I got a nice follow up question and as it is most likely a very common question I like to answer on here with permission of the e mail .
Q: The concepts sounds great, but far to complex to be used anywhere. ( Time , cost and more )
A: May be and as I am biased and work since years in this thought process , I may often forget, that we talk a different language , when we explain basic ideas. This is the case in many other areas we start to look into and I think it is more a question of giving it at least a try to see, whether we can understand it. I see often, that the main hindrance is the fact, that some classical ideas are getting somewhat under scrutiny and instead of asking the same questions we get for MOXY's limitation and use , we should apply the same question on what we do for the moment with VO2, lactate FTP and more.
Often we have a kind of a hesitation there to ask critically whether, what we do, may need once in a while some reviews to see, whether it still applies to what we learn new.
I like to show 2 critical questions: My point for FTP.
FTP is a perfect system to give you a very objective feedback on the average wattage and perhaps average HR you where able to sustain over a 60 min cycling load on a relative accepted circuit under this days conditions and this temperature and metabolic state of your body and many more factors.
All the same factors , which will influence HR or lactate or MOXY values.
Now once I have the FTP result I can easy calculate % of this one point value and than create calculated Zoning.
Than the rest is hope . I hope that every time I do a workout the body will react physiologically the same otherwise I am in trouble.. If I agree, that the body will not change performance, no matter , whether I am depleted with glucose or I had a bad night of sleep or the temperature is very different, than this system is perfect.
I f I may have some small doubts , that I do not feel every day up to the same task to reach the same average watt FTP , than I have to accept, that I may be off in my physiological stimulation despite being in the same wattage zone meaning I push the same watt load objectively for a watt load point of view.
Okay lets' make it easier. Here an example form two studies . One form Australia and widely published d and one form us small kitchen never publish but easy to repeat if somebody needs a paper to write.
Summary.. Guiding your workout daily with watt feedback has some clear limitation to see, whether the same watt is really the same physiological stimulus.
Here a second critical feedback form a study which is highly accepted.
The question, whether there is such a thing like a real LT. There are at least 20 plus different concepts and ideas out there on how we may or may not find a Lactate threshold. Does that may ask a question, why we have at least 20 top research who do not agree on one single idea of LT ?
Thee are even under this 20 + ideas three clear trends.
a) The once who believe in an absolute lactate number like 4 mmol or another absolute number.
b) the once who believe in a specific slope of a lactate curve by using a tangent or any model like 1 mmol increase over at least 2 steps or more, Using an angle against the curve like a 45 degree angle or 49.5 or 51 degree ???
Than the MAX LASS believer where you have to be able to maintain a relative plateau with some accepted increase over at least 16 min or other time frames.
The MAX LASS concpet makes actually lot's of sense. and it most liley can be " repalced" to ifnd MAX LASS by using MOXY's SmO2 information.
Determination of maximal lactate steady state in healthy adults: can NIRS help?
Bellotti C, Calabria E, Capelli C, Pogliaghi S.
Department of Neurological, Neuropsychological, Morphological and Exercise Sciences, School of Exercise and Sport Sciences, University of Verona, Italy.
We tested the hypothesis that the maximal lactate steady state (MLSS) can be accurately determined in healthy subjects based on measures of deoxygenated hemoglobin (deoxyHb), an index of oxygen extraction measured noninvasively by near-infrared spectroscopy (NIRS).
Thirty-two healthy men (mean ± SD age = 48 ± 17 yr, range = 23-74 yr) performed an incremental cycling test to exhaustion and square wave tests for MLSS determination. Cardiorespiratory variables were measured bbb and deoxyHb was monitored noninvasively on the right vastus lateralis with a quantitative NIRS device. The individual values of V˙O2 and HR corresponding to the MLSS were calculated and compared to the NIRS-derived MLSS (NIRSMLSS) that was, in turn, determined by double linear function fitting of deoxyHb during the incremental exercise.
V˙O2 and HR at MLSS were 2.25 ± 0.54 L·min (76% ± 9% V˙O2max) and 133 ± 14 bpm (81% ± 7% HRmax), respectively. Muscle O2 extraction increased as a function of exercise intensity up to a deflection point, NIRSMLSS, at which V˙O2 and HR were 2.23 ± 0.59 L·min (76% ± 9% V˙O2max) and 136 ± 17 bpm (82% ± 8% HRmax), respectively. For both V˙O2 and HR, the difference of NIRSMLSS from MLSS values was not significant and the measures were highly correlated (r = 0.81 and r = 0.76). The Bland-Altman analysis confirmed a nonsignificant bias for V˙O2 and HR (-0.015 L·min and 3 bpm, respectively) and a small imprecision of 0.26 L·min and 8 bpm.
A plateau in muscle O2 extraction was demonstrated in coincidence with MLSS during an incremental cycling exercise, confirming the hypothesis that this functional parameter can be accurately estimated with a quantitative NIRS device. The main advantages of NIRSMLSS over lactate-based techniques are the noninvasiveness and the time/cost efficiency.
