Development Team Member
Registered: 1440802274 Posts: 2
I hope this is the correct location to post my information and experience using SmO2 to monitor the current lifting phase.
Back squats: Phase 3 of 4 hypertrophy period. Lifting four days/week with a full break on Wednesday. Monday and Thursday are heavy lift days (65, 70, and 75% of one-repetition-maximum -1RM). Tuesday and Friday are light lift days (60, 65, and 70% of 1RM respectively.) Each percentile level consists of two sets of 10 to 12 repetitions each separated by 1.5 to 2 minutes of rest. Stiff-legged dead lifts: three sets of eight repetitions each separated by 1.5 to 2 minutes rest 51 year old, male, road-racing since 2009, firm user of periodization plans and quantified, goal-oriented training Routine: warm-up with 2 minutes of running stairs and no-load squats at the top/bottom of stairwell. Here's the results:
Starting SmO2 level (~50-70%) appears as expected at the left vastus lateralis location based on other workouts The recovery baseline was met in all squat lifts except after the second (~8:19:21) The target, or depletion baseline was met in all squat lift attempts SmO2 re-stock seems to replenish sufficiently, although the trend slope is steeper/quicker during intervals on the bike trainer comparatively Stiff-legged dead lifts (SLDL) follow the squats after weight change on the bar The current weight level of the SLDLs do not appear to produce the same SmO2 depletion rate as the squats previously The SmO2 SLDL re-stock rate seems rather slow compared to the squats rate Weight bar/rack clean-up occurs after the last SLDL (~8:39)
Monitoring format was based on the guidance from "Moxy Strength Training eBook." Full recovery was used between lifts as a starting point. Unfortunately, my device does not expose the tHb metric, although the text mentions using this metric as a performance indicator. (Would love to have a Moxy device of my own.)
Warm-up and bar setup ends at about 8:16. One difficulty was the inability to observe the real-time measure of SmO2 during lifting by use of the Tablet software application. The squat rack is outside and exposed to the weather, which in the current Seattle, Washington weather, would likely render the device unusable. Between-lift breaks are controlled with a stopwatch. I think in order to use the other recovery protocols, I would need to observe the SmO2 measures in real-time, or use appropriate stopwatch durations based on re-stock trends for like workouts.
It's likely that I didn't rest long enough after squat #2 in changing weights to the next level (65% 1RM,) hence the insufficient recovery level.
I'm not certain that the depletion target (~43%) meets requirements? Is this target sufficient to cause hypertrophy adaptation? Thoughts? I think that the SLDLs required their own recovery/target baselines since they are a different lift pattern. Thoughts?
I think I'm generally on the right track in order to achieve the plan intent and outcomes. My plan is similar to last year's; and contains corrections for lessons-learned. Your comments and thoughts are welcome! Thanks for reading.
(174.59 KB, 22 views)
Development Team Member
Registered: 1380484167 Posts: 1,501
Thanks so much for opening a discussion in this section of our forum. I am surprised this did not happened earlier on, as for strength workouts NIRS is possible a great choice. No please do NOT take anything I write here and we may have perhaps a long discussion and ideas exchange on here personal. I am getting it completely on what you do with your training ideas as I was brought up in the hay days of periodization's in Europe. I like to start as usual very different tan expected. Many many years back I asked myself the question. Does it has r to be really : No pain no gain Could we replace this perhaps with NO brain no gain ? Now lets' start there. The fundamental difference between a physiological feedback live guided workout and a calculator prepared workout. In a simple picture e it would look like this So let's dive into your great feedback. Back squats: Phase 3 of 4 hypertrophy period. Lifting four days/week with a full break on Wednesday. Monday and Thursday are heavy lift days (65, 70, and 75% of one-repetition-maximum -1RM). Tuesday and Friday are light lift days (60, 65, and 70% of 1RM respectively.) Each percentile level consists of two sets of 10 to 12 repetitions each separated by 1.5 to 2 minutes of rest. Not personal remember. But how do we know we can do another workout tomorrow just from using numbers and days ? Do we know whether you recovered. what's happened when your muscle after a workout looks like this here. As you can see from the date 1984 no new question. This is a muscle biopsy after an eccentric overload. Straight leg dead lifts for example are eccentric loads at least for you hamstrings and other muscle groups. So timing of repair between loads is a very important part of performance improvement or more important injury prevention. So the timing can be figured out with using NIRS in combinations with some other tools like SEMG and some blood markers as well. Using this combination help us to get some ideas, how to use NIRS feedback , when we can not