Thanks and great feedback.
Allow me to ask some critical questions not with the intension to take anything apart, but to show you how we differ more and more form the great "classical" theories we all know and used and try to adpapt and integrate ideas now available thanks to new technology.
The below questions based on the answer above form yoru coach are for us again a greta way to show you, that we would have given the same answer 10 - 15 years back, than went through a phase of major confusion ( and are sometimes still conused ) as more and more studeis started to question classical believes due to new technology.
So the questions are an example of loud thinking on our part. that is it , and not a critic on anybody out there.
So PLEASE do not look at this as a we know it all and you know nothing , but look at it as a challange we all face together in the comming years.
So before we do some questioning with some feedback I love to use a section from T. Noakes paper
How does a foundational myth become sacred scientific dogma?
The case of A.V. Hill and the anaerobiosis controversy
by Tim Noakes
Lessons from a medical training
The first great lesson of medicine is to teach oneâ€™s supreme level of personal stupidity. Indeed there is a collective level of medical ignorance, so brilliantly described by Dr Lewis Thomas (1985: 10):
The greatest single achievement of science in this most scientifically productive of centuries is the discovery that we are profoundly ignorant. â€¦ I wish there were some formal courses in medical school on medical ignorance; textbooks as well, although they would have to be very heavy volumes. We have a long way to go.
Indeed, the beauty of the Textbooks of Ignorance would be their accuracy. I am reminded of these quotations whenever a scientist expounds the ignorance of absolute certainty. Regardless of any appearance of individual brilliance, we are each profoundly ignorant. And never more so than when we are absolutely certain of our most brilliant opinions.
This distinctive characteristic of modern medicine to challenge the truth (Le Fanu 1999), explains the intellectual paradox captured in the classic quotation attributed to a former Dean of Harvard, Dr Sydney Burwell by G.W. Pickering (1956: 14), himself formerly Professor of Medicine at the University of London and a protagonist in one of the classic medical arguments of the twentieth century (Swales 1985): â€˜My students are dismayed when I say to them, â€˜â€˜Half of what you are taught as medical students will in 10 years have been shown to be wrong. And the trouble is, none of your teachers know which halfâ€™â€™â€™.
The second great advantage of my medical education was that it included nothing about the exercise sciences, other than that which I taught myself. Learning in this way has important disadvantages, but one unique advantage is the avoidance of indoctrination, which is the tendency towards a stubborn, if subconscious, acceptance of a specific scientific mindset or prejudice that we acquire from our venerated tutors whom we assume to be intellectually infallible (Waller 2002). This could perhaps be termed the Tyranny of the Founder Effect.
So below now questions we had to ask ourself and again I use the answers from what we all would answer.
1.) Improvement of the anaerobic lactic capacity by improving the lactic production, buffering and tolerance of the muscles (aka winning the final)
a) what if there is no such thing like anaerobic ?
Richardson et al have concluded that: â€˜â€˜â€¦intracellular pO2 remains constant during graded incremental exercise in humans (50â€“100% of muscle VO2max)â€™â€™ so that: â€˜â€˜With respect to the concept of the â€˜â€˜anaerobicâ€™â€™ threshold, these data demonstrate that, during incremental exercise, skeletal muscle cells do not become anaerobic as lactate levels suddenly rise, as intracellular pO2 is well preserved at a constant level, even at maximal exerciseâ€™â€™ (p. 63168). They also conclude that: â€˜â€˜Net blood lactate efflux was unrelated to intracellular pO2 across the range of incremental exercise to exhaustionâ€™â€™ but was â€˜â€˜linearly related to O2 consumptionâ€™â€™ (p. 62768). Another study confirmed these conclusions: â€˜â€˜â€¦consequently these data again demonstrate that, as assessed by cytosolic oxygenation state (deoxy-Mb) during incremental exercise, skeletal muscle cells do not become â€˜â€˜anaerobicâ€™â€™ as lactate levels rise, because intracellular PO2 is well preserved at a low but constant level even at maximal exerciseâ€™â€™
b) what is lactic capacity ? how do we meaure this , when we do not know what is produced nor what is used. Nor do we know when the value we read is produced in a 10 x 30 seconds workout or a 3 min step test. We have a number from teh finger that is all.
