Maximal RSA test
Athlete runs specifically defined test course (it can involve agility too) with MAX effort (altought the speed will decrease over time). For example
10x40m with 30sec rest (walking)
From this test we can get:
Best 40m time
Worst 40m time
Average time
Standard deviation
Total time (summ of all 40m runs)
Fatigue Index [ (Worst-Best)/Average * 100]
For all of those 6 variables I would love that someone provide the following resuts:
Correlation with VO2max tests (direct, indirect : shuttle runs, both speed at VO2max and ml/min/kg )
Correlation with LT (both runing speed, and VO2max at LT)
Wingate test correlation with all of those variables (For measuring of anaerobic lactic production)
Some other Lactate toleration test, like repeated 300m runs or suicides for basketball
When we collect those correlation, both with cross and longitudinal studies, we can say something, but till then we can only speculate…
Sub Maximal RSA test
Athlete runs specifically designed test course with submax speed, expressed in absolute terms (m/sec, or distance time) or in relative terms (80% of best sprint).
For example
Repeat 40m runs @85% (best 40m) with 30sec rest.
When the athlete is unable to repeat runs around definded time + 5% the test is stoped and the number of reps represent test results.
This test give us the folowing:
number of reps of repeated sprint with submax speed while the athlete is able to manage to do the setted time
Speed reserve expressed as MAX best time on 40m run minus submax speed at which 40m is run.
The test should be repeated with various submax speeds.
What we are looking for here is the following
The correlation of speed reserve with number of reps done
Correlation of VO2max (speed and ml/m/kg), LT (speed, %VO2max, ml/m/kg) with number of reps
Correlation of Wingate with number of reps
Correlation of some lactate capacity test with number of reps done
Correlation of number of reps with Fatigue Index from maximal RSA test!
Repeat for various submax speeds
UNTIL we have both tests done, we cannot say what affects anything with certainity… We can only speculate till that!
From this my post, someone could easily propose 20 experiments… This would answer questions like: which energy systems defines RSA both max and submax, what is relation of speed reserve with submax RSA!
The example is someone benching 90kg, and would love to improve number of reps at 70kg.
I think that he should first develop greater reserve (improve 1RM), because there is a lot of correlation of number of reps with submax weight (until 70%) with 1RM value.
While the 70kg falls into 70% zone, improved 1RM will improve number of reps with 70kg.
After the 70kg falls below 70% of 1RM, that athlete should spend more time improving somekind of strength endurance.
Thus, we can cetrainly say that athlete A with 90kg 1RM will do more reps with 70kg than athlete B with 80kg 1RM… The line here is 70%, under that zone, reserve (1RM-kg which they would like to lift) DOES NOT PLAY IMPORTANT ROLE as does strength endurance!
Where is this line with repeated submax runs and speed reserve? Also 70%?
I think that 80% will be more appropriate with submax RSA.
Take an example:
Athlete A: max speed 40m 4.3s
Athlete B: max speed 40m 4.7s
Who will do more reps at 5.0s repeated 40m?
Athlete A: speed reserve = 0.7secs (16%)
Athlete B: speed reserve = 0.3sec (6%)
I would give my money on athlete A, that he is going to do more reps!!!
When the submax speed drops down even futher, exiting from 80% of max, then speed reserve will have minor role and the result will depend on some other factor: be it ‘general endurance’ or something more precise term
Off top of my head LaFontaine et al. (1981) would give you a very short answer to part of your questions regarding Max RSA Test, i.e., between sprint and LT -the latter defined as one of the many ways in the literature…
If peak running velocity correlates well with most of the performance variables mentioned above and for a great range of distances, I would expect the same to happen with any pure-speed drill as well. Speculation, of course…
If you can execute, or find a longitudinal such study, please let me know…
Duxx,
In your example…
[b]Where is this line with repeated submax runs and speed reserve? Also 70%?
I think that 80% will be more appropriate with submax RSA.
Take an example:
Athlete A: max speed 40m 4.3s
Athlete B: max speed 40m 4.7s
Who will do more reps at 5.0s repeated 40m?
