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Larry Flessland

Fortiori Design LLC
Posts: 38
I just completed a 5-1-5 exercise as you can see in the attached graph.  Here’s the equipment I used:
  • (4) MOxy’s – Larry (left leg), User_127 (right leg), User_289 (left deltoid), User_290 (right deltoid)
  • Garmin Premium heart rate monitor
  • Garmin GCS-10 speed/cadence sensor
  • Travel Trac Comp Mag+ trainer
  • PeriPedal software with 5-1-5 workout plan.  Calculated power based on trainer.
On the PeriPedal screenshot you can see the 5-1-5 power target for user Larry along with SmO2, Thb, heart rate and speed/cadence.  This is the topmost of the four trends.  The other three trends (User_127, User_289 and User_290) show SmO2 and Thb for the exercise.
I am a runner but like to do workouts on the trainer.  What I would really like is to come up with a 15-20 minute workout based on this 5-1 -5 exercise that I can do in the morning before going to work or during my lunch break when time is limited.



Posts: 266
Does anyone have any thoughts on what causes the slow oscillations in Thb and SmO2 at some points during the test?  I've seen something similar when doing some isometric biceps contractions in a very few cases and did not understand what was causing it.  The graph below is a zoom in on the first run of the 4th load right around the 40 minute mark.  You can see that THb in both arms and SmO2 to a lesser extent oscillate 4 times during the last 2 minutes of that interval.  If you look close, you can see a much smaller oscillation in the leg THb and SmO2.

The oscillation cycle is about 32 seconds long from peak to peak in this particular case.

Green is SmO2, Brown is THb.  Thick lines are legs, Thin Lines are arms.  Dark color is left, Light color is right.  HR is Red.  I've smoothed the THb over 10 seconds.

There are other oscillations throughout the test.  I just highlighted this one.  Other oscillations were faster or slower.

My observations and thoughts so far:
  • It seems to be systemic because all 4 sensors show the effect at the same time.
  • On each sensor, the SmO2 and THb move the same direction at the same time.
  • It's too slow to be driven directly by respiratory frequency
  • The effect is larger in the arms than the legs
  • The legs and arms THb seem to oscillate in opposite directions

THb and SmO2 Oscillations.jpg
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
First to Larry's question on a  15 - 20 min workout  on a bike trainer  as a runner.
 If we  have a bike test as you delivered  we will be able to tell you the limiter  and potential compensator on the bike  in this test.
 Problem. So we can set up a program to make you a better  cyclists based on the  information form a bike test.
 BUT  if your  goal is to use the bike for a potential improvement in running we need a running 5/1/5 test, find the limitation and possible compensation there  and than  go back to the bike test  and see, whether we  have a  way of challenging your running weakness  with a bike  workout or not.
 Your bike HR is  very low  and it may be because you have  a great stroke volume  and slow  HR therefor.
 BUT it may as well be because you have a  muscular limitation in biking  so your cardiac system really never has to be working  too its potential limit.
Here an example we did  10 years ago.
 It shows the different metabolic reaction    same person but first load on the bike and than loading in running. As you can see the challenge may be very different.

intervall with different speeds.jpg  

and here one where we  as well looked  and  cardiac hemodynamic with Physio flow .
JJ  intervall bike run.jpg 
As you can see this is a very old  case study , where we still believed in our lactate balance point idea so the idea  was developed  30 years ago in the midst of a time  ., where 2 and 4 mmol was the real gospel  and  some  groups  slightly  at least  tried to challenge this towards a more  individual  approach. One of them was  lactate balance point.
 If you like a 15 - 20 min idea  to improve  some of your biking ability we  can use your  assessment you sent.
 If you like to  use your bike  as a potential idea of improving some weaknesses you may have in the running we need a running test to see your limiter there and see, whether we  can  use the bike to  work on this.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
To the    question of Roger  and oscillation  in arms and legs  with phase  set off reactions. So tHb up in arms    than down in legs  and vica verca.

