identifying the correct species of metabolic substrates and products.
Note this next part!
However, failure to apply the entirety of physicochemical principles leads to the incorrect and misleading conclusion that lactate– is unrelated to the metabolic acidosis of exercise. We do contend, therefore, that the accumulation of lactate–within skeletal muscle directly contributes to intracellular acidosis, by virtue of the fact that it is a strong acid anion that fundamentally alters the behavior of water. With respect to acid-base balance, it is inappropriate to consider each biochemical reaction independently, and it is similarly inappropriate to try to link them temporally or in biochemical sequence. Acid-base balance changes instantaneously; therefore, a more complete understanding of the acidosis of exercise considers the simultaneous biochemical, transport, and proton buffering reactions, as well as their instantaneous and simultaneous physicochemical interactions with water, at any point in time. As stated by Norman Jones in 1980 (16): "The simple biochemical relationships above yield only a shortsighted view of proton release because the ionic state of the reactants is ignored. As they may exist in either acidic or basic forms, the net charges need to be taken into account. Reference to a biochemistry text (20) will show that the equations may be written more accurately and the source of protons is not what it seemed at first."
The whole article:
Am J Physiol Regul Integr Comp Physiol 289: R891-R894, 2005; doi:10.1152/ajpregu.00225.2005
Hit the submit button below if you want us to review the post.