afford all the other goodies. So this the point of how often as a number versus how often as physiological feedback. Next up : hypertrophy periodThere are as usual different ideas on how to load to create hypertrophy. The common discussion is done in % calculation, as we all do or id based on 1 rep max load. As all max loads 1 rep is a very mentally changing number and highly depends on daily motivations. And much more Where most agree is that the load should bee 65 % and up from your 1 rep max. The hyper trophy takes place so empirically this seem to work inmost of us . The one reason , which seem to trigger hypertrophy is HYPOXIA Here a great short info on this Hypoxia increases muscle hypertrophy induced by resistance training. Nishimura A 1, Sugita M, Kato K, Fukuda A, Sudo A, Uchida A. Author information 1Department of Orthopaedic Surgery, Mie University Graduate School of Medicine, Tsu City, Mie Prefecture, Japan. Abstract PURPOSE:
Recent studies have shown that low-intensity resistance training with
vascular occlusion (kaatsu training) induces muscle hypertrophy. A local hypoxic environment facilitates muscle hypertrophy during kaatsu training. We postulated that muscle hypertrophy can be more efficiently induced by placing the entire body in a hypoxic environment to induce muscle hypoxia followed by resistance training. METHODS:
Fourteen male university students were randomly assigned to hypoxia (Hyp) and normoxia (Norm) groups (n = 7 per group). Each training session proceeded at an exercise intensity of 70% of 1 repetition maximum (RM), and comprised four sets of 10 repetitions of elbow extension and flexion. Students exercised twice weekly for 6 wk and then muscle hypertrophy was assessed by magnetic resonance imaging and muscle strength was evaluated based on 1RM.
Muscle hypertrophy was significantly greater for the Hyp-Ex (exercised flexor of the hypoxia group) than for the Hyp-N (nonexercised flexor of the hypoxia group) or Norm-Ex flexor (P < .05, Bonferroni correction). Muscle hypertrophy was significantly greater for the Hyp-Ex than the Hyp-N extensor. Muscle strength was significantly increased early (by week 3) in the Hyp-Ex, but not in the Norm-Ex group.
CONCLUSION: This study suggests that resistance training under hypoxic conditions improves muscle strength and induces muscle hypertrophy faster than under normoxic conditions, thus representing a promising new training technique. So here is where we now with live feedback of NIRS have a great step forward. a) do we create a hypoxia b) how do we know the SmO2 value shows hypoxia or the muscle will have to go hypoxic with the load I apply ? Here a case study from our own kitchen done by a student from UBC ( university of BC) during his summer break in my office . Nick Mc Lean. We assessed maximal contraction force using SEMG and NIRS. Than we loaded different % of max NIRS activity to find out how Rhonmerts idea of reduction in blood flow due to muscle compression really looks in reality. So by what % of contraction force do we see a reduction in blood flow due to muscle compression. Here the result by 67 % of maximal contraction force and what we see in NIRS The vertical line is where he quit( his decision) Color: Green is as usual SmO2 %. Blue is HHb ( deoxygenated Hb /Mb) Red is O2Hb so oxygenated Hb /Mb Purple kind is thB ( total hb /Mb) You can see SmO2 simply indicates, that he used immediately O2 . ( which asks the critical question of " anaerobic" versus newer ideas of O2 immediately involved in any activity ) More fun is to follow tHB trend. Look carefully. Do you find a) compression outflow ? Or as we discussed perhaps better reduction of tHb or reduction in blood volume. I like from a visual point n of view the wording outflow ( but it may bee wrong ) b) thb increase. " outflow restriction due to higher compression force form outside /muscle contraction , than vasodilatation effect form CO and other vasodilatation options. c) complete occlusion situation. and already motivational problems or brain protection and early release of complete occlusion till hee gives up. In a subsequent forced occlusion test he was able as he had no choice to drop SmO2 down to 0 % so very low. Was he hypoxic ?? We will get back to this perhaps But first stay in general. NIRS: SmO2 alone can give some indication but it is not a great way to control strength loads as suggested. What we know is that trained people working on these idea of hypertrophy can desaturation very low. meaning that they really go very low on O2 content so hypoxic. Now as in the article you can do this very local on a muscle group or you can do it systemically. a) locally . You have to see, how your workout improves the drop in SmO2. The bets way to force SmO2 to drop is to be able to create an occlusion. To see, whether you are able to do this you can use tHB trends. See below an example of squatting. Green is SmO2 , yellow/brown is tHb trend # sets and than the body told us , that's it. Extreme version. Numbers versus physiology. Physiological guided workouts are mentally hard to do. You do not know how many sets you will have to do, you do no t know how long rets in between you do not know how often during the week. You really know nothing. Now workout based on numbers. You know everything what concerns the operation organisational plan. How much do you know what really goes on ? Why 10 - 13 2 reps , why 1 min break and so on. Physiological guided workouts are very short if the gaol is to deplete as low as posisbel and as fast as possible. They can be very long if you do not push yourself and than change the idea of stimulation. What we know is , that stimulation of GH growth hormones are not based on number of sets but intensity of load. and possible % of muscle mass involved in total body workouts versus isolated body workouts. So this leads us to a first summary. Strength workouts are based when you use physiological feedback like NIRS on your goals setting as usual. 