Athlete A: speed reserve = 0.7secs (16%)
Athlete B: speed reserve = 0.3sec (6%)
I would give my money on athlete A, that he is going to do more reps!!!
When the submax speed drops down even futher, exiting from 80% of max, then speed reserve will have minor role and the result will depend on some other factor: be it ‘general endurance’ or something more precise term [/b]
For athlete A (4.3) a 5.0 second run is 85%
For athlete B (4.7) A 5.0 second run is 94%
So I believe undoubtably that Athlete A is going to be able to do more reps. After all this is what speed reserve is all about!!
It becomes more tricky when you have a 4.3 and 4.5 guy (Note in a 40 .2 is a large difference). For these athletes…
Athlete A (4.3) a 5.0 second run is 85%
Athlete B (4.5) A 5.0 second run is 89%
Now what?? Who is better now? And at what point do you shift your training towards more aerobic stuff or “stuff” to specifically improve there RSA?
YOU DONT!! The faster you are the quicker you can get to the ball and the the better speed reserve based on your top speed the better off you are. As we said (as proved in studies) V02 Max have very little coorelation to RSA and when trying to improve the aerobic system you must be aware of the ceiling effect that exists. So it seems like we need to decide what do we need to acheive as optimal aerobic capacity and how can we measure this?
Also I like your ideas in Test #1. However test 2 does not seem worth doing. What if the athlete trys to pace himself and accidently falls off one rep which by your instructions would stop the test prematurely.
It seems as though strategy would play a large role in this test.
Nik,
We dont disagree!!
Were just trying to figure some things out (more details) and how we can relay our points to other people/coaches with proof and examples.
I agree with Quik, test one seems to be a solid test, another way to go about it would be to use something like you purpose for the 2nd test, you could have the runners run at max speed over whatever distance, and have them repeat the sprint until their performance drops by a certain percentage of their predetermined max say somewhere in the 7% range maybe, just a thought.
Also the 2nd test will be very hard to perform just with my experience of trying to run at set percents for tempo runs, and depending on the subjects you may have some subjects coming in at 95% and wearing out fast and other coming in right at the 85% range, and others coming in at 84% who still have plenty of energy in the tank.
Also (what types of athletes will you be testing) perhaps it won’t be that big of a deal, but I would expect strength athletes to be able to still put up impressive numbers (charlie’s example of the shot putter being able to run with the sprinter the first few step) for one or two reps then their numbers following off more dramatically then say a sprinter or soccer player.
For example, in highschool I was a football player (lots of strength training and single jumps minimal sprinting) and in track I was a mid/long distance runner. I had endurance, i had strength, I would kill at our preseason combine in 40yd, however when we would have conditioning before the season started I would get beat by most of the team in repeat 10-20x40yd with 36 sec rest.
Quik, i think you have the right idea here. But, when do we know when we are putting too much time in working on trying to get someone faster and missing out on training other beneficial qualities? Law of Diminishing Returns…are we gonna kill ourselves trying to knock off that extra .05 when there may be other important “stuff” that we could be training that would be beneficial to RSA?
Which leads me to Scott’s last post about “specific endurance”. This is the other “stuff” we are talking about. I hope Scott gets back on here soon because i am a bit confused on the “specific” part. In his HIIE paper he basically stated that a well trained aerobic system is the best way to buffer bLA and improve RSA (unless i am fogetting something, its been a while since i read it). Now, is this the “specific” endurace you are talking about…even though it may be a general means of training? Or, are you in agreement with Duxx that as the season nears max accels with short recovery are good for “specific endurance”? Not sure if i misunderstood something.
Wish i could add more right now but am getting killed at work and will get on here asap.
I tottally agree with you guys regarding that submax RSA test… hardly done! There is a problem on running distances within 2secs, and we are here talking about tenth of seconds… unposible!