1. Look at the  time  frame, when it starts.  It takes about  2 - 3 min till we get a  cycles  of plus minus 30  sec of   " sinus wave " form.
 In 1977 Secher net all  had the courage to challenge  common  and still existing believes , that CO  and  respiration is never a limitation.
 He  in very short terms  showed. that when using a big large muscle mass we  may have a competition between upper an lower body  MAP  situation. So we will have a  phase, where reflexes try to   maintain or optimize  blood pressure in the working leg muscles but than   may have to readjust    for the upper  body area.  I was no yet  checking the  sinus=us  wave  at the first easy load  and  at the last load but perhaps somebody could do that and show it on here.
 The fluctuation reaction time  of blood gases  as well of  hormonal sinus wave of  blood vessel activating    substances   is somewhere  in and around 30 +- sec.
 So what we look at is the  initial Alarm phase  and its  time needed to actually create a  homeostasis   so that this reactions can be seen.
 As we   discuss since  along time , I believe a  3 min step length does not optimally allow  this regulations  and as   such we  loose  lot's of important information.
 That's  one as well of the reason of 5/1/5.
 Here in very shorty term.
 The  oscillation  can be  potentially a  regulatory feedback information on MAP  in combination of the duration of Gas exchange    and therefor the MBF.

 Here  a very old   feedback on that  from the mid  19 70  form one of my old  old   scripts, where I collected a many of the  ideas, which at that time where considered  out of the box  and non confirm  with traditional ideas and therefor  where not accepted  to be used   in education and school.
 So my Question.
 Is this oscillation  seen in MOXY  one of this  reactions and shows the incredible  sensitivity of the NIRS  information. ?
MB and MAP.jpg 
 This  was done by a load of  10 watt in upper body work over a 3 min span You can see that the MBF  needed  longer to reach " oscillation" app. 30 sec  and than we have  about  2  - 3   waves over a  1 min section. This  was not done by  NIRS. but as much I can remember  and t is 40 + years back it was done  with a Doppler.

Interesting would be to see the thb  reaction  as bog as roger showed it here in the first step  and the last step  as well.
 Why. Would be interesting to see, whether in a very low intensity  there may be no need  on adjustment  and in a very high intensity there  may be  a  situation, where priority may be in the working muscles only  and therefor  we  may loose the  fluctuation in the arms.
 Why higher amplitude in the arms.
   Possibly :
 no muscle compression in the non involved muscles  so much easier   vasodilatation in the arms  due to lack of the muscular compression. ? The muscular  compression diminish the   MAP  and the amplitude  will drop. 
IF  and only IF  this is the case  we may have a baseline to see, when CO  may start to be  of a limitation ???


Posts: 266
I'm following up on this oscillation phenomenon a little bit more.

WebMD lists 4 ways that the body controls blood pressure.  I imagine there's more, but let's start simple.
  • The heart can speed up and contract more frequently.
  • The veins can expand and narrow.
  • The arterioles can expand and narrow.
  • The kidney can respond to changes in blood pressure by increasing or decreasing the amount of urine that is produced.

We can see from the data that the heart rate does not have the same sinusoidal pattern as the THb and SmO2 so I think we can rule that out.

Veins contracting and narrowing would primarily affect the preload on the heart and therefore cardiac output.  If this were the cause, then I think we'd see the arms and the legs responding in phase rather than in opposite directions.

The kidneys changing the amount of water in the blood would also be a preload effect, plus it would be way too slow of an effect to oscillate with a 30 second period.

Arterioles expanding and narrowing seems like a plausible explanation IF we assume that it's mainly the arms that are reacting.  When the arterioles in the arms narrow, THb and SmO2 in the arms will go down and Mean Arterial Pressure (MAP) will go up slightly due to the increased vascular resistance. The increase in MAP will cause a slight increase in THb and SmO2 in the legs.

I don't want to jump to the conclusion that this is THE explanation for the oscillation effect, but at this point I don't see any conflicts with our observations and I don't have any other explanations.

The next layer of question is "What would drive the arterioles in the arms to narrow and expand in oscillaition?"