Thirdly, an alternate or a complementary explanation to the pattern of plasma ]La-] response to ramp exercise can be suggested. According to this explanation, lactate is produced in the working muscle: (1) as soon as the exercise begins, as suggested by Brooks (1985); or (2) following a delay, according to the theory of the anaerobic threshold (Davis 1985). Under both hypotheses the onset of lactate production within the working muscles occurs at comparatively low work rates. At that time: (1) the amounts of lactate produced and the gradient between muscle [La-] and plasma [La-], and the amount of lactate released from the muscle remains small; (2) cardiac output and muscle blood flow are also low and do not favour lactate release
from the working muscles and its distribution into S; and (3) the small amounts of lactate released are diluted within the comparatively large S, thus resulting in a very small increase (if any) in plasma [La-]. Therefore,
a delay could be expected between the beginning of lactate production within the working muscles and the parabolic rise in plasma [La-] in response to ramp exercise in a similar way that, in response to a short period of severe exercise, the peak value of plasma [La-] is only observed following a several-minute delay into the recovery period (see Hirvonen et al. 1987, 1992). Consequently, plasma [La-] concentration at a given t during a ramp exercise does not reflect lactate production in the muscle at that precise t and at the
exact corresponding work rate, but at a previous t minus ~ of unknown and probably variable length, and at the corresponding work rate. This phenomenon might have been overlooked in the development of the theory
of the anaerobic threshold which implicitly assumes that plasma [La-] at a given t reflects lactate production and thus the metabolic state of the muscles at that precise t, and at the exact corresponding work rate. This is very unlikely to be the case, particularly during the exercise protocols of short duration and with steep increase in work rate used for the detection of the anaerobic threshold (Anderson and Rhodes 1989). In this type of protocol, where VO2 significantly lags behind the value expected for the corresponding
work rate (Whippet al. 1981), it may be expected that plasma [La-] also tracks the metabolic state of the working muscles with a significant delay, particularly at the beginning of exercise for the reasons presented above.
d) why do you have to tolerate lactate when in fact adding lactate improves performance.
Respiration and respiratory training, more than just for fun.
: "Because lactate is combusted [metabolized] as an acid (C3H6O3), not an anion (C3H5O3), the combustion of an externally supplied salt of lactic acid, CHO3H5O3- + H+ + 3O2 Â¨ 3H2O + 3CO2 effects the removal of the proton taken up during endogenous lactic acid production (Gladden, L. B. and J. W. Yates, J Appl Physiol 54:1254-1260, 1983). A side benefit of alkalizing the plasma
by feeding lactate would be to enhance movement (efflux) of lactic acid from active muscles into plasma, a process which is inhibited by low (relative to muscle) blood pH.
(Brooks, G. A. and D. A. Roth, Med Sci Sports Exerc 21(2):S35-207, 1989; Roth, D. A. and G. A. Brooks, Med Sci Sports Exerc 21(2):S35-206, 1989). Moreover, maintenance of a more normal blood pH during strenuous exercise would decrease the performer's perceived level of exertion. The conversion of lactate to glucose in the liver and kidneys also has alkalizing effects by removing two protons for each glucose molecule formed, 2C3H5O3 + 2H+ Â¨ C6H12O6. Thus, whether by oxidation or conversion to glucose, clearance of exogenously supplied lactate lowers the body concentration of H+, raising pH."(22)
e) does the person with the highest o2 independent ability wins the race or the person with the better O2 availability ?
Glycogen Turnover Forms Lactate during Exercise
Robert G. Shulman
Department of Diagnostic Radiology, Yale University School of Medicine, MR Research Center, New Haven, CT
Could it be, that the athlete with the higher ability to maintain ATP production over O2 may win the race and not the guy with the short term timebomb ability to use somewhat more O2 independent energy sources. How far down can you drop with ATP ?