Here is another expand of your example Quick:
Athlete A (4.3) a 5.0 second run is 85% (Had large Fatigue index @max RSA test)
Athlete B (4.5) a 5.0 second run is 89% (Had small fatigue index @max RSA test)
Who will do more reps? I’ll bet on Athlete B… But if we reduce speed even more so its fall in “aerobic zone” who will dominate… We are talking about different abilities here! Thing are way to complex…
So to conclude:
The success at submax RSA test (or submax runs in game situations) depends on complex relations between Speed Reserve, Fatigue Index, Submax Speed! Key word here is COMPLEX!
So to conclude, submax RSA test is not posible to do, it will give small number of information except it is done with great number of submax speed… Lets keep a discussion on max RSA test!
Couple of thoughts:
Is it worth spending enourmous number of time in increasing soccer player’s 40yard dash for 0.05 sec to increase his “game speed”?
Note that game speed involves (a) appropriate tactics, thus being at the right time on the right place or to say slower 40yard dash will be faster at 20m then faster 40yard dash player at 30m from the ball, (b) apropriate slection of stimuly (where does the player looks - experience - hips, ball, eyes, field etc), (c) reaction speed, (d) selection of appropriate motor response, (e) optimal programming of that response, (f) raw speed, (g) cutting, stoping etc… Note that this is only simplification
Where is the line here?
Note that soccer speed can be trained in more Specific conditions. For example: two players stands at 1/3 of the field, coach kick the ball to the goal, players try to take a ball from each other and to score a ball. The first to the ball attacks and the another defends the goal… there is numerous of posibilities… This brings me to the next point:
Altought I believe that short sprints with short rest will dramatically increase RSA I dont think they are needed to be trained separatelly, because game practice, various games with a ball etc will cover it in more specific way…
Altough this may be better than “shuttles” at max effort for 20-40sec for improving RSA. This brings us to the solution that, with a good base of general speed and aerobic conditioning (via high intensity, @70%, interval aerobic training), RSA will be improved by the game practice itself!!!
My opinion is that speed work, as the prep period goes on, should be developed in more and more specific situations… This will allow to use the new levels of speed in soccer specific situations and to peak into sport form… Somewhere in the middle of the season (depends how long it is) the speed work again switch to general without ball starts etc to maintain raw speed, prevent from boredom, maintain sport form etc…
“Work capacity work”, as a base for RSA, should progress from submax shutles (start and stop at submax speed - preparation for speed and agility work), tempo work (as agility and joint stress increase due general specific means in speed), aerobic games with a ball (to allow peaking, like zones games, criss-cross runnning with passes etc), then again tempo due joint stress from games itself… There is no need for short sprints with short rest work, 400m runs etc, the game(s) and practice will cover this issue… But this is just mine opinion!
A well trained aerobic system is necessary and will aid in the oxidation of lactic acid during rest periods. However, the point of the paper was to review the research regarding how well the aerobic system needs to be trained for RSA. Obviousy, there is some necessary standard that needs to be met - after that other factors come into play.
I am in agreement with Duxx that as the season nears some type of max accel with short rest (in the form of linear work or agility work depending on the sport) is necessary for specific endurance - especially the ability to buffer La - and please don’t read too much into this - but also to develop some level of ‘mental toughness’ (without being stupid about it).
So, as you said it seems like we need to decide what do we need to acheive as optimal aerobic capacity and how can we measure this?
Please forgive me if this has been answered in your paper. I haven’t had a chance to read the full version in its entirety.
I am really glad to see you contributing to this thread!! As you know this is a not yet well researched area and discussion this kind is very productive! I wish only that Spencer and Bishop were here
Regarding your post…
The premise that oxydative system helps remove LA and thus increase RSA is based on the idea that LA is a “poisonuous toxin” which cause fatigue, which is not true. Altough bLA raise follows raise in H+ (or decrease in pH) it is not direct cause of fatigue. Some research says that H+ is not the cause of fatigue too. Some “point finger” to inorganic phosphate (P) or disturbance between Na/K inside and outside the cell. The last, but not the least, is the CNS contribution to fatigue, but this is another story!
