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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #1 
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.
 

Mitochondria Adaptations

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.

 

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
I like to add   some more  ideas  towards this topic.
  The way we approach  hypoxic  intensity  depends  very  strongly on the bio availability  of O2.
  We  can  have a  hypoxic  load  and still see very high  SmO2  values  or we  can have a hypoxic  load  and see  low SmO2  values.
  As we discussed  far back. The  timing  of the   loads    have a direct influence  on the physiological reactions.
  Give  it some thoughts  and I  will show you here a NIRS    info. There  where 2 different   step tests  done ( 5 min step  length and 1 min step length.) 
  But look the different   levels  of   oxygenation resp.  deoxygenation.
  This  study result  was  done  and  sent to us    by the Red Bull research group.( Per Lundstrom)

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