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Some feedback  to the next layer of questions:

Local and Autonomic Control of the Vasculature Smooth muscle surrounds each blood vessel, and the tension of these cells controls the radius of the vessel. 


Vasoconstriction is caused by contraction of the smooth muscle cells, and vasodilatation occurs passively, powered by BP as the vascular muscle relaxes.


Vessel tone is controlled by local factors and autonomic mechanisms.  All of these are short-term corrections to changes in blood pressure.

This is most likely  what we visual   with MOXY as we  can see

 In the long term, control of blood pressure is determined by fluid balance--fluid   intake vs fluid output.  Thus, the kidneys are the most important organs in control of BP.This is not visual  with MOXY tHb reactions ( too slow)


The fluctuation is due to BP changes  and adjust ments  and in  sports  with big  % of muscle mass involved teh blood pressure si needed  to balance the “ weakness” of the heart as it can ‘t maintain the  O2  demand  from all the involved muscles and  the central governor  has to make some  “decisions” on where is  what needed to survive.

 The non-involved  muscle will be the one  we see the most fluctuations  .


Smaller arteries and arterioles have a basal tone, that is the muscle is always partially contracted at rest.  This is       necessary to provide for vasodilation, which can only be accomplished by relaxing the muscles.  That means       that tissues capable of large increases in blood flow (such as skeletal muscle) have a high basal tone.  Basal   tone is slight in most veins.






Local control of blood vessels:


Local temperature:  Especially important in the skin.  High ambient temperatures cause cutaneous arterioles and veins to dilate.

TSI % in NIRS, which are based on a stable tHb  show some interesting variation. If we use  a  NIRS, who takes  skin  O2 information  and  pair it up with MOXY , who takes  muscle SmO2  we  will see  that  whne  Skin flow goes up  SmO2  drops  and when  Skin flow drops  SmO2  goes up.

 See test we showed with  compression  garments.   Cold causes vasoconstriction, which conserves heat and safeguards core temperature.


External pressure compresses the vessels and impairs blood flow.  May be caused in muscle by muscle  contraction (myocardial or skeletal), or in skin by sitting, kneeling, or lying.

All this can be nicely demonstrated using MOXY. The interesting question is often what overrules  what.


Autoregulation--the relative constancy of tissue perfusion in the face of pressure changes.  Independent of the nervous system.  Vessels respond directly to changes in arterial pressure.  A rise in pressure evokes arteriole vasoconstriction (and increased vascular resistance), while a fall in pressure evokes vasodilation (and reduced resistance).  Account for near-constancy of blood flow.  A change in arteriole radius takes 30 to 60 seconds to develop fully, so a sudden change is pressure elicits an initial brief change in flow (Increased pressure, increased blood flow).  Keeps capillary pressure stable.  Myogenic mechanism--an increase in    vascular pressure causes vascular smooth muscle to contract; reduced pressure causes muscle relaxation.


Endothelium-derived relaxing factor (NO)--released in response to shear stress to cause vasodilation.


A balance between autoregulation and EDRF is largely responsible for regulation of vessel diameter.


Local metabolites--

Local hypoxia causes vasodilation of arterioles

Carbon dioxide causes vasodilation

Extracellular K+, which can double in contracting muscle, causes vasodilation

Autacoids, vasoactive chemicals that are produced locally, released locally, and act locally (in effect, local hormones);  they include histamine, which participates in inflamation.  Histamine (a derivative of the amino acid, histadine) is released in response to trauma and allergic reactions.  It dilates arterioles and contricts veins.


Reactive hyperaemia--after inadequate blood flow (i.e., from compression of skin), the blood flow immediately after release is much higher than normal.  Vasodilator metabolites accumulate.  Resupplies oxygen and nutrients to ischemic tissue very rapidly.

Increased blood flow (caused by an increase in arterial pressure), vasodilator products of tissue metabolism are     washed out and their interstitial concentration declines, increasing vessel tone.