The true story regarding source of H+ ions in cell is the breakdown of ATP/CP and NOT of glycolisis (anaerobic) (Gladden, Robergs). The mitochondria uses both LA, H+ (+O2, +Glycogen) and thus prevents from H+ buildup. If the ATP/CP break-down is faster than mitochondria phosphorilation (due lack of enzymes, number and size of mitochondria, O2 -> capilarization, trasport capacity of blood, heart minute volume etc), or H+ influx is larger that H+ eflush to mitochondria, then the H+ buildup will happen… and the lack of ATP/CP used for energy… and here is when glycolisis starts to produce new ATP/CP and LA! So, build-up of H+ and LA are timely related but not directly connected… The question is: DO THEY DEVELOP FATIGUE?
Another thing that confuses me here is that is “believed” that ATP/CP break-down is the fastest energy-producing process, followed by glycolisis, folowed by oxydative phosphorilation. But new research found that during Wingate test oxygen is used more powerfully than thinked… thus suggesting that aerobic processes are not so slow than thinked…
Note that muscles have thousands of motor units (MU), and all of them have their properties like number of capilaries, mitochondria etc. So, HOW the brain RECRUITS them may present a crucial factor in increasing endurance. Also, there is a LA shuttle between them, so they can help each other by using LA produced.
I have never consider (any) running as “aerobic event” because during the foot-strike and push-off the more powerfull MU are engaged and energy is created by “anaerobic” processes, while during the leg swing phase the homoeostasis is put back to normal with aerobic processes… So, any type of movement is a COMBINATION of “homoeostasis perturbation” and “homoestasis return” like in the case of running. If those two processes are not in “harmony” fatigue develops, but not as “catastrophe impairment”, but rather as a protective mechanism which reduces the “homoestasis perturbing” activity (in this case the running speed). So, classification of aerobic/anaerobic is flawed… very flawed!
I don’t know why I am writing this essey, but I got inspiration and I hope you are still following me here…
As you have written in you Final paper, HIIE may induce more level of bLA level due the nature of activity itself and larger FT MU used…
On my opinion, during sprints (in HIIE), FT twich are recruited due their powerfull contraction. Their aerobic capacity is fairly low, thus to return homeostasis to normal (ATP/CP level), larger proportion of glycolisis is used and the byproduct is LA. Created Lactate and H+ shuttles to more ST fibers and blood during recovery. ST fibers (which are also used more in sprints and jogs during recovery) uses LA and H+ to return their homoeostasis to normal (ATP/CP cell level). The excess H+ is buffered with bicarbonate buffers (and others), which transport them to lunges (kicked out as CO2 and H2O) kidney and liver. LA also serves as a buffer (it protects from fatigue and not cause it). Because blood is redistributed to muscles, bLA uptake by liver, kidney is reduced. Thus bLA level rasies more because of reduced LA uptake than production…
So, to be successfull in HIIE sports, with regard to RSA and under the “cardiovascular/anaerobic model” approach athlete should:
Improve power of FT fibers (speed training)
Improve the shuttles of H+ and LA from FT fibers to blood and ST fibers (via capilariyation and lowering cell membrane resistance)
Improve the uptake of LA and H+ of ST fibers
Improve the oxydative capacity of ST fibers (both central and peripheral) without affecting FT fibers. If ST fibers have low oxydative capacity they would not be able to use byproducts of FT fibers and would also use more glycolisis to return their own homoeostasis, and this will increase H+ even more and the fatigue onset will be faster.
Improve the LA uptake by various organs including heart
Improve the blood redistribuition during rest, so that the ANS fastly increase blood flow trough kidneys and liver during rest periods -> Improve “switching of blood redistribution”
Improve the H+ buffering and transoprt to lunges and kidneys
Improve the RECRUITMENT order during activity and during recovery periods
Improve heart, kidney, lunges, liver function and their ANS control
As contrary to 99% physiological books, in factors affecting HIIE performance I included both CNS and ANS!!!
