Thanks again for the great feedback. Yes the Grassi's paper was an interesting study and we have it some where on this forum at the beginning of our discussion.
i tried or we try to avoid further discussions on lactate as we do this now since the early 1980. The main interesting situation is, that we somehow accept these fact , that lactate is not what we learned in school ( but we still have a problem to get rid of the use of the old idea in sport.
How come that we still have so called lactate tolerance workouts, when in fact we know, that if we add lactate to a working muscle we can go longer and faster ???
What is the reason we learned in school why we should cool down ???
Well if lactate is not the reason anymore what is the new reason.
Why would we like to drop lactate after a workout, when in fact it is a fast option as a shuttle to refuel the liver ???
And many more question we collected over the last over a quarter of a century.
Yes there is a connection with lactate and SmO2 reactions as both have a connection to energy production over O2.
I will look back where we did many years back the same. We desperately tried to hang on to the lactate idea , Threshold idea and so on and we tried over hundreds of test to create a LT threshold with NIRS (Portamon ) but as longer we tried as worse was the outcome as we started to understand more ( not all yet ) how O2 utilization and energy production are influenced.
We think it is great , if people try to use NIRS to do a noninvasive lactate test? The question simply is up for discussion on how to I find a lactate threshold if perhaps there is no such think like a lactate threshold, and if there is one what concept do I use ( Simon , Keul , Kindermann, Bunc, Broumann ,Tegtbour ????) but a great imagination may always find something..
Depending where we go here I may copy some of many many hours of discussion on lactate on here as we go along.
Our idea simply is to look what MOXY is doing , what we can measure and what it tells us, without trying to force it in any existing theory we may simply like to defend out of many different reasons.
As such I like to how here a very short perfectly written summary in where lactate really seems to be and to go.
Have fun and great discussion and yes many different options.
Lactate metabolism: a new paradigm for the third millennium
L B Gladden
Department of Health and Human Performance, 2050 Memorial Coliseum, Auburn University, Auburn, AL 36849-5323, USA
Corresponding author L. B. Gladden: Department of Health and Human Performance, 2050 Memorial Coliseum, Auburn University, Auburn, AL 36849-5323, USA. Email: ude.nrubua@blddalg
Author information ► Article notes ► Copyright and License information ►
Received November 25, 2003; Accepted April 29, 2004.
Copyright © The Physiological Society 2004
This article has been cited by other articles in PMC.
For much of the 20th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage. Since the 1970s, a ‘lactate revolution’ has occurred. At present, we are in the midst of a lactate shuttle era; the lactate paradigm has shifted. It now appears that increased lactate production and concentration as a result of anoxia or dysoxia are often the exception rather than the rule. Lactic acidosis is being re-evaluated as a factor in muscle fatigue. Lactate is an important intermediate in the process of wound repair and regeneration. The origin of elevated [lactate] in injury and sepsis is being re-investigated. There is essentially unanimous experimental support for a cell-to-cell lactate shuttle, along with mounting evidence for astrocyte–neuron, lactate–alanine, peroxisomal and spermatogenic lactate shuttles. The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional and whole body metabolism. Overall, the cell-to-cell lactate shuttle has expanded far beyond its initial conception as an explanation for lactate metabolism during muscle contractions and exercise to now subsume all of the other shuttles as a grand description of the role(s) of lactate in numerous metabolic processes and pathways.
In 1950, von Muralt distinguished four different eras in the development of muscle chemistry: pre-lactic acid, lactic acid, phosphorylation, and myosin. The pre-lactic acid era began in 1808 with Berzelius's discovery of an elevated concentration of lactate in ‘ the muscles of hunted stags’ (see Brooks & Gladden, 2003). Although there were several studies of lactic acid (HLa) in the next 99 years (see Brooks & Gladden, 2003), confusion reigned until the landmark studies of Fletcher & Hopkins (1907). Their paper ushered in the lactic acid era during which A. V. Hill's studies suggested that HLa was the immediate energy donor for muscle contractions and Meyerhof demonstrated that glycogen was the precursor of lactate (La−) (e.g. Meyerhof, 1920). Between 1926 and 1932, ATP and PCr were discovered and investigations were begun to determine which of these phosphagens might be the direct energy donor for muscle contraction (see Brooks & Gladden, 2003). These discoveries and new ideas changed the field of muscle energetics so profoundly that A. V. Hill (1932) called the experiments over the 1926–32 time period ‘the revolution in muscle physiology’. Accordingly, the 1930s marked the beginning of the phosphorylation period of muscle chemistry. In 1939, the myosin period began with the finding that the enzyme responsible for ATP hydrolysis was associated with the muscle protein, myosin (see von Muralt, 1950 for details and references). By the early 1940s, the full Emben-Meyerhof (glycolytic) pathway had also been elaborated.
If we restrict our considerations to HLa and its metabolism, we might term the period from the 1930s to approximately the early 1970s the dead-end waste product era. During this period, La− was largely considered to be a dead-end metabolite of glycolysis resulting from muscle hypoxia (Wasserman, 1984). Lactic acid was also believed to be the primary cause of the slow component of the O2 debt (Margaria et al. 1933) and a major cause of muscle fatigue (Hermansen, 1981). Since the early 1970s, a ‘lactate revolution’ has occurred. At present, we are in the midst of a lactate shuttle era which began in 1984 with the introduction of the lactate shuttle hypothesis by George Brooks (1985a).