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Other/Mixed Studies and/or research on anti glycolitic training?

Other strength modalities (e.g., Clubs), mixed strength modalities (e.g., combined kettlebell and barbell), other goals (flexibility)

North Coast Miller

Level 8 Valued Member
Are we reading the results the same way? 🤔

To me it seems to line up with the AGT style of training:
The SS group had the less acidic pH overall.
The SS group also had lower "markers" (if that's the right word)for glycolysis: lower pyruvate and lactate levels.
The SS group had a lower reduction in muscle ATP as well.
Also, the G-6-P is interesting. If I'm not mistaken that's a molecule which is part of glycolysis.
I'm not sure what to make of it. When I read it it looks like the SS group was more reliant on glycolysis than the LS group:
"Rate of muscle glycolysis was similar in SS and LS during the first sprint, but twofold higher in SS than LS during the last sprint (P < 0.05)."

"Muscle [phosphocreatine] before the last sprint was 1.5-fold lower in SS than LS (P < 0.001). "

"PCr utilization during a single sprint was smaller in SS than LS, but PCr availability before the last sprint was lower in SS than LS....suggests that limitations in PCr availability may have played a more prominent role in peripheral fatigue development during the multiple short- than the long-sprint protocol." - this statement doesn't maybe make sense compared to the next observation

"Thus, even though intracellular [Pi] was not measured in the present study, it is conceivable that Pi-dependent alterations in sarcoplasmic reticulum Ca2+ cycling contributed to the larger degree of peripheral fatigue observed in LS."

Which is consistent with other studies linking accumulation of Pi to reduced contractile forces independent of lactate and hydrogen ion accumulation.

And again maybe playing devil's advocate, is this just showing a logical pattern of fatigue? The longer you sustain an effort the greater the accumulation of PhosphoCreatine byproduct. This study seems to show the duality of increased glycolysis magnitude in LS also increasing PCr stores, but the inorganic phosphate from using it reduced contractile force anyway. So maybe supporting the SS as a training approach for increasing output, but this study didn't last long enough to measure adaptive response over time to the different protocols. Reading it, it doesn't seem to support the metabolic aspect although I certainly could be missing a great deal - much of the chemistry is WAY over my head.

This research does a good job of isolating the effect in mice:
"Even after 100 fatiguing tetani, force was not significantly affected in CK–/– fibers (lacking creatine kinase), whereas by this time force was reduced to <30% of the original in wild-type fibers"

 

ali

Level 6 Valued Member
Is it me?
The paper states the work was matched in 2 groups....ss, 18x5 s and ls, 6x20 s.
So that's 90 s v 120.

How is that matched? Haven't read it all but is there a difference in intensity? Somewhere? Or another variable?

Don't get it.

Greater fatigue in ls...well, they sprinted more.

Did they sprint at the same power output or different and so total work was on a par?
 

bluejeff

Level 6 Valued Member
Is it me?
The paper states the work was matched in 2 groups....ss, 18x5 s and ls, 6x20 s.
So that's 90 s v 120.

How is that matched? Haven't read it all but is there a difference in intensity? Somewhere? Or another variable?

Don't get it.

Greater fatigue in ls...well, they sprinted more.

Did they sprint at the same power output or different and so total work was on a par?

Perhaps this will clarify:

From the paper (underlining and bold by me):
The exercise protocols were matched for mechanical work, intensity, and exercise-to-recovery ratio, but differed in sprint and recovery duration.
The exercise protocols were matched for mechanical work (SS: 81 ± 3 kJ; LS: 80 ± 3 kJ) and exercise-to-recovery ratio (1:6). SS included 18 × 5 s “all-out” efforts interspersed with 30 s of passive recovery, whereas LS included 6 × 20 s “all-out” efforts interspersed with 120 s of passive recovery. Preliminary trials were conducted with four subjects to determine the number of 5-s sprints necessary to elicit the same mechanical work sustained during 6 × 20 s sprints, resulting in 18.3 ± 0.3 sprints.
During cycling, when a pedaling frequency of 100 rpm was reached, the dedicated software automatically applied the workload and started the timer.
So:
They did a test to find out what intensity to use on the bike to get the same level of mechanical work. The cycle ergometer they used has a system that applies "braking" to apply the resistance.

Edit: adding the url of the paper in case a search engine brings someone here:
 

ali

Level 6 Valued Member
Having now read it, the most interesting take from it isn't surprising to me...as a sprinter...but will surprise some.
The rate of glycolysis in short sprints.
Full on.

Precisely why speed and performance sprinting should be higher carb, lower in fat for ratio of energy intake.
Better performance. Better recovery.
Better fatigue management.
 

North Coast Miller

Level 8 Valued Member
Having now read it, the most interesting take from it isn't surprising to me...as a sprinter...but will surprise some.
The rate of glycolysis in short sprints.
Full on.

