It is fun to get older, as many ideas show up about every 50 years again or every 25 years. So every new generation of researcher repeat more or less what was done already. Perhaps with some new equipment, but often still based on the idea of lactate as a reason of fatigue or the myth , that there is something called anaerobic intensity in activities, despite the fact, that there are no studies out showing that, but studies are out showing, that there is no such thing like an anaerobic load.
In one of the many great blogs in Moxy monitor, we have again the discussion of HIIT and slow endurance.
If you look carefully , than the study results are not fitting with the title at all , but it is often used in this way.
The key for the critical readers is to see, why MOXY will actually finally help us to assess the effect of HIIT and slower workouts to see, what and how individual react on specific loads ( MOXY info ) and what actually will trigger a functional reaction and what will lead to a structural adaptation.
The 2 studies for HIIT and slower load mentioned, where done in a similar way ( just not yet on humans) 1/2 century ago already . Here a small summary.
As a solution to the problem of inadequate aerobic metabolism, Hadd provides a training prescription supported by two research studies – a 1960s study by John Holloszy and a 1982 study by Gary Dudley. Using these studies, especially the study by Dudley, Hadd promotes the idea that training at very specific intensity levels will cause an increase in mitochondria density and an increase in aerobic metabolism.
“Way back in the late 1960s a professor called John Holloszy got some rats to run on a treadmill for various lengths of time up to 2hrs per day at around 50-75% of the rats’ VO2peak (easy running, therefore). After 12 weeks, he found that the rats had increased the mitochondria (vital for aerobic energy production) in their running muscles (compared to control rats that did no training). This was a seminal piece of work, because it explained why runners get better with training.”
“The next question was logical. How long should people run for to optimally cause this effect?
Back to Holloszy and his fellow researchers who formed 4 groups of rats to train: one group running 10mins/day, a second running 30mins/day, a third running 60mins and a fourth running 2hrs/day. All at the same easy 50-60% VO2peak, and for 5 days/week for 13 weeks.
Perhaps logically, the 2hr-group had the greatest increase in mitochondria at the end of the training period.”
“But what about intensity? Were mitochondria only created while running long and slow?
In 1982, a guy called Gary Dudley decided to explore this question. He had several groups of rats training five days/week (but only for 8 weeks). Like Holloszy, he also used a range of different training durations, from 5-90 mins per day. However UNLIKE Holloszy (whose rats all trained at the same pace) he also used a range of training intensities. Dudley’s rats trained at either 100%, 85%, 70%, 50% or 40% VO2peak. He also examined how different intensities and different durations affected different muscle types (fast twitch white, fast twitch red or “intermediate”, and slow twitch).”
“…the best way to cause improvements in slow-twitch fibers was to run long and slow at 70% VO2peak (adaptation began from as low as 50% VO2peak pace). Faster was not better. Although Dudley found that 90 mins was not better than 60 mins, Holloszy had shown that 2hrs was definitely better than one…”
“So, to sum up:
To improve your LT (which will have a direct impact on your race performances), you must increase the mitochondria in your running muscles (in a neat move, the optimal training to improve mitochondria is also the optimal training to improve capillary density).”
“The more mitochondria, the less lactate at every running pace. But mitochondrial adaptation in each fiber type is training-intensity dependent. If you want to maximize the number of mitochondria in each fiber type, you must train at the correct pace for that type. (remember; the more mitochondria, the less lactate; the less lactate, the faster the racing pace and the more economical you are at any pace, meaning you can keep that pace up for longer.)”
In summary, based on the research work of Holloszy and Dudley, Hadd promotes the belief that training for long durations of up to 2 hours at 70% VO2peak is the best method for increasing slow twitch muscle fiber mitochondrial density. He further believes that training at intensities of about 80% VO2peak and above will not cause these same adaptations in the slow twitch fibers. He states that an increase in mitochondrial density results in the runner being able to run at increasingly faster paces all the while meeting his muscles’ energy needs via aerobic metabolism.
You can enjoy many of the reasoning with lactate and see, where we are stuck and what we may have learned.
When you look at the Blog title
The Effect of Mitochondrial Density on Athletic Performance
One such study, conducted by MacDougall et al. in 1998, was carried out on healthy male undergraduate students. For three days a week, the subjects carried out four to 10 maximal cycling sprints lasting 30 seconds with four-minute recovery intervals between each. After seven weeks, levels of the oxidative enzymes succinate dehydrogenase in the skeletal muscle had increased by 65 percent, citrate synthase by 36 percent, and malate dehydrogenase by 29 percent. Higher levels of these mitochondrial enzymes led to improved skeletal muscle metabolic function.
So as the study shows HIIT increased function , no word on actual increase in mitochondrial numbers nor density.
What both studies show is the open question, whether hypoxia may be a great stimulator of mitochondrial function and if properly done even on mitochondria density and numbers.
How do we know, when using 30 seconds on 4 min off, whether our client actually reaches a hypoxic load. And why 4 min off ?.
well this studies where done in a time, where we did not had any ideas in general of using NIRS MOXY to actually have control over oxygenation deoxygenation and reoxygenation.
So today the study would most likley look different and more individual as we now can see , when we actually stop deoxygenation and when we start to add hypoxic stimulation to the load.
True most likely 30 sec hard out will deoxygenate , but do we reach every time the same deoxygenation and stay the same time frame hypoxic.
The regular reader can see, where we come in with MOXY.
Here to end the story of functional versus structural. A very old pic from 1/4 century back showed at a training camp in Spain.