Evidence That Glycogen Rather Than PCr Generates ATP during Contraction
The conventional view of short-term muscle energetics is that PCr supplies almost all of the energy needed for a sustained burst of contractions lasting less than 10 s, after which it is replaced by glycogenolysis. This view is not supported by experiments. In a recent review, Greenhaff and
Timmons (5) report, â€œIt is now accepted, however, that PCr hydrolysis and lactate production do not occur in isolation, and that both are initiated rather rapidly at the onset of contraction.â€
The proposal that glycogenolysis is the ultimate energy source for exercise is supported by studies on patients with McArdleâ€™s disease. In this genetic metabolic disorder, glycogen phosphorylase is completely inactive. Patients experienced exercise intolerance and muscle cramping.
31P NMR studies (11) of the resting muscle in these patients showed normal PCr, ATP, and Pi levels, but a decidedly higher pH 7.2) than in control subjects (7.02 0.01). During either moderate or high-intensity short-term exercise, PCr decreased much more rapidly in the patients than in the control subjects, whereas the pH remained high, and ATP levels remained constant. The inferred minimal lactate production
in the McArdleâ€™s patients relative to control subjects is evidence that normal muscle uses glycogen to satisfy its contractile energy requirements. Furthermore, the normal levels of PCr present in these patients did not supply enough energy to support mild exercise in the absence of glycogenolytic flux.
Additional evidence that PCr is not the exclusive direct energy-supplying pathway comes from genetic knockout experiments.
Watchko et al. (15) created mutant mouse strains missing either or both forms of creatine kinase and compared functional diaphragm muscle performance with control animals during isotonic activation. Both singly mutated forms showed no difference from control animals in force, velocity, power, time of sustained shortening, and work output, whereas these e reduced in the doubly mutated animal CK( /): a 20%
decrease in the velocity of shortening, 16% decline in maximal power, 30% reduction in work, and a 40% attenuation in the time to sustain shortening during repetitive isotonic activation. However, in contrast to these moderate functional decreases, the creatine kinase activity in CK( /) mutants had decreased
to less than 1% of control values. These results showed that PCr did not serve as a steady-state source of energy. With only 1% of creatine kinase activity, muscle force was only partially
20%) reduced (14). These experiments force us to discard the notion that PCr provides the entire short-term energy for a contraction. Although there is a role for PCr in providing the proximate energy for contraction by buffering ATP, the temporal coordination of oxidative and nonoxidative pathways supply
the ultimate energy for contraction. ATP would not be well buffered in the CK( /) mutants, which presumably accounts for the partial reductions in force.
1.What if lactci acid does not exist in the human body , what do we do with all what we learned on lactate the good the bad and the ugly ?
Does lactic acid exist in humans?
According to Professor Matthew Hickey, head of the Human Performance Research Lab at Colorado State University, â€œThe bottom line is, no. There is no lactic acid in human beings.â€
Why then do we still talk about lactic acid in our bodies? Because of â€œsimple historical inertia,â€ said Hickey. â€œIt has stuck in the minds of lay audiences, coaches, athletes, etc. But it is based on a misunderstanding about the chemistry.â€
.) Improving the cycling technique under heavy loads
Under heavy load we first of all use the main coordination muscle chain and if we overload too long heavy ( see 400 m runners) than the technique ( coordination )falls apart completely and we " teach " how to survive with what we have left, which is not a great coordination training , but a survival and high riks injury load.
See in a wingate tests or a 30 seconds all out test 10 x, how the technique realy falls apart.
Perhpas we should look live how long we supply O2 or better supply if we can and utilize O2 and stop the heavy load in duration and numbers of sets and reps, as soon we loose the coordination as a goal.
So the training would be not 10 x 30 seconds but would be based on live individual feedback from the athlete .
Improving the explosive capacities
How do we improve explosive capacity in 10 x 30 seconds hard loads.
What is explosive capacity and how do we see, whether we work on this ?
Woudl a very high SEMG activity be one way to look at this and how can we translate this in the workout live in the field ?
Many open questions and little answers when we justify workouts based on lactate and terms .
Sounds good and I used this all the time, hoping nobody would ask me what it all means and where are the papers showing this ideas .
So for us at least time to give it a closer look on what we did and what we can adjust because of newer ideas and studies.
Here to end the discussion , a reminder my son Andri sent me lately, when I got too much carried away.
"You must conform your beliefs to the evidence, and not the evidence to your beliefs."