Fortiori Design LLC
Registered: 1355349061 Posts: 1,530
We hope to have n short a E book ready for MOXY users with teh goal to use same wording and same explanations as we fast increase MOXY users all over teh world and we have to talk a common language.
One of our goals is to avoid from the beginning the idea, that we try to push moxy trends and information into a : classical: system with compassion of ANT, AT. LT, VT and all the threshold concepts out there. We like to have a new start here for us and simply use MOXY information to explain what we see and how we use this information. Here an interesting paper: Muscle oxygenation trends during dynamic exercise measured by near infrared spectroscopy. Source
Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Canada.
During the last decade, NIRS has been used extensively to evaluate the changes in muscle oxygenation and blood volume during a variety of exercise modes. The important findings from this research are as follows: (a) There is a strong correlation
between the lactate (ventilatory) threshold during incremental cycle exercise and the exaggerated reduction in muscle oxygenation measured by NIRS. (b) The delay in steady-state oxygen uptake during constant work rate exercise at intensities above the lactate/ventilatory threshold is closely related to changes in muscle oxygenation measured by NIRS. (c) The degree of muscle deoxygenation at the same absolute oxygen uptake is significantly lower in older persons compared younger persons; however, these changes are negated when muscle oxygenation is expressed relative to maximal oxygen uptake values. (d) There is no significant difference between the rate of biceps brachii and vastus lateralis deoxygenation during arm cranking and leg cycling exercise, respectively, in males and females. (e) Muscle deoxygenation trends recorded during short duration, high-intensity exercise such as the Wingate test indicate that there is a substantial degree of aerobic metabolism during such exercise. Recent studies that have used NIRS at multiple sites, such as brain and muscle tissue, provide useful information pertaining to the regional changes in oxygen availability in these tissues during dynamic exercise. between the lactate (ventilatory) threshold We all know the ongoing discussion due to lack of real values. We know that in some cases studies show that the lactate is increasing at the same time , where we see a clear shift in respiratory response like in VE. Therefor this groups state that VT = AT or LT. On the other side there are great studies showing that this is not really the case. We argue, that it is not the case , but if respiration is a LIMITER than we see the need of the body to find energy ( ATP ) production with less help of O2 so we will see an increase in lactate as a metabolic marker that glucose is used with some less help of O2 . In this cases the lactate increases at a similar place as VE may increase. If the respiratory system is the Limiter, than we will see at that stage a drop in SmO2 as a sign of delivery problem due to respiratory limitation and now we have at the same place a change in lactate ( metabolic sign  , a change in VE ( respiratory change) and a change in SmO2 ( oxygenation information.) In this case we have logically at the same time all the reaction we would expect , if respiration is the limiter as the body tries to change the behaviour of respiration with VE up , but we have to look why RF or TV or both or one down the other more up . Than we can see, if the respiration is the limiter as a metaboreflex reaction, so we not only have SmO 2 drop but as well tHb drop due to vasoconstriction. This leads to less O2 delivery for the same load and lactate will go up as a sign of a metabolic shift. CO2 will go up stressing repiration even more and this is the reason why in that client VT and SmO2 drop may be close to or at the same place in the same step. Now for "players" if at this stage you force yourself or the client to breath either very fast or very deep and slow ,you will have a change in lactate as well as a change in VT VE. but as well a change in SmO2 trend depending what you do. Try ity out and come back.
Fortiori Design LLC
Registered: 1355349061 Posts: 1,530
Here is an example we like to show to avoid confusion.
The regular reader is well aware by now, that we use the idea of LIMITER and compenator. So as an example. If I have in my clinic a client with a cardiac problem I know that the cardiac problem my be the Limiter. This is not always true as the respiration could have been the limiter and over years the cardiac system had to compensate so that it finally fails. That's when we have to go back and work on respiration and on cardiac training. Now back to our point. If the cardiac system is a limiter, the ECGM system will create under load a reduction in motorunit recruitment and as such by a simular load compared to a non cardiac limiter client the SmO2 will drop earlier and tHb will drop earlier. ( Portection of the vital systems on cost of the extremity muscle systems . The drop in motor units will create a higher contraction for the left over, still working units , to achive the same performance, there will be a compression on capillarise and as such tHb will drop, which makes it even harder to maintain performance as less O2 is delivered so SmO2 drops further ( delivery problem ) . The task to try to maintain performance is now moved to more involvment of the O2 independent energy deliver which creates a higher CO2 output as well as a higher H + production. so lactate will besides be used as energy , help as a buffer system moving H + out of the overloaded area . therefor we add to the already higher CO2 level additional CO2 over the H + situation, which increases the respiratory load which may now hit a limitation and vasoconstriction will increase ( metaboreflex). and so on. This has very little, in fact for us ,nothing to do with the lactate threshold, but it is still used from many places as they belive l lactate is the reaosn of fatigue . Here to enjoy Monitoring skeletal muscle oxygenation during exercise by near infrared spectroscopy in chronic heart failure. Source
Servizio di Cardiologia Riabilitativa, Istituto Lancisi, Ancona, Italy.
