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Registered: 1451945333 Posts: 61
or worse, now i see, it may not be asthma, but actual exercise induced hyperventilation!
http://www.ncbi.nlm.nih.gov/pubmed/10400486 Exercise-induced hyperventilation: a pseudoasthma syndrome. Hammo AH, Weinberger MM. Abstract BACKGROUND: Exercise-induced asthma is common and generally responds well to an inhaled beta2 agonist. OBJECTIVE: We examined the physiologic changes in airflow and gas exchange that occurred during standardized treadmill exercise in patients previously diagnosed with exercise-induced asthma whose histories appeared atypical or where conventional treatment, including an inhaled beta2 agonist, was ineffective. METHODS: During a 1-year period 32 patients, aged 8 to 18, met these criteria. All had been previously diagnosed as having exercise-induced asthma. Exercise consisted of treadmill running at a time when the patients had received no inhaled beta2 agonist, cromolyn, or nedocromil for at least 4 hours. Spirometry was done before and at 2, 5, 10, and 15 minutes after exercise; oxygen saturation was monitored by pulse oximetry; and end-tidal CO2 was monitored with nasal cannula. RESULTS: Despite their previous diagnoses of exercise-induced asthma, 11 patients who described chest tightness during exercise had decreases in FEV1 less than 15% with all but one of those less than 10% (mean decrease 5.6%) but demonstrated decreases in end-tidal CO2 greater than in all of the other 21 patients (mean 23.2 versus 9.8%, P < .01). Only 4 patients had unequivocal evidence for bronchospasm with cough and wheezing accompanying chest tightness in association with decreases in FEV1 from 18 to 22%. Seventeen patients had neither their symptoms reproduced nor physiologic abnormalities. CONCLUSIONS: These data show that chest discomfort perceived as dyspnea during vigorous exercise may be associated with hypocapnia from hyperventilation without bronchospasm in children and adolescents previously misdiagnosed and treated as having exercise-induced asthma.
Development Team Member
Registered: 1380484167 Posts: 1,501
Sandor , wwoww thanks so much for this replay as it gives me a perfect opportunity to show the fundamental changes in exercise physiological testing. I originally had a whole sets of graphs from rowing ready to explain the data's you sent in comparison to some world class rowers I have the fortune to support with some ideas and suggestions.
So here what I will try as I have approximately 50 mails who all will benefit from this section here. My original hope was, that VO2 classical believers would actually trigger his discussion but as so often it works out differently. Here what I hope to get done on the weekend. I gently but clearly will show and disagree with the abstract and the full study you use to back up the idea of an exercise induced hyperventilation during workouts. I will try to make the case, that the equipment and data collections they used move the conclusion in a very different direction, than what we see when we combine VO2 (EtCO2 ) but we never would use EtCO2 alone as it is only a small help as we need to know the reactions intracellular or in the blood so to start out look what EtCO2 means, where it is it tested and is EtCO2 really under activity = PaCO2 and PA co2. Is RQ under activity like a harder workout really RER. Why does RQ definition for fat and glucose between 0.7 AND 1.0? But RER is often above 1.0 ? We have to accept the limitation in EtCO2 and FeO2 % in VO2 test equipment when compared to the actual location we look with NIRS ( same for lactate lovers) EtCO2 and FeO2 % are tested at the mouth or nose level as an indirect, delayed feedback on gas exchange from the muscular level plus some dead space interference in between. Than because it was the at the time bets and easiest way to test we simple equaled EtCO2 = PaCO2 ??? The interesting time will be soon here, where thanks to COSMED Italy we now have more people doing what we do since years comparing live directly mask or nose gas values with actual changes intramuscular with NIRS or actual blood gas analyzing with sampling blood. So the new VO2 equipment from Cosmed can be combined with MOXY. ( And the above study could be reviewed again with data's from different places and not just EtCO2 at the mouth level. We will have for classical VO2 user some sleepless nights ahead if we not start thinking in a combination and accept the fact that classical VO2 is a team summary of what happens in different teams members and will confuse many initially (as it did it to us ) Here to start very short. The time lag in EtCO2 values compared to the SmO2 reaction and tHB trend will be the topic of discussion. You will have a very low EtCO2 depending