Tempo running bellow 70% (HI “aerobic” training) will produce great effects with HIIE athetes, because:
it uses FT fibers but not so strenuously or too long to transform them or to affect speed sessions
it forces ST fibers to uptake LA and H+ produced during a a run
it stimulates ST oxydative capacity
it increase capilariyation in whole muscle
it produces LA and H and thus stimulates buffering capacity
it improves recruitment order and control of blood redistibuition, heart, kidney and liver because of its intermitent nature
its intermitent nature “teaches” optimal control of CNS and ANS in homoeostasis control
It have greater hip movement
It spares joints and glycogen compared to continuous running.
bla, bla, bla (outlined in Tempo??? thread)
Why HI shuttles and SE2 work sucks:
it forces FT and ST fibers to use glycolisis during a work periods (instead during recovery to return homoeostasis to normal)
it transforms FT fibers in more economic glycolitic machines instead in more ATP/CP breakdown machines (read slows them down)
cant be done with enough number of reps to affect ANS control of blood redistribution, etc.
It affects speed session
But they improve buffer capacity
I hope you are not have fallen in a deep sleep till now… I had some inspiration to write this… I hope it will direct futher discussion into “new and unexplored”…
Svass said that “aerobic system is necessary and will aid in the oxidation of lactic acid during rest periods. However, the point of the paper was to review the research regarding how well the aerobic system needs to be trained for RSA. Obviousy, there is some necessary standard that needs to be met - after that other factors come into play.”.
Oxydative capacity is measure with VO2max, and as stated it contribute to RSA till some point, after that some other factors come in play… Some of the factors outlined in this post may have the important role.
Note that Bishop & Spencer found great increase in RSA performance in interval group compared with continuous group of aerobically trained athletes. Physiological variables suchs as VO2max, LT, betam, La, etc were not significally different between them, thus improvement in RSA is not explained by those factors… But they didnt thinked about improved RECRUITMENT of CNS and increse of his “upper limit” regarding what is safe… One EMG measurement should be done too!
This open a milion o questions, espeially when CNS and ANS are involved…
“As complexity rises, precise statements lose meaning and meaningful statements lose precision”. --Lotfi Zadeh
Duxx - VERY nice summary. Hope you haven’t lost too many people.
“As complexity rises, precise statements lose meaning and meaningful statements lose precision”. --Lotfi Zadeh
Exactly - when you get down to the actual science that backs up what you are seeing in training, the answer often comes down to - “We have a good idea, but we’re not really sure.” Trying to sum everything up in a thread like this is pretty damn hard.
Robergs, Robert A., Farzenah Ghiasvand, and Daryl Parker. Biochemistry
of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol
287: R502–R516, 2004; 10.1152/ajpregu.00114.2004.—The development of acidosis
during intense exercise has traditionally been explained by the increased
production of lactic acid, causing the release of a proton and the formation of the
acid salt sodium lactate. On the basis of this explanation, if the rate of lactate
production is high enough, the cellular proton buffering capacity can be exceeded,
resulting in a decrease in cellular pH. These biochemical events have been termed
lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the
biochemistry of acidosis for more than 80 years. This belief has led to the
interpretation that lactate production causes acidosis and, in turn, that increased
lactate production is one of the several causes of muscle fatigue during intense
exercise. This review presents clear evidence that there is no biochemical support
for lactate production causing acidosis. Lactate production retards, not causes,
acidosis. Similarly, there is a wealth of research evidence to show that acidosis is
caused by reactions other than lactate production. Every time ATP is broken down
to ADP and Pi, a proton is released. When the ATP demand of muscle contraction
is met by mitochondrial respiration, there is no proton accumulation in the cell, as
protons are used by the mitochondria for oxidative phosphorylation and to maintain
the proton gradient in the intermembranous space. It is only when the exercise
intensity increases beyond steady state that there is a need for greater reliance on
ATP regeneration from glycolysis and the phosphagen system. The ATP that is
supplied from these nonmitochondrial sources and is eventually used to fuel muscle
contraction increases proton release and causes the acidosis of intense exercise.