Patients with chronic heart failure (HF) have a reduced skeletal muscle blood flow which can in part explain reduced exercise tolerance and increased ventilation. All the techniques commonly employed to measure skeletal muscle blood flow have limitations that reduce their accuracy and clinical application. Near infrared spectroscopy (NIRS) is a noninvasive, inexpensive, and reproducible technique able to monitor muscle oxygenation both at rest and during exercise, providing information about tissue perfusion. The principle of NIRS is based on the observation that the light absorption characteristics of hemoglobin (Hb) and myoglobin (Mb) in the near infrared region (700-1000 nm) change depending on their relative saturations. In humans, NIRS has been employed to monitor skeletal muscle oxygenation during exercise and/or after cuff-induced limb ischemia in normal subjects as well as patients with chronic HF. Patients with chronic HF have a reduced Hb/Mb oxygenation at any matched work rate and a more rapid deoxygenation above
the anaerobic threshold than normal subjects. More recently, NIRS has been used to determine the kinetics of muscle oxygenation in recovery after constant work rate exercise, providing evidence of an inverse relation with cardiac function as assessed by peak oxygen uptake. In conclusion, NIRS appears to be a new promising noninvasive technique for studying muscle oxygenation in a variety of experimental models. (c)1999 by CHF, Inc. For us it is NOT the anaerobic threshold as the system is not anaerobic in the first place . it is the limitation of delivery and in some cases utilization of O2 due to protection of vital systems as well to avoid a critical drop in ATP.
Fortiori Design LLC
Registered: 1355349061 Posts: 1,530
As mentioned , the key is to try to have an open mind towards a new idea and try to blend out common confusing "classical" concepts.
The main info on mails I am getting from people is that they try to find a common value in classical ideas we have in our brains and MOXY an than they often do not fit together. Example: Interval MOXY and lactate. If you do a 200 or 300 m interval on your track and you take a lactate sample at the end of the run immediately, you may have a very low lactate value, which never ever fits the " feeling " you have. A few minutes later you may have a very high lactate value but. With the low value at the end of the run you felt "terrible" and with the high value 5 min later you are ready to go again ????? The SmO2 value is very low as well immediately after the run.Therefore fits your " feeling" after you just made a very strong energy demanding effort and as a part of the ATP demand you needed to take O2 as long and as much as possible. If it was not anymore delivered or the utilization was higher than the delivery SmO2 will show that immediately as you go. At the moment when you stop lactate will be low and SmO2 will immediately shoot up as a sign of refueling the O2 storage ( Mb ) and reloading Hb. So now you have actually a very high SmO2 and a very low lactate. During the run you have a steady dropping SmO 2 till to a certain level and you may have a plateau. A few minutes after the load SmO 2 may actually come down again but lactate may still go up. This is the difference between a real live on sport assessment with MOXY and an indirect information over a blood sampling on a finger . The lactate is a trend information of some metabolic changes but has very little info on where this problem may have occurred and where we may take lactate as energy source before it even shows up on the finger. When you start using MOXY try to add the info tHb can give you and start to think that your body works as a team ( rowing team) so what can influence what reactions instead of looking , where you may find a specific mathematical angel, a threshold or what ever. Here a direction more an more groups take now when using NIRS ( MOXY ) and it is great for us to see, that our many years of insisting in the idea of using more than just TSI % or SmO2 we can look at additional trend s from NIRS/ MOXY. Haemoglobin oxygen saturation as a biomarker: the problem and a solution. Source
Optics Division of the Martinos Center for Biomedical Imaging, Harvard Medical School, Massachusetts General Hospital, 149 13th St rm 2301, Charlestown, MA 02129, USA.
Near-infrared spectroscopy measures of haemoglobin oxygen saturation are often used as an indicator of sufficient oxygen delivery to assess injury susceptibility and tissue damage. They have also often been used as a surrogate measure of oxygen metabolism. Unfortunately, these measures have generally failed to provide robust indicators of injury and metabolism. In this paper, we first review when haemoglobin oxygen saturation does work as a robust indicator, and then detail when and why it fails for assessing brain injury and breast cancer. Finally, we discuss the solution to obtain more robust measures of tissue injury and cancer
by combining oxygen saturation measurements with measures of blood flow and volume to more accurately estimate oxygen metabolism. PMID: 22006898 [PubMed - indexed for MEDLINE]