16 seconds for 100yd is 17mid for 100m. He said small skill guys. Even at 180-200lbs, if you are able to run 9mid 100yd (what he says), that is a joke.
I understand you don’t want to cause lactic. I get that. I also understand you want to be fresh for your speed days as those are the most important, but why even bother doing those volumes if those are the goals? The speed here is so slow that even if you are doing 30 second rests, there is not going to be much fatigue until you get into significantly high volumes. That is what I am trying to figure out.
In short, the increased acidosis generated during lactic efforts, specifically when the 4mmol mark is approached and surpassed, destroys the mitochondria in the active skeletal muscle fibers.
Can you please post the literature that indicates this to be true (without complementary mechanisms in place)?
I ask this because of how it goes completely against the majority of the empirical evidence (with athletes who do more training in acidosis tending to have greater mitochondria development).
I personally can get lactic build-up anywhere up to 19s if I’ve done enough repeats (on grass)… on track or any other surface changes things completely and I’m ok in the low 16’s. But then I time the recoveries at 30s/60s rather than walking (i’m sure 50m walk is longer than 30s, also as you get more tired you tend to walk slower)
I can’t see this being the case, like fogelson said the actual research would be nice to see. Looking at somebody like KitKat’s schedule for 400m there are 4 days a week where lactic most likely exceeds 4mmol. In fact almost any SE2 work would theyby inhibt ability because it would destroy mitochondria.
I agree, but why do high volumes we see prescribed then (2000m 3x a week).
I am sure you know how easy these paces are that are described. While around the speeds (100m pb/ability) described, I do not have “tremendous work capacity” and have done 2x10x100m in mid 15 walk 50m rest (which is under 40 seconds) without any hint of lactic… Tired, but not lactic.
Charlie himself that tempo can (and should be in GPP) difficult and tough. No lactic and you should be able to finish at the pace you started, but it should be tough. Again, the paces and workouts described are a glorified warm-up. I don’t have anything against that and do things like that myself, I am just trying to get clarification mostly from Charlie here about the role of tempo because if it is primarily to just loosen up and get blood flowing, then I don’t see the reason in doing such high volumes. I think he may have some other reasons though, hence my questions.
How many repeats to get “lactic” in the 19s 100m range? When I’ve timed 50m walk, the longest (towards the very end) is 45seconds rest with most in the 30-40sec range. What is the PB level?
Local hypoxia will yield mitochondrial biogenesis in the myocardium; yet destroy these same structures in the skeletal fibers. (read zhelyazkov and Dasheva)
Ministry of Education of the Russian Federation
Penza State University
The Department of Traumatology, Orthopedics and military and emergency surgery Term Work When insufficient flow of oxygen for normal aerobic cellular metabolism of hydrogen ions are formed. The resulting acidosis rapidly destroys the cells and stops just in metabolism, if only a certain amount of hydrogen ions does not appear in the conversion of lactate piruvata, and then to lactic acid. Thus, although an excess of lactic acid is considered to be dangerous, it represents an important compensatory mechanism in preventing cellular damage due to acidosis.
Understand that there is an enormous amount of research on this subject from overseas sources. You merely have to search for it via the proper channels.
Some more from a friend and colleague of mine from the National Sports Academy in Sofia Bulgaria: mitochondrial damage or/and dysfunction is caused by : i) high acidosis ii), Moderate work (medium intensity) - Should not exceed anaerobic threshold. Doing so leads to hypoxia and destruction of mitochondria.
Some authors for your consideration are Zhelyazkov/Dasheva, Issurin, Seluyanov,
Correct, as Nikoluski has described, the physical effort for an athlete of sufficient preparation may be quite manageable yet still yield counter intuitive adaptations.
Niko, thank you, but I have read the site, read the materials, watched the videos, things still aren’t that clear when you get posts from James like this.
Example, NT in the Peaking When It Counts video was running tempo very slowly. Charlie called him out on running tempo this slowly and told him to run it faster. The paces are not much different from what James is describing here. If Charlie wants his athletes to run the tempo faster, this doesn’t seem to make sense.
This then leads me to wonder if people understand what Charlie is saying or if some of us misunderstand it or are interpreting it wrong. That is all I am asking.
Sorry, but these are not studies and do not really tell us anything. What you are essentially saying is that 400-800m runners, bodybuilders, and road cyclists (three separate groups of athletes whose training has historically had tons of lactic work at the threshold you describe (>4mmol nearly daily) have destroyed all their mitochondria. I am just pointing out how absurd this sounds without some context or explanation.
Hi James! What date are the quotes above? I am not sure of the mechanism described here (i.e., hydrogen ions) and the definition of hypoxia…
Just to clarify, I meant that 4 mmol.l-1 is most probably a small value for a sprinter, i.e., produced easily/quickly. Pfaff has mentioned much higher values for sprinters and anyway, it’s not rocket science to figure that out vs. (some) endurance runners.
I don’t have the date from the first study, however, my friend Svetoslav sent me the information from the second quote within the last 6 months. Svetoslav has recently been offered a position at the NSA for next year so I consider him to be as reliable a source as there is with respect to current sport science research.
Essentially, while I wouldn’t use the phrase “destroyed all their mitochondria”, you are correct.
If we accept that these athletes are routinely exposed to intensive anaerobic-glycolytic loads then while glycolytic power or capacity is developed it is coincidentally inhibiting the oxidative capacity of the active skeletal fibers by destroying mitochondria.
So they are inhibiting their oxidative capacity. Well, I’d love to hear to what extent, because these are athletes with some of the greatest oxidative capacities of any athlete in sports. My point here is that you haven’t really shown any studies and the only ones I am even aware of that show mitochondrial damage from generating lactic are ones that have pathologically induced or pharmocologically induced acidosis for long periods of time (not acutely through exercise which may have complementary means).