on respiration ( TV, RF and dead space and respiratory pattern like ratio of inspiration to expiration time ) But you may see a very fast drop in SmO2 due to a very high intramuscular PaCO2. But a very low EtCO2 at the mask level . Why ? Than you may have a very high EtCO2 but an increase in SmO2. Why ? Very similar to lactate dynamic combined with SmO2 trends. A drop in SmO2 ( fast drop ) may not show up as an increase in lactate in a test sample but we may have an increase in SmO2 and than an increase in lactate ???? Hope you see where we go with this. Now start to read carefully the pdf file not the abstract from Sandors used research. I used that exact study about 4 years ago with my grade 11/ 12 student to show the relative risk off using studies blindly even if pear review if the data collection misses certain crucial reactions. Here what you search in the study.as it is a interesting section where they contradict their own conclusion. 1. Hyper ventilation as per definition will reduce CO2 pH up . these creates a left shift of the O2 disscurve . which increases affinity of O2. and SpO2 will go up. Look for : Mean decreases in O2 saturation and end-tidal CO2 in those patients were similar to that seen in the four patients who experienced wheezing and coughing in association with chest tightness
What causes O2 sat SpO2 as they tested it to drop ? Or in other words where does the O2 diss curve has to shift to have the affinity to create the drop in SpO2 ?
If this may be the case what happens there to CO2 and pH if the O2 disscurve shifts to get this affinity reaction ? How can the CO2 concentration in the moth test influence the O2 diss curve in the body. Here a practical experiment the grade 11/ 12 student had to do. 1. Hold your breath. test MOXY reaction in the biceps and quadriceps as you hold the breath. Describe be what you see and why. 2. Repeat the experiment but measure the EtCO2 as soon you have to give up holding your breath . What do you see e and why ? 3. Repeat the test but breath shallow ( using only dead space TV. So you will have to v create a RF of 3o / 40 / 50 . Look at the live EtCO2 values and live SmO2 values , what do you see and why ? 4. What do e expect when testing PaCO2 in the blood as the names suggest and the DEtCO2 with the capnometer you use. . What is the conclusion form this basic experiment ? follow up discussion we had.
a) how will a biased close look on O2Hb and HHb look when we have a delayed EtCO2 reaction.
Draw a hypothetical tHb O2Hb and HHb trend. b) explain the below values and meaning and why they support the O2Hb and HHb reaction of the squatting exercise ? What causes the lack of re saturation O2Hb trend in the left activity compared to the right. The above data's are courtesy to Per Lundstrome form the seminar we had at the Red Bull research center in Santa Monica California.
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Registered: 1380484167 Posts: 1,501
Only 2 responses ( mails ) so far. so like to give some more hints.
. Definition of dead space. What influences dead space at rest and what during a load ? - If we look at EtCO2 in combination with SpO2 than we have always if we test during a load look as well at VE ( l/Min and how VE is created over RF and TV. Here three examples for a real situation . VE ( l/Min is 90 l/min) VE 90 Athlete 1: RF 30 / min A 2 : 45 / min A 3 : 60 / min TV ? dead space % ? Here result from 3 rowers sent to us from a USA test center which starts to combine VO 2 and MOXY. ( The head coach doing this assessment is from Europe ) Below three athletes and you see the graph of Respiratory frequency development during a VO2 max test Now below the same athletes same test . Tidal volume reaction now how could this affect the EtCO2 and the PaCO2 ? here the CO2 ( EtCO2 trend of all three below Now if we look how the CO2 and O2 reacted taken one out of the three see below. Which of the above 3 atheist is this O2 CO2 reaction what TV and what RF ? The result will be a very low EtCO2 O2 diss curve shift to the left ???? Hmm where is the CO2 ??? so O2 disscurve shift to the right ??? If it is a exercise induced " hyper ventilation " than we have O2 disscurve to the ??? and SpO2 would be ???? Now here the study graph where they concluded it is an exercise induced hyper ventilation. below graph from the study You can see EtCO2 drops so "conclusion " hyper ventilation which would mean O2 disscurve to the left see below because if EtCO2 low due to systemic low CO2 than PaCO2 will be low as well. If this is the case we have an easy way to " glue " O2 so SpO2 will go up. This is the reason why fetal Hb can take on O2 as the mothers O22 disscurve is more on the right so easy give up and O2 and fetal Hb easy pick up as more on the left. Now to proof