Thanks Roger great question and a great chance not to critics but to show the disconnect in many exercise physiological studies to the real world of physiology.
1. Lactate has only a limited feedback ability to the trend in SmO2.
a) we can have 4 different situation and it is up to the regular reader to explain what happens in the body when I explain the 4 different options.
a1. We can see an increase in SmO2 and an increase in lactate at the same time Why and when ?
a2. We can see an increase n SmO2 and a decline in lactate
a3 We can see a drop in SmO2 and a drop in lactate
a4 we can see a drop in SmO2 and an increase in lactate.
Lactate has no direct impact on the O2 diss. curve at all.
It is the H + ( lactate is a buffer of H + ) as well CO2 besides other reason , who shift the O2 diss curve.
In this case above, the fact , that VO2 and lactate where not different in the two groups simply indicates, that they did a step test ( classical VO2) test with too short steps in the first place to actually create a clear information on what and why some where low in SpO2 ( nearly 50 % ).
A drop in SmO2 means , that they where looking at the end of the test for O2 and the O2 was found in the storage and the regular training stimulated in this people the ability to deoxygenate better. ( Different reason for this ability like CO2 levels H + levels change in hormones as explained in the articles before.)
The fact remains, that they still had O2 they where able to use due to the better deoxygenation ability and there was a similar amount of VO2 used over all.
In the group with a " normal' SpO2 there the O2 needed or used at the end was delivered over blood flow , so they where not digging into the storage, as it was not needed as the delivery system to the blood was still working well. So same O2 use just delivered instead of used from storage.
. This examples show exactly the big reserve we have to improve performance.
Athletes with an EIH have a different limitation and a different compensation. Limitation may be respiratory system or vascularisation or muscular . Compensation is a better utilization of O2 ( bio availability ). The other group has a utilization limitation and has a compensation over , for example , muscular ability.
So the key is to find the Limiter and than work on the Limiter to improve performance.
So the EIH group would have to work on the ability to load O2 and maintain the ability to utilize and they have immediately more O2 available for a better performance. The other group would have to work to improve utilization and maintain delivery and again a performance gain.
That's and exactly that is , why we do our 2 different assessments. Finding delivery limitation and utilization limitation with MOXY and combine it in actual test centers with Physio flow and VO2 equipment.
The main reason why this is not common used as of yet is the inability we all have to accept, that we can make progress and do not have to hang on a now nearly 100 year old concept of VO2 max or 2 and 4 mmol lactate, when we actually agree, that there is no such thing like a VO2 max but a VO2 tested peak. and that lactate is most likely an energy source and a great shuttle tool for many important ideas in the body.So the "effort' from many groups to force NIRS result into a mythical idea of LT ANT and so on slows done the progress of looking at new options.
So the fact than in this study VO2 and lactate is used but did not correspond with NIRS trend shows nicely why we desperately try to avoid , that NIRS MOXY is getting used to be a part of an artificial kept alive theory to all costs. For us MOXY is a new start into a new area of life in the field information , which can be combined with " classical " ideas but is so much more direct than lactate and VO2 , that it is not a great idea to try to force MOXY trends in non existing lactate thresholds or % of VO2 max and so on.
VO2 and lactate have a direct result based on test protocols and we can't use them as actual physiological information in most of the short term test ideas.
See here a small statement form the University of Maastrich research ideas in Cycling Pro and amateur comparison.
"A study protocol with 3-minute stages was used in this study, starting with 2 W/kg and
increasing every workload step with 0.5 W/kg. Other research investigating differences
between professionals and amateurs, mainly Lucia and Chicharro, used different study
protocols with stages of 25 W/min (17, 18, 37, 39-44). Sallet et al. used a ramp protocol of 30
Watts every 1 minute and 30 seconds (55). These differences in ramp protocols may hamper
comparisons between the several studies. For example, the ramp protocol of 25 W/min
generally requires less total time than the protocol used in this study"
If we have real physiological parameters, than protocols should not influence physiological reactions if the body had a chance to try to react. If the protocols are based on physical ideas too much and the lag time of some of the physiological systems, including the lag time for the equipment. ( VO2 testing at the mouth to concluded, what happens in the muscle, lactate testing at the finger to conclude what happens in the muscle ) , than we simply create nice looking ideas with very little ability to find limiter and compensator.
The drop in the study of SmO2 is due to the shift in O2 diss curve due to respiratory limitation. There is a fundamental difference in metabolic acidosis, where lactate can be one of many bio markers to show, that we start mixing o2 dependent ATP production with O2 independent ATP production, which can create a shift in O2 curve due to change in H + level and pH.
and the respiratory acidosis which creates H + and CO2 an therefor a shift in O2 diss curve as well. We can create a respiratory acidosis with low SpO2 and high CO2 and a shift in SmO2 and a better deoxygenation with out even moving a leg or an arm and with put increasing HR really. See pic from a case study done by Brian Kozak. look the deoxygenation and he did this by simply sitting at home. What was he doing.
Many questions you have to answer in this respond. I am looking forward to a critical response and ideas. Here a short info on acidosis and alkalosis
Some basic information
Normal pH value for the body fluids is between pH 7.35 and 7.45. If the pH of body fluids is below 7.35, the condition is called acidosis, and if the pH is above 7.45, it is called alkalosis.
Metabolism produces acidic products that lower the pH of the body fluids. For example, carbon dioxide is a by-product of metabolism, and carbon dioxide combines with water to form carbonic acid. Also, lactic acid ( lactate + H ) is a product of oxygen independent metabolism, protein metabolism produces phosphoric and sulfuric acids, and lipid metabolism produces fatty acids. These acidic substances must continuously be eliminated from the body to maintain pH homeostasis. Rapid elimination of acidic products of metabolism results in alkalosis, and the failure to eliminate acidic products of metabolism results in acidosis.