1. Do you like to keep delivery somewhat open so tHb may drop only. 2. Do you like to keep inflow going but create a stop in outflow than tHB will increase till you quite. Immediately after you quite you see a drop in thB as a sign of a outflow after occlusion or outflow restriction. 3. Do you like like in your case to create a Hypoxia for triggering hypertrophy you can do that over a local reaction or a systemic reaction. No you have to create a stable tHb ass a feedback of an arterial occlusion. or you have to be able to drop SmO2 not just locally but systemically as a sign of a hypoxia generated in the systemic circulation. For this you can sue one NIRS and one SpO2 sensor. or 2 NIRS one on the involved muscle group and one on a minimal involved muscle group. At the end the workout would look. Squatting to exhaustion weight unimportant . As heavier as faster you may desaturate as you can easy cravat an occlusion but as faster you may cheat as well and get injured. How many sets. : depending on the goal. Do you like to recover back to baseline. ( complete recovery do you like to over compensate do you like to incomplete recover Below 2 of the three options : what is what ? Both examples from NEXT Level coaching Brian Kozak One form a swim workout in thee water using NIRS and one from an ice hockey ion ice workout. Simply looking at metabolic recovery What does NIRS SmO2 tells us in metabolic feedback ? A brief review of the use of near infrared spectroscopy with particular interest in resistance exercise. Pereira MI 1, Gomes PS, Bhambhani YN. Author information 1Departmento de EducaÃ§Ã£o FÃsica, Universidade Gama Filho, Rio de Janeiro, Brazil. Abstract
There is growing interest in resistance training, but many aspects related to this type of exercise are still not fully understood. Performance varies substantially depending on how resistance training variables are manipulated. Fatigue is a complex phenomenon usually attributed to central (neuronal) and/or peripheral (muscular) origin. Cerebral oxygenation may be associated with the decision to stop exercise, and muscle oxygenation may be related to resistance training responses. Near infrared spectroscopy (NIRS) is a non-invasive optical technique used to monitor cerebral and muscle oxygenation levels. The purpose of this review is to briefly describe the NIRS technique, validation and reliability, and its application in resistance exercise.
NIRS-measured oxygenation in cerebral tissue has been validated against magnetic resonance imaging during motor tasks. In muscle tissue, NIRS-measured oxygenation was shown to be highly related to venous oxygen saturation and muscle oxidative rate was closely related to phosphocreatine resynthesis, measured by (31)P-magnetic resonance spectroscopy after exercise. The test-retest reliability of cerebral and muscle NIRS measurements have been established under a variety of experimental conditions, including static and dynamic exercise. Although NIRS has been used extensively to evaluate muscle oxygenation levels during aerobic exercise, only four studies have used this technique to examine these changes during typical resistance training exercises. Muscle oxygenation was influenced by different resistance exercise protocols depending on the load or duration of exercise, the number of sets and the muscle being monitored. NIRS is a promising, non-invasive technique that can be used to evaluate cerebral and muscle oxygenation levels simultaneously during exercise, thereby improving our understanding of the mechanisms influencing performance and fatigue.
Development Team Member
Registered: 1364386800 Posts: 168
Skipper / Juerg, hi. I second, it's great to read some activity from the ST topic.
I do a little MOXY guided ST at my gym and usually process like this: 15 min. Client warm up period for calibrating individual oxy/deoxy levels
60-75 min. Client is coached within live display of muscle oxy/deoxy range
1. Load to the minimal SmO2 level achievable, try to maintain for a rep or two at most and move to recovery (usually see a deflection of SmO2). RECOVERY: 1. Recover back to highest SmO2 or 'warmup level'. 2. Recover briefly to stay below SmO2 'warm up level'. 3. Recover longer to see if we can "overshoot" the SmO2 'warm up' level. 3a. Load as soon as we see an "overshoot" of the SmO2 'warm up' level. 3b. Load after the SmO2 "overshoot" decreases and again client reaches the SmO2 'warm up' level.