Nervous Control


Sympathetic vasoconstriction

Neural vasoconstrictor regions are tonically active (averaging approx 1 impulse per second at rest) contributing to    basal tone.   Reflexes that enhance this activity result in more frequent impulses (as high as 10 per second)       to the terminals containing norepinephrine, which is released and elicits constriction.

Affects both arteries and veins, but has most important effects on small arteries and arterioles.   Capillary pressure is reduced by arteriole vasoconstriction.

Skin responds more profoundly to sympathetic activation--Skin more sensitive to sympathetic stimulation and also     has lower basal sympathetic tone than most other tissues, so greater change is possible.

If sympathetic outflow is generalized, results in rise in BP (by increased peripheral resistance and increased cardiac   output).


Circulating catecholamines (E, NE from adrenal) have similar but less profound effects.



Parasympathetic vasodilation

Parasympathetic fibers generally not found on arterioles.  Parasympathetic innervation of arterioles in salivary glands



Baroreflex--vasodilation caused by fall in sympathetic activity

Baroreceptors are stretch receptors located in the carotid sinuses (where internal and external carotids split) and in     the aortic arch.  Impulsed from them travel up the 9th and 10th nerves to the NTS.  Stim of NTS inhibits sympathetic outflow to peripheral vessels (depressor effect) -- (also causes bradycardia via parasympathetic mechanisms, which also lead to reduced BP).

Baroreceptors are also located in heart and pulmonary vessels.

Provide short-term adjustment, but long term changes in blood pressure are achieved by changing the fluid balance     (via the kidneys).

The baroreceptors in the heart and pulmonary circulation also has a diuretic effect on the kidneys to decrease blood volume.


Hypothalamus is sensitive to changes in brain temp, and shunt blood to skin to diffuse heat or away from skin to      concerve heat.


Forebrain--Emotional responses often elicit vasodilatory and depressor responses (blushing, fainting).

Pain also effects BP.  Cutaneous pain raises BP, while visceral pain lowers it.

Lung stretch receptors--Inflation of lungs causes systemic vasodilation, while deflation causes vasoconstriction.


The brain and heart are controlled primarily by intrinsic factors.  Thus, in acute hemorhage, when there is massive   sympathetic discharge to contrict vessels, blood flow to the brain and heart are not greatly reduced.


In the skin, external vascular control is dominant.


In skeletal muscle, both are prominent--at rest, external (sympathetic) vasoconstrictor tone is dominant.  In anticipation of, and at the start of exercise, blood flow to leg muscles increases.  After the onset of exercise,    vasodilation occurs as a result of local increase in metabolites.  Vasoconstriction occurs in inactive tissues as   a result of general sympathetic discharge, but constrictor impulses  reaching  vessels of active muscles are     overridden by local metabolic effect.  This allows increased blood flow where needed and shunts blood away   from areas that don't need it
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here some additional  parts of the discussion.
 In non involved muscles  the arterioles  reaction is much easier to see as there is no "counter force' There In activity involved muscles  we have a  muscle contraction force
 " Arterioles expanding and narrowing seems like a plausible explanation IF we assume that it's mainly the arms that are reacting "  This   explains why we see this   reactions much nicer in the arms.
  One  email I got is the  question n an abstract  from Secher.
 Here  a short abstract on a topic   where discussion started in  the late 1970 .

Are the arms and legs in competition for cardiac output?

Secher NH, Volianitis S.


The Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, University of Copenhagen, Denmark.


Oxygen transport to working skeletal muscles is challenged during whole-body exercise. In general, arm-cranking exercise elicits a maximal oxygen uptake (VO2max) corresponding to approximately 70% of the value reached during leg exercise. However, in arm-trained subjects such as rowers, cross-country skiers, and swimmers, the arm VO2max approaches or surpasses the leg value. Despite this similarity between arm and leg VO2max, when arm exercise is added to leg exercise, VO2max is not markedly elevated, which suggests a central or cardiac limitation. In fact, when intense arm exercise is added to leg exercise, leg blood flow at a given work rate is approximately 10% less than during leg exercise alone. Similarly, when intense leg exercise is added to arm exercise, arm blood flow and muscle oxygenation are reduced by approximately 10%. Such reductions in regional blood flow are mainly attributed to peripheral vasoconstriction induced by the arterial baroreflex to support the prevailing blood pressure. This putative mechanism is also demonstrated when the ability to increase cardiac output is compromised; during exercise, the prevailing blood pressure is established primarily by an increase in cardiac output, but if the contribution of the cardiac output is not sufficient to maintain the preset blood pressure, the arterial baroreflex increases peripheral resistance by augmenting sympathetic activity and restricting blood flow to working skeletal muscles.



