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Juerg Feldmann

Fortiori Design LLC
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 #1 
Here a nice  inside view in some ideas from Italy :

Blood lactate accumulation and muscle deoxygenation during incremental exercise

1.   Bruno Grassi1,

2.   Valentina Quaresima2,

3.   Claudio Marconi1,

4.   Marco Ferrari2, and

5.   Paolo Cerretelli1

+ Author Affiliations

1.    1 Istituto di Tecnologie Biomediche Avanzate, Consiglio Nazionale delle Ricerche, I-20090 Segrate (MI); and

2.    2 Dipartimento di Scienze e Tecnologie Biomediche, Università di L’Aquila, I-67100 L’Aquila, Italy

       Submitted 25 August 1998.

       accepted in final form 10 March 1999.

Next Section

Abstract

Near-infrared spectroscopy (NIRS) could allow insights into controversial issues related to blood lactate concentration ([La]b) increases at submaximal workloads (w˙). We combined, on five well-trained subjects [mountain climbers; peak O2 consumption (V˙o2peak), 51.0 ± 4.2 (SD) ml ⋅ kg−1 ⋅ min−1] performing incremental exercise on a cycle ergometer (30 W added every 4 min up to voluntary exhaustion), measurements of pulmonary gas exchange and earlobe [La]b with determinations of concentration changes of oxygenated Hb (Δ[O2Hb]) and deoxygenated Hb (Δ[HHb]) in the vastus lateralis muscle, by continuous-wave NIRS. A “point of inflection” of [La]b vs.w˙ was arbitrarily identified at the lowest [La]b value which was >0.5 mM lower than that obtained at the following w˙. Total Hb volume (Δ[O2Hb + HHb]) in the muscle region of interest increased as a function ofw˙ up to 60–65% ofV˙o2 peak, after which it remained unchanged. The oxygenation index (Δ[O2Hb − HHb]) showed an accelerated decrease from 60– 65% ofV˙o2 peak. In the presence of a constant total Hb volume, the observed Δ[O2Hb − HHb] decrease indicates muscle deoxygenation (i.e., mainly capillary-venular Hb desaturation). The onset of muscle deoxygenation was significantly correlated (r2 = 0.95;P < 0.01) with the point of inflection of [La]bvs. w˙, i.e., with the onset of blood lactate accumulation. Previous studies showed relatively constant femoral venous levels at w˙ higher than ∼60% of maximal O2consumption. Thus muscle deoxygenation observed in the present study from 60–65% ofV˙o2 peak could be attributed to capillary-venular Hb desaturation in the presence of relatively constant capillary-venular levels, as a consequence of a rightward shift of the O2Hb dissociation curve determined by the onset of lactic acidosis.

 

the question whether lactate accumulation in muscle and blood at submaximal workloads is attributable to an imbalance between O2 supply and O2 requirement in the working muscles, that is, to muscle hypoxia, is controversial (6, 14, 17). The issue is further complicated by the fact that lactate concentration in blood ([La]b), as usually determined in the exercise physiology laboratory, cannot be considered a direct index of lactate production by muscles, because muscles, as well as other tissues and organs, are also consumers of lactate by oxidative metabolism for their energetic needs (6). In additon, lactate distribution throughout body compartments appears to be regulated by complex mechanisms (14, 16). Apart from its involvement in energy metabolism, other roles of lactate have been recently suggested. For example, according to Stringer et al. (35), lactic acidosis in muscle would facilitate O2Hb dissociation and therefore increase O2 extraction while preserving the O2 pressure gradient from capillary to mitochondria.

Some further insights into these issues could be obtained by the utilization of near-infrared spectroscopy (NIRS), a noninvasive method that allows the monitoring of muscle oxygenation on the principle that the near-infrared light absorption characteristics of hemoglobin (Hb) and myoglobin (Mb) depend on their O2 saturation [see, for instance, the recent reviews by Ferrari et al. (13) and by Mancini (22)].
Juerg Feldmann

Fortiori Design LLC
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 #2 
Now to add more insult to the discussion.
 When looking at classical ideas of lactate or any use of the idea of lactic acid, than it may be fun to read this book her or if not enough time a great part  of the book  in a blog.  So if you not like to get bored with chemical formulas  below  I let them out so you just can enjoy the explanation.

 

Principles of Biochemistry, 5/E
Laurence A. Moran, University of Toronto
Robert A Horton, North Carolina State University
Gray Scrimgeour, University of Toronto
Marc Perry, University of Toronto


Muscles and the Lactic Acid Myth

If you've been watching the Olympics, you've heard the story many times from coaches, athletes, and even team doctors. They all tell you that the performance of endurance athletes is limited by the buildup of lactic acid in their muscles and this is what causes the pain and limits their ability to win a gold medal.