Volume for each ST exercise:
Move to next exercise/lift when no longer can reach SmO2 'warm up' baseline level within a sensible reload period...
OR Move to next exercise/lift in sequence when no longer can reach greatest DEOXY level, despite best effort to maintain proper/safe lifting. Inter Set / Intra Workout Variations:
Explore both break down sets and progressive loading increases with limited recovery to further decrease SmO2 Level
As mentioned in other topics... we now try to move the focus of lifting exercises from intermuscular - intramuscular. Juerg mentions below that hypoxia is one of the main mechanisms associated with hypertrophy outcome. I'm curious to discuss this idea of hypoxia-induced hypertrophy a little further from a perspective of tHb trends and wonder if the hypertrophic effect will be best from a series of workouts using an increased tHb (muscle pump) load OVER a series of workouts using a decreased tHb effect (muscle compression outflow) load. Thoughts ? PS, I mostly work with non-athletes and generally see the tHb drop 9 of 10 times during most lifts when we first get started.
Development Team Member
Registered: 1380484167 Posts: 1,501
As mentioned in the article and as we do since many years. we choose two option.
1. Local hypoxia 2 systemic hypoxia. 1. local hypoxia is used when we do rehab on specific target muscles . so little coordination is involved. This is a great idea for rehab, as we often can do full muscle slings or muscle chains yet due to restrictions like weight bearing or other forces which may be not applied in that stage. It is not a great idea of strength for health but as well as for sport, as it completely misses the neurological as well as dynamic motion pattern. Sorry big fitness chains, but I believe the development of this huge gyms with this huge equipment collection is doing minimal to nothing besides being a good business for overall health and prevention in our population. It may not even be true that it is better than nothing ( Smile ) I just can't see the physiological value of a biceps curl equipment for a few thousand dollar to make a single joint single movement pattern as a progress in our health and fitness promotion. Movement have to be as soon as possible full patterns of natural motions to actually benefit from the workout. We name it DNA as a pattern which shows up in any movement with a natural idea and will run in a kind of a spiral motion like a DNA pattern. So I do not think a cyclist benefits relay from a double leg squatting for his sport that great. He needs a DNA pattern. Same with many other sports. The interesting part is that the sport where we see thee most amazing strength development and ability to move the body is gymnastiques. Non of this world class athletes ever sets a foot in a gym to lift weights. Exception again if they are injured you may have to make some exception for some time. So when we do local hypoxia wee initially trry, whether the contraction force in the target muscle can create arterial occlusion so that we can deoxygenate down so we have a hypoxic reaction. Now I have two option if I can no yet create this contraction force like in beginners. a) I add some restriction in delivery to it and monitor. b) I create a insufficient bio availability for O2 2. Systemic hypoxia. This is used, when I work in our DNA pattern. I can again have tow options. a) create first a hypoxia and than immediately follow with the exercise b) create the hypoxia during the exercise. Now I can create hypoxia two way's 1. By really stimulate utilization so I drop SmO22 as far as possible . 2. I reduce the bioavailability of O2 so SmO2 will actually increase during the load So many options to do that. I often do 2 sets +- sometimes just one set for one DNA pattern. Sometimes two just to confirm really that the first one did its job and overloaded. So therefor I often do not use the recovery of SmO2 but I often use the tHb trend in recovery. Occlusions tend to create an increase in tHb after each load. Now this is the case, when we do an actual occlusion artificially. In a natural created occlusion we have a different reaction after we let go with a much more pronounce occlusion outflow due to the integration of a much higher CO. The small problem is , that lab work and studies have to do this as of yet as in the pats there are very few studies looking at the blood flow or volume reactions besides what we do practically. There is one nice newer study recognising some problem with blood flow. Too bad that they did not look at tHb as they had all there to see it. Evidence for restricted muscle blood flow during speed skating. Foster C, Rundell KW, Snyder AC, Stray-Gundersen J, Kemkers G, Thometz N, Broker J, Knapp E. Source
University of Wisconsin-LaCrosse, 54601, USA.
firstname.lastname@example.org Abstract INTRODUCTION:
We have previously hypothesized restricted muscle blood flow during speed skating, secondary to the high intramuscular forces intrinsic to the unique posture assumed by speed skaters and to the prolonged duty cycle of the skating stroke.