Lactate production increases under these cellular conditions to prevent pyruvate
accumulation and supply the NAD needed for phase 2 of glycolysis. Thus
increased lactate production coincides with cellular acidosis and remains a good
indirect marker for cell metabolic conditions that induce metabolic acidosis. If
muscle did not produce lactate, acidosis and muscle fatigue would occur more
quickly and exercise performance would be severely impaired.
Lactate analysis has been used by many athletes and physiologists over the last decade as a tool for predicting endurance performance. Specifically, the higher the percentage of VO2max, or the higher the pace at which the lactate threshold occurs, the fitter the athlete. Many researchers have placed the lactate threshold - the maximum concentration that an athlete can maintain during a steady state effort - at around 4mmol/L. But others have found that lactate concentrations can vary widely, with some athletes capable of maintaining concentrations as high as 8mmol/L over sustained periods.
A new study has measured the lactate response to a cycling time trial in which the participants were instructed to cycle as far as they could in a period of one hour, with lactate samples collected every 10 minutes. The athletes averaged 40.8k during the trial at an average 83% of maximum heart rate. Lactate concentrations ranged between
5 and 12mmol/L, with an overall average of 7.6mmol/L. Mean lactate concentrations and pace remained relatively stable throughout, suggesting the athletes were maintaining a constant maximum steady state effort.
The implication is that when athletes select their own pace, a constant effort can be maintained despite high lactate concentrations. This raises serious doubts not just over whether 4mmol/L can be regarded as the lactate threshold point but whether the concept of a lactate threshold is relevant to athletic performance. It may be that the long-term accumulation of lactate during a race or time trial is much higher than the levels found during incremental tests in the laboratory, which questions the validity of lab-based lactate testing as a way of predicting performance.
The study found a wide degree of variation in lactate concentrations between athletes. Since there was no correlation between lactate concentration and performance, this suggests a link with individual muscle fibre type. For example, an athlete with a greater proportion of type IIa fibres will produce more lactate than one with more type I fibres, even with identical performances.
So is there any point in lactate testing? Certainly the observed variations in concen-trations that can be maintained for long periods would cast doubt on its use for predicting performance. And there may be little association between lactate found in the lab and that found in competition conditions.
Lactate testing may need to be restricted to individual longitudinal tests at a fixed workloads. For example, testing the lactate response to a 20-minute run at 12kph would be an objective measure of aerobic fitness for an individual athlete which, if repeated regularly, could be used to determine training status and assess the effects of a training programme on the aerobic system.
Medicine and Science in Sport and Exercise 33(1), 152-156
C’mon guys, are you scared with little physiology?
I have just recieved an e-mail letter from David Bishop, one of the most prominent researches of RSA in the field, in which he send me couple of his sci papers! We have the support from the best people in the field regarding this “project”…!!!
I am just in a proccess of applying the theme of my final paper, but I have some troubles with mentor, because Faculty Policy demands that my mentor have to be the chief of my department, and he is an assh* who stole from me my seminar work and put it in his textbook as his own words… BTW my seminar has 30pp and his book 280pp, so I should be co-author of the book… Anyway, I still have 3 exams under that assh and I plan to prosecute him on a court!!! What do you guys think about this?
I’m not sure how it works over there, but at the very least I would have him brought in front of the university ethics committee. That is complete BS (stands for bullsh*t in english Duxx).
I have just sent a letter to University rector (dean) regarding this issue… The problem is that I still have 3 exams under this ASSHOLE and according to faculty policy he should be my mentor for my final paper BS! He don’t even know what does HIIE and RSA stands for MF! I am really pissed-off… I am not scared to bring this to light, includig calling the news services…
You should love to know what are they doing on other faculties here in Serbia: they give students for final paper to do some project (architecture, melioration etc) and when they defend it the teacher SELL it as a project for some firm and get money for student work… I am really sick of academc criminal here in Serbia! First posibility and I am out of this country and region!!! BS!