The major effect of acidosis is depression of the central nervous system. ( Feedback loop over the Central governor and for us over the ECGM extended central governor) When the pH of the blood falls below 7.35, the central nervous system malfunctions, and the individual becomes disoriented and possibly comatose as the condition worsens.
A major effect of alkalosis is hyperexcitability of the nervous system. Peripheral nerves are affected first, resulting in spontaneous nervous stimulation of muscles. Spasms and tetanic contractions and possibly extreme nervousness or convulsions result. Severe alkalosis can cause death as a result of tetany of the respiratory muscles.
Although buffers in the body fluids help resist changes in the pH of body fluids, the respiratory system and the kidneys regulate the pH of the body fluids. Malfunctions of either the respiratory system or the kidneys can result in acidosis or alkalosis. (Mal function can be create due to limitation of the task the respiratory system suppose to do. )
Acidosis and alkalosis are categorized by the cause of the condition. Respiratory acidosis or respiratory alkalosis results from abnormalities (or weakness /limitation) of the respiratory system.
Metabolic acidosis or metabolic alkalosis results from all causes other than abnormal respiratory functions.
Inadequate ventilation of the lungs causes respiratory acidosis. The rate at which carbon dioxide is eliminated from the body fluids through the lungs falls. This increases the concentration of carbon dioxide in the body fluids. As carbon dioxide levels increase excess carbon dioxide reacts with water to form carbonic acid. The carbonic acid dissociates to form hydrogen ions and bicarbonate ions. The increase in hydrogen ion concentration causes the pH of the body fluids to decrease. If the pH of the body fluids falls below 7.35, symptoms of respiratory acidosis become apparent.
Buffers help resist a decrease in pH, and the kidneys help compensate for failure of the lungs to prevent respiratory acidosis by increasing the rate at which they secrete hydrogen ions into the filtrate and reabsorb bicarbonate ions.( As well a limiter Kidney will get help from the compensator Respiratory system. )
In sport however the short term need of balance of H + only can take place over a perfect respiratory system. However, the capacity of buffers to resist changes in pH can be exceeded, and a time period of 1 or 2 days is required for the kidney to become maximally functional. Thus the kidneys are not effective if respiratory acidosis develops quickly, but they are very effective if respiratory acidosis develops slowly or if it lasts long enough for the kidneys to respond. For example, kidney cannot compensate for respiratory acidosis occurring in response to a severe asthma attack that begins quickly and subsides within hours. However, if respiratory acidosis results from emphysema, which develops over a long period of time, the kidneys play a significant role in helping to compensate.
Respiratory alkalosis results from hyperventilation of the lungs. This increases the rate at which carbon dioxide is eliminated from the body fluids and results in a decrease in the concentration of carbon dioxide in the body fluids. As carbon dioxide levels decrease, hydrogen ions react with bicarbonate ions to form carbonic acid. The carbonic acid dissociates to form water and carbon dioxide. The resulting decrease in the concentration of hydrogen ions cause the pH of the body fluids to increase. If the pH of body fluids increases above 7.35, symptoms of respiratory alkalosis become apparent.
The kidneys help to compensate for respiratory alkalosis by decreasing the rate of hydrogen ions secretion into the urine and the rate of bicarbonate ion reabsorption. If an increase in pH occurs, a time period of 1 or 2 days is required for the kidneys to be maximally effective. Thus the kidneys are not effective if respiratory alkalosis develops quickly. However, they are very effective if respiratory alkalosis develops slowly. For example, the kidneys are not effective in compensating for respiratory alkalosis that occurs in response to hyperventilation triggered by emotions, which usually begins quickly and subsides within minutes or hours. However if alkalosis results from staying at a high altitude over a 2 or 3 day period, the kidneys play a significant role in helping to compensate.
Metabolic acidosis results from all conditions that decrease the pH of the body fluids below 7.35, with the exception of conditions resulting from altered function of the respiratory system. As hydrogen ions accumulate in the body fluids, buffers first resist a decline in pH. If the buffers cannot compensate for the increase in hydrogen ions, the respiratory center helps regulate the body fluid pH. The reduced pH stimulates the respiratory center, which causes hyperventilation. During hyperventilation, carbon dioxide is eliminated at a greater rate. The elimination of carbon dioxide also eliminates excess hydrogen ions and helps maintain the pH of the body fluids within a normal range.
If metabolic acidosis persists for many hours and if the kidneys are functional, the kidneys can also help compensate for metabolic acidosis. They begin to secrete hydrogen ions at a greater rate and increase the rate of bicarbonate ion reabsorption. Symptoms of metabolic acidosis appear if the respiratory and renal systems are not able to maintain the pH of the body fluids within its normal range.
Metabolic alkalosis results from all conditions that increase the pH of the body fluids above 7.45, with the exception of conditions resulting from altered function of the respiratory system. As hydrogen ions decrease in the body fluids, buffers first resist an increase in pH. If the buffers cannot compensate for the decrease in hydrogen ions, the respiratory center helps regulate the body fluid pH. The increased pH inhibits respiration. Reduced respiration allows carbon dioxide to accumulate in the body fluids. Carbon dioxide reacts with water to produce carbonic acid. If metabolic alkalosis persists for several hours, and if the kidneys are functional, the kidneys reduce the rate of hydrogen ion secretion to help reverse alkalosis