Precisely why speed and performance sprinting should be higher carb, lower in fat for ratio of energy intake.
Better performance. Better recovery.
Better fatigue management.
After reading how cheetahs rely on glycolysis, combined with how the true culprit for chemically induced muscle fatigue is byproduct from PCr, it really looks like the PCr pathway is a metabolic stop-gap intended to run for the 8-10 seconds glycolysis needs to get up to full reaction speed from a dead start. The body will continue to use it as it becomes available, but it sounds like we'd be better off if it shut down after 30 seconds or so.
 

ali

Level 6 Valued Member

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bluejeff

Level 6 Valued Member
Interesting study here:


There's a sweet spot but we knew that already.....
Hmmm. I will have to take some time to unpack this, and find access to the full study text. However, depending on what the HIIT protocol was, it makes sense....

Speaking broadly, the whole idea of AGT is to avoid precisely this. Without getting into the nitty-gritty of the biochemistry (yet) it seems like evidence which may support the idea that too much glycolysis (too often) leads to negative side effects.
 

North Coast Miller

Level 8 Valued Member
Going to need the details for this one, and how they measured mitochondrial impairment. Also, was the drop a temporary lull in adaptive response prior to a recovery phase. Looking at the graph it appears all markers including performance were going back up when they terminated the study, but was that due to a week off?
 

ali

Level 6 Valued Member
I was hoping to read the whole study - it is paid for access but usually I can get most studies via my university log in but it is not available at the moment.
Yeah, of course, more details rather than the abstract may lend better info.
 

North Coast Miller

Level 8 Valued Member
Have found a few references to the study where they discuss the protocols:

During the high-intensity interval training, or HIIT, subjects warmed up, and then were asked to maximize their power output over either 4- or 8-minute intervals, interspersed with 3-minute breaks. The training started out relatively light, with 36 total minutes of high-intensity intervals, spread out over the week, not including warm-up or rest times. In the following, moderate week, subjects completed 90 total minutes of intervals. Among other findings, the researchers determined that a measure of metabolic efficiency known as intrinsic mitochondrial respiration improved over that time, as did physiological parameters such as oxygen consumption.

That changed in the third week, designed to represent excessive training, during which the participants completed a grueling 152 minutes of intervals over the course of the week. After that, the subjects’ intrinsic mitochondrial respiration fell by an average of 40 percent compared with the samples taken at the end of the moderate-intensity week, the researchers report......After a recovery period, during which participants completed 53 minutes of intervals spread across the week, most measures rebounded. The subjects’ oxygen consumption and power output during exercise, as measured by how hard they pedaled, were higher after recovery than at baseline or at any other point during the experiment.
Hmmm....
Study coauthor Mikael Flockhart, also at the Swedish School of Sport and Health Sciences, says that it’s not clear where the “tolerable limit of training” is, especially because the study indicates that overexercise doesn’t necessarily lead to a decline in actual athletic performance.


 

ali

Level 6 Valued Member
Making the point there that 'excessive' is beyond the point where most people exercise.....it taps into San Milan's research that suggests similarities between untrained and elite endurance athletes' mitochondrial function: both being abnormal (paraphrasing) compared to 'healthy' individuals.

I firmly sit on the fence. Excessive exercise/burnout/overtraining consists of a complex input of physiological and psychological stressors. Difficult to tease them apart experimentally.

A case here.....excessive amount led to a decrease in mitochondria using the same timing protocol as less demanding exercise but over time they bounced back up.

As expected. Really.

Greater the intensity/volume greater recovery time.

So....back to regular day to day high-ish intensity....it shouldn't be so high to require more rest days.

Higher intensity less frequent bouts need more recovery.

Huge variability person to person and in-person variability with psycho-social changeable stressors and changeable reaction to and management of them.

My own confirmation bias but a stress model of exercise is a better measure, if ill-defined and vague, of exercise and timing of more demanding 'excessive' training, rather than a single function.
 

North Coast Miller

Level 8 Valued Member
Making the point there that 'excessive' is beyond the point where most people exercise.....it taps into San Milan's research that suggests similarities between untrained and elite endurance athletes' mitochondrial function: both being abnormal (paraphrasing) compared to 'healthy' individuals.

I firmly sit on the fence. Excessive exercise/burnout/overtraining consists of a complex input of physiological and psychological stressors. Difficult to tease them apart experimentally.

A case here.....excessive amount led to a decrease in mitochondria using the same timing protocol as less demanding exercise but over time they bounced back up.

As expected. Really.

Greater the intensity/volume greater recovery time.

So....back to regular day to day high-ish intensity....it shouldn't be so high to require more rest days.

Higher intensity less frequent bouts need more recovery.

Huge variability person to person and in-person variability with psycho-social changeable stressors and changeable reaction to and management of them.

My own confirmation bias but a stress model of exercise is a better measure, if ill-defined and vague, of exercise and timing of more demanding 'excessive' training, rather than a single function.


The study also noted that after rebounding they were at their peak of metabolic efficiency and power output. Hard to see how mitochondria could have been much damaged if a week later they were burning fat better than they had been previous. More likely they had impaired enzyme function/production and the mitochondria were fine. It would be nice to see what the speculated reasons were for the negative responses

Overreach, pull back, improve.

Further, if they had worked up to that level over a period of 12 weeks instead of two, the outcome might have been a good bit different - you don't remodel/adapt that quickly outside of an Arthur Jones laboratory...
 
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