It's the acid that does it and that acid is caused by synthesis of lactic acid taking place during anaerobic exercise, or so the story goes. That happens under extreme conditions when the energy needed by working muscles exceeds the ability to produce it by normal aerobic oxidation. It all sounds so logical ... and so biochemical.

It's all a myth. Lactic acid has nothing to do with acidosis (the buildup of acid in the muscles). In fact, it's not even clear that acidosis is the problem, but let's deal with that another time.

Assuming that acid buildup in muscles is what causes the pain of the long distance runner, where does that acid comes from? In order to answer that question we need a brief lesson on acids.

Acids are molecules that can give up a hydrogen ion (H+), or proton. Hydrochloric acid (HCl) and acetic acid are classic examples. They can both dissociate into H+ and a negatively charged ion; either a chloride ion in the case of hydrochloric acid (Cl-) or an acetate ion (CH3COO-) in the case of acetic acid.

 

 

The strength of an acid depends on how easily it dissociates into hydrogen ions. Hydrochloric acid is a strong acid because it dissociates almost completely and acetic acid is a weak acid because it only partially dissociates in water.

The concentration of hydrogen ions is what makes solutions acidic and we describe that concentration by referring to the pH of the solution where the "H" stands for hydrogen ions. The pH scale is a log scale and it is the negative log of the hydrogen ion concentration (don't ask). Solutions with low pH have very high concentrations of hydrogen ions.

Muscles need biochemical energy to do their work and that energy is supplied by ATP, the common energy currency in the cell. As ATP is used up, it needs to be regenerated and the quickest way to do that is to makes make more ATP using creatine phosphate, a high energy molecule stored in muscle cells. When the creatine phosphate is depleted, muscle cells mobilize their store of glycogen converting it to glucose that is then metabolized by the glycolysis pathway. The end products of this pathway are pyruvate, ATP, and NADH. The ATP produced during glycolysis is used by the muscle cells.

 

 


Under normal conditions, pyruvate enters a pathway called the citric acid cycle and this pathway regenerates NAD+ from NADH so that glycolysis can continue. This reaction is coupled to synthesis of more ATP by mitochondria, a process that requires oxygen.

Here's where things get tricky for athletes. Their muscles are often working so hard that the resupply of ATP by glycolysis and the citric acid cycle can't keep up with the oxygen supply, no matter how hard the athletes are breathing. Pyruvate begins to accumulate in the muscle cells because it can't be metabolized quickly enough in the citric acid cycle.

Under these conditions, pyruvate is converted to lactate in order to generate more NAD+ so that glycolysis can continue. This is often referred to as anaerobic metabolism. Look closely at the reaction.

 


The product of this reaction is lactate, not lactic acid. Lactate is not an acid because it can't give up a proton. The overall reaction doesn't produce acid (H+), it actually consumes it. Muscle cells do not accumulate lactic acid, they accumulate lactate and that's not the same thing.

So what causes acidosis in muscles? It may come, in part, from the reaction that consumes ATP but this can't be the whole story because ATP is rapidly regenerated, using up the hydrogen ion.

 


Some of the acidity may be indirectly due to a buildup of lactate affecting buffering capacity but this doesn't seem to be a likely cause of acidosis.

The important point is that lactic acid is not produced in muscles so it can't be the source of acidosis. This has been known in the scientific literature for twenty years but it doesn't seem to have entered the biochemistry textbooks until recently. The myth of lactic acid has been debunked in newspapers and science magazines but it's still believed by athletic coaches and trainers and by the athletes themselves. It doesn't really matter since training is able to overcome the limits of muscle metabolism whatever the cause. It's likely that training and hard exercise increase the number of mitochondria in muscle cells and this could be the real benefit since it allows for more aerobic metabolism.


Andri

Fortiori Design LLC
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Posts: 65
 #3 
The irony of the situation is that lactate measurements are useful to a certain extent (less and less with expanding technology such as NIRS), just that the reasoning or understanding was wrong. Blood lactate accumulation represent an increase in glycolysis to beyond the point of oxidative capacity, and therefore lactate is produced to create reducing equivalents (NAD) to maintain further glycolysis. Therefore, blood lactate indirectly can help us understand metabolism changes. Therefore the use of blood lactate values for training guidance was and is actual somewhat useful and for this reason (maybe) it became widely accepted, because it proved effective, even though it was based on wrong science....luck? What is important now is to recognize that, even though lactate and lactic acid may not be what they once where, many points from Hill and colleagues anaerobic theory are still on the forefront of physiology and training science. If we still believe that oxygen uptake and utilization is key to metabolism, but that blood lactate is no longer the most effective way of identifying changes in metabolism (talking from a broad population point of view), what other tools exist or are being developed that can help us understand individual metabolism during exercise.
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