Now below some more critical feedbacks on LT and its " existance
LT most likely could be just MAX LASS, but MAX LASS may depend on duration of the load.
MOXY's SmO2 is a live steady feedback so you can see, whethr you sustain a stable SmO2 by the same wattage or whether you have to reduce wattage to sustain a stable SmO2 trend.
Lactate and O2 during exercise: is lactate an anaerobic metabolite?
Numerous studies beginning with those of Pasteur (see Keilin, 1966) in the 18th century demonstrated that anoxia and hypoxia stimulate cellular HLa production. For example, in 1891, Araki (cited in Karlsson, 1971) reported elevated La− levels in the blood and urine of a variety of animals subjected to hypoxia. Then, Fletcher & Hopkins (1907) found an accumulation of La− in anoxia as well as after prolonged stimulation to fatigue in amphibian muscle in vitro. Subsequently, based on the work of Fletcher & Hopkins (1907) as well as his own studies, Hill et al. (1924) postulated that HLa increased during muscular exercise because of a lack of O2 for the energy requirements of the contracting muscles.
There is no disagreement that PO2 values in the range of ∼0.5 Torr or less result in O2-limited cytochrome turnover, and therefore O2-limited oxidative phosphorylation, a condition termed dysoxia (Connett et al. 1990). However, problems have arisen because of the application of the converse of this construct, i.e. that elevated HLa production and accumulation necessarily indicate the presence of dysoxia. This supposition formed the groundwork for the anaerobic threshold concept, which was introduced and detailed by Wasserman and colleagues in the 1960s and early 1970s (see Wasserman, 1984). The basic anaerobic threshold paradigm is that elevated HLa production and concentration during muscular contractions or exercise are the result of O2-limited oxidative phosphoryation. Similarly, standard medical practice has accepted an elevated blood La− concentration ([La−]) as the herald of O2 insufficiency (Mizock & Falk, 1992).
Over the past 35 years, considerable evidence has mounted against the idea of dysoxia as the primary cause of increased HLa production and accompanying increases in muscle and blood [La−] during submaximal exercise (e.g. Connett et al. 1986) and in some clinical situations as well (see below). Recently, Richardson et al. (1998) used proton magnetic resonance spectroscopy (1H-MRS) to determine myoglobin saturation (and thereby estimate intramuscular PO2) during progressive single-leg quadriceps exercise in humans. Increasing La− efflux with increasing work rate did not appear to be the result of inadequate O2 and thereby O2-limited oxidative phosphorylation. Instead, as the intramuscular PO2 (iPO2) decreases, oxidative metabolism becomes O2 dependent (see Gladden, 1996). Within some low range of iPO2 (< 20 Torr?), larger increases in [NADH]/[NAD+] and ([ADP][Pi]/[ATP]) are required to maintain adequate stimulation of cellular respiration to meet the aerobic ATP demand. The connection to increasing La− production and higher muscle and blood [La−] is that the requisite increase in ([ADP][Pi]/[ATP]), to compensate for the lower iPO2, is a potent stimulus of glycolysis. (For further details of this paradigm, see Connett et al. 1990; Gladden, 1996.) Accordingly, the best evidence indicates that O2 is only one of several interacting factors that cause an increase in muscle and blood [La−] at submaximal exercise intensities. Additional factors are listed in Table 1 and some are discussed in detail by Gladden (2003).
Lactate efflux is unrelated to intracellular PO2 in a working red muscle in situ.
Connett RJ, Gayeski TE, Honig CR.
Blood flow, lactate extraction, and tissue lactate concentration were measured in an autoperfused pure red muscle (dog gracilis). Muscles were frozen in situ during steady-twitch contraction at frequencies of 1-8 Hz [10-100% of maximum O2 consumption (VO2max)]. Myoglobin saturation was determined spectrophotometrically with subcellular spatial resolution. Intracellular PO2 (Pto2) was calculated from the oxymyoglobin-dissociation curve. Tissue lactate was well correlated with VO2 but not with Pto2. Lactate efflux increased markedly above a threshold work rate near 50% VO2max. Efflux was neither linearly correlated with tissue lactate nor related to Pto2. Pto2 exceeded the minimum PO2 for maximal VO2 in each of 2,000 cells examined in muscles frozen at 1-6 Hz. A small population of anoxic cells was found in three muscles at 8 Hz, but lactate efflux from these muscles was not greater than from six other muscles at 8 Hz. Our conclusions are that
1) the concept of an anaerobic threshold does not apply to red muscle and
2) in absence of anoxia neither tissue lactate nor blood lactate can be used to impute muscle O2 availability or glycolytic rate. A mechanism by which the blood-tissue lactate gradient could support aerobic metabolism is discussed.
Now I drifted as usual far off. So next up is the practical answer to show you how easy it is to use MOXY' and how far and how many different levels you can apply after you started to integrate the basic idea of using MOXY. So stay tuned for a practical session on this.