To test this hypothesis, we studied speed skaters (N = 10) during submaximal and maximal cycling and in-line skating, in both low (knee angle = 107 degrees) and high (knee angle = 112 degrees) skating positions (CE vs SkL vs SkH). Supportive experiments evaluated muscle desaturation and lactate accumulation during on-ice speed skating and muscle desaturation during static exercise at different joint positions.
Consistent with the hypothesis were reductions during skating in VO2peak (4.28 vs 3.83 vs 4.26 L x min(-1)), the VO2 at 4 mmol x L(-1) blood lactate (3.38 vs 1.93 vs 3.31 L x min(-1)), and cardiac output during maximal exercise (33.2 vs 25.3 vs 25.6 L x min(-1)). The reduction in maximal cardiac output was not attributable to differences in HRmax (197 vs 192 vs 193 b x min(-1)) but to a reduction in SVmax (172 vs 135 vs 134 mL x beat(-1)). The reduction in SV appeared to be related to an increased calculated systemic vascular resistance (354 vs 483 vs 453 dynes x s(-1) x cm(-1)). During maximal skating there was also a greater % O2 desaturation of the vastus lateralis based on near infrared spectrophotometry (50.3 vs 74.9 vs 60.4% of maximal desaturation during cuff ischemia). The results were supported by greater desaturation with smaller knee angles during static exercise and by greater desaturation and accelerated blood lactate accumulation during on-ice speed skating in the low vs high position. The results of this study support the hypothesis that physiological responses during speed skating are dominated
by restriction of blood flow, attributable either to high intramuscular forces, the long duty cycle of the skating stroke, or both.
[PubMed - indexed for MEDLINE]
Here is an example of an ACL recovery patient where we have different levels of contraction strength so occlusion is reached with a very different pattenr yet and he is ready to go back to high performance sport when this pattern is equal. If he goes to early high riks for a reinjured situation .
Development Team Member
Registered: 1380484167 Posts: 1,501
I had some e mail exchange yesterday after my comment on here with some interesting people. Discussion point.
How low SmO2 should drop and how long should it stay that low ? Here is where many have to understand the limitation in a local NIRS application and how a local respond connects to a systemic situation. If you go to the long discussion we had on U shape tHb trends you see what I mean. There is a idea out there we all leaned and that is the great idea of the Fick equation. What we as well know now is that the Fick equation is a feedback forma systemic point of view. But there is more and more evidence, that there is a very great local reaction on blood flow or better oxygenation ability build in our physiological systems so that O2 is getting there where it is most needed. Now there is a difference when we look at local muscle strength with small muscle groups or individual muscles involved as pointed out and systemic workouts so whole muscle chain involved like a DNA workout. When we look blood flow regulation and O2 delivery in endurance sport we have to look at the much bigger picture than when we look a local biceps curl. On the other hand when we look bigger muscle chain workouts we are getting much closer or equal respond as we get with endurance loads. Here as a repetition for strength coaches on the systemic view . Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation? Calbet JA, Joyner MJ. Author information Department of Physical Education, University of Las Palmas de Gran Canaria, Campus Universitario de Tafira s/n, Las Palmas de Gran Canaria, Spain. email@example.com Abstract
In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle.
The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [approximately 300 mL (100 g)(-1) min(-1)], but the pumping capacity of the human heart is limited to 20-25 L min(-1) in untrained subjects and approximately 35 L min(-1) in elite endurance athletes. My add on > So a STEADY " FIGHT" OR BALANCE BETWEEN VASODILATATION TO PLEASE o2 DEMAND OVER A GOOD Delivery AND A Steady VASOCONSTRICTION OPTION TO Maintain the NEEDED Local AND SYSTEMIC BP. . This means that when more than 7-10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when approximately 80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure.
PMID:So what I think and see form years of using this idea is, that hypoxia alone is not an optimal tool as we may see a reduction in recruitment pattern when we stay too long in a hypoxic or very low SmO2 situation.