that the EtCO2 is really due to hyper ventilation they have to show the respiratory reaction so VE TV RF as shown above plus as well use PaCO2 blood test to see, whether their conclusion is true.. I can not see any of the back ups in the study. So if SpO2 drops than we may have a O2 disscurve to the right so harder too pick up O2 in the lungs to the blood but easier to use O22 from the blood to the cell. Question . How can we use MOXY now here, if we can not afford an I start or a blood testing blood gas option. What would we see in SmO2 reaction and what would we see in tHb reaction when we suddenly stop the load so CO and VE are up but no demand anymore of O2 or better less demand of O2 and no muscle compression influence on tHb ? Summary . Their explanation paired with their graph indicate a drop in EtCO2 due to respiratory reasons rather than a hyper ventilation as EtCO2 down in the mouth area but SpO2 down as well in the blood ) Hyper ventilation would create a low ETCO2 and a low PaCO2 and a increase and high SpO2. Hyperpnea but hyper capnia in the muscle will create a low EtCO2 / a high PaCO2 which can not escape due to the respiratory limitation and will therefore shift to the right the O2 disscurve so back up for this over a drop in SpO2 ( hypoxia hypercapnia ) and the next back up will come over MOXY trend of tHb and SmO2 . how is that trend looking ? or best blood gas support. When we talk in respiration on this issue we have either a hyper ventilation, which can be voluntary or a reaction ins certain situation or we have a exercise create hyper pnea Why is this interesting. Well for ay coaches who may earlier or later start to use physiological stimulation over performance created stimulation ,as you may like to know what you create or like to stimulate you have to understand how respiration, cardiac reactions, blood flow and delivery/ utilization actually influence each other daily, no matter what % of a training zones you believe in. . Physiological training means I apply a specific stimulation in a very specific load so I can decide the reaction I like to archive.
Registered: 1363469067 Posts: 45
I am hoping the new equipment we are bringing to market will help this discussion along, by CLEARLY indicating breath rates and tidal volumes, as well as adding information on VO2. Please feel free to have a look at our short video, and imagine how easy it will be to assess respiratory factors with the vo2 Master. Even more exciting for those reading this forum will be the implications of using live respiratory feedback in TEACHING athletes to breathe better, much like we used to do with the simple Bioharness, but now, improved data and simple app to help with analysis.
Development Team Member
Registered: 1375288126 Posts: 51
Hi Andy, great work! Something, that I was looking forward to have for a long time :-)
Could you just explain littble bit about the technology? How do you measure flow and FeO2 and, and how do you calculate other measures. Thanks! Jiri
Registered: 1363469067 Posts: 45
The technology is a pantented process for measuring volumes that is not much different than some of the lab-based desktop vo2 monitoring devices. We were able to eliminate the moving parts, and incorporate the oxygen sensor into the small mouthpiece. From the flow volume measurements and FeO2 data, it is simply a matter of calculating the difference between the inspired oxygen content and the expired content to yield the volume of oxygen consumed. The big leap forward was removing the wires and cables, which we were able to accomplish with the help of a very smart engineer. We are just producing our Version 2 at the moment, with testing starting again in the next few weeks. We hope to have Juerg's feedback from a unit we will send him in August, once we clean up a few challenges and improve the accuracy, which currently sits at 2-3% different from pan-based equipment. However, I am confident that some of that perceived error is actually on the lab unit, which samples continuous air flow through a long tube, with the inherent error that occurs with that method. Our unit has a much higher sampling rate, located much closer to the source, who'd I believe will yield more accurate and more reliable values.
If you see the website, you will see we are taking pre-orders, at a price of only $999, which means you can purchase a unit for about the same cost as it currently takes to pay for two vo2 max tests at a "testing centre".
I will try to post csv data from a 5-1-5 this weekend, along with Moxy data to show changes due to training from this spring. I will look forward to feedback, and comments, but mainly am excited to see how the VO2 data can help with the discussions and training ideas Juerg is bringing to this great group.