[PubMed - indexed for MEDLINE]

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
We  got lost as so often on some very interesting findings.
 So here back to the actual  question :
 What I would really like is to come up with a 15-20 minute workout based on this 5-1 -5 exercise that I can do in the morning before going to work or during my lunch break when time is limited.

As  explained. the 5/1/5  n the bike will gives us some nice indication where you have  some  limits in biking.
If the limits are delivery limits, than  we  can address this on the bike   or the same holds  true  for utilization.
 BUT. A  delivery problem on the bike may not be a delivery problem in running.
So straight forward answer.
 The 5/1/5  test on the bike  will not be of a lot of value for you to try to use the bike  for running.
 We need a  5/1/5  from running and than we can see, whether the weakness ( limit ) can be addressed on the bike.

You have one interesting " weakness" on the bike, which is a very asymmetrical  use of your legs. A spin scan  would  potentially confirm this.
Due to this asymmetric  reaction we would take the arm SmO2    as a guide  for training intensity but would use the  next few weeks to work on a symmetrical  pedal stroke training in the morning , which may or may not help in the running.
 If we look your SmO2 trends in 2 legs  and one arm it looks  pretty nice  with one leg  more dependent on a good utilization.

2 legs  1 delta smo2.jpg

Now  before  we  look just SmO2  we   look as well the delivery  situation tHb.


You can see in  a big difference in the tHb reactions  in the right and left leg  and when looking  at SmO2  you would not have expected this  extreme difference.

Look at the red  circle  and it gives you some very interesting  feed backs.
Due to this  very asymmetric  situation we  can assume that one leg is  limiting  an optimal performance  and in a load the other may start to compensate.

Just in short if this would be a biker.
 We would run the test with a  power crank the same way.

 In this case we see that SmO2 trend in delta  and legs are very    similar so we can go back to delta information for a zoning idea.

 Now before we do that we liked to see, whether this asymmetric situation as well in the upper body   and than we would have a problem. So here the SmO2  trend of both delta muscels. ( Polyn)
smo2  delta both.jpg 
and now  both tHb  reactiosn of both delta. Reember the chance to have it exactly at the same spot is   zero so we look at the trend not the absolute numbers.

delta both thb poly.jpg

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Another interesting observation in this case is the following section

4 th step.jpg

You see the trend in SmO2  where in the first load it drops initially  and  increases a bit  and in the repeat  he  actually has it higher  and more stable.
 You see the step before a similar reaction and you can see who created the drop in SmO2  . look at the HR.  ( spike ) there are different feedback we can get from moxy on this  spike as well.
 Now lets' stay by the 4 th step.
 The increase in SmO2 indicated  a change in  efficiency in either delivery  or utilization.
 Something happened here. So to get some ideas we  can go and see the "delivery information  at that 4 th step.
So here  what we see at the same step in tHb reaction on one side
4th step thb.jpg

you can see, that despite the same wattage load  ( same step ) he  changed something which changed the  delivery  due to either pressure  change  by the muscels ( different RPM)  or other options Now look at tHb spike at rest.
 They  did a  great job by changing 6  and 12 o clock position so in each step  we have both options to avoid a problem interpretation from there. The relaxation in this 3 / 4 step is different and we have  out of  what ever reason a   not optimal  thHb rebound  at the 1 min rest.???

Now  for the advanced MOXY coach  here the ultimate information on this  by looking at the biased  HHb  and O2Hb trend   