Now is the SmO2 " good " or bad when low. It all depends on tHb. If I have an arterial occlusion I will lower SmO2 due to delivery stop and as such I may loose an optimal feedback on SATP levels and too long may be bad on a low SmO2 level. What as well happens here is the at we see a reduction in SEMG activity most likely as a protection to reduce ATP use as long as possible to maintain a stable mingle needed level for survival of the cell. If I look low SmO2 levels in systemic workouts and I have a still normal or open tHb reaction than I do not worry at all. What we often see is a flat SmO2 a flat but still same level SEMG and we may see an overall reduction or no further increase in performance. But what we often see if performance is still improving is an additional inter muscular help form other muscle groups who can support this movement Now you can see why I lie to have SmO2 and tHB in the same picture One for metabolic feedback situation SmO2 and how much I have left in the tank to give me an option to push more as I may be able to utilize more or whether I simply are balanced but no further chance to increase performance and tHb which gives me feedback on volume or thB concentration change in the observed area.
Development Team Member
Registered: 1440802274 Posts: 2
Thank you for your thoughts and references. I hope my interpretations in the following outline are reasonably correct. The items are in no particular order: Interpretations o At the system level Â§ Quantification is difficult. I know of methods such as: Â· Rated perceived exertion (RPE) Â· Morning heart rate compared to average or baseline Â· Heart rate variability tracking and comparison o At the locomotor/peripheral level Â§ Possibly subjective, such as â€œOuch, my legs really ache this morning.â€ Â§ No other method known to me P1h lifting plan is similar to the Kaatsu test method Dropping SmO2 o Locally/peripherally Â§ Best way to drop SmO2 locally is to produce an occlusion Â§ Best way to detect an occlusion is to observe tHb trend Â§ Occlusions tend to increase tHb after load o Systemically Â§ Options to produce hypoxia Â· Stimulate utilization to drop SmO2 as far as possible Â· Reduce the bio-availability of O2 so SmO2 actually increases during load Â§ Hypoxia alone is not an optimal tool regarding the recruitment pattern as a protection to reduce ATP use Pituitary gland secretes GH based on intensity of load (>65%? 1RM) After re-reading your responses and references, I asked myself "What one change can I make to improve my method based on my new understanding?" It appears that stimulating a hypertrophic response can be likely done by producing work at the muscle(s) of interest under a system hypoxia. I thought a conservative test change (incomplete recovery/reduced bio-availability of SmO2) would be to reduce the recovery time from 2 minutes to 1 minute between sets. Reader, please note that my device does not provide access to tHb measures, only SmO2. Figure 1. The workout before: We can see that squat SmO2 level recovers to the baseline in Figure 1. Figure 2. Reduced or partial recovery In Figure 2, I performed a static, non-movement measurement with my device for 3 minutes, then a warm-up for two minutes before moving to the squat bar outside my home (denoted by "1".) Unfortunately, when I finished and downloaded my data file, I noticed that my device attachment to my left VL was faulty, which produced the "signal loss" areas in the graph. Questions In Figure 2. I see that the reduced wait-time between sets did not allow SmO2 to recover to Figure 1 levels. So maybe this change contributed to a beneficial, (local) hypoxic condition contributing to hypertrophy? In Figure 2, should the recovery baseline point be located at the end of the warmup period ("red line")? If this is correct, then isn't my recovery excessive for a local hypoxia to occur?
As always, thank you for your thoughts,
Development Team Member
Registered: 1380484167 Posts: 1,501
Nice and great summary.
Not a lot to add to the summary. There are different options you can look for systemic recovery and less optimal once for local recovery as you point out. I showed somewhere in the forum how we assess recovery for endurance sports. What can you do different. Well if you are successful do not change anything. The feedback form the SmO2 form your squatting is hard to analyze as we do not knwo , whether you actually had a chance to be hypoxic or drifted towards hypoxia. A dropping SmO2 indicates a higher utilization than delivery at that time in that muscle. So as the word says higher utilization , but u you still use O2. There are some fun practical approaches we did in the past with lactate believers and people using a dropping SmO2 as an indication of lactate increase( Boulder Colorado workshop ).. It is easy to show , that we can drop SmO2 and when we create this situation we use more O2 and we may see lactate actually dropping and not increasing. So a dropping SmO2 ina squatting ca mane , great O2 use or it can mean problem with delivery and you move towards a hypoxic direction. tHb will tell you this whether you load that you can achieve a hypoxia or whether you load and create perfect O2 utilization stimulation. Depending of your goal you like to see one or the other. In fact I use often the opposite situation to be sure I can go hypoxic . I try during the load to stop SmO2 drop by changing O2 bio-availability in the system and a s soon this happens I load to create an arterial occlusion either with muscle contraction if possible or with a specific pressure pump system . With athletes I never use a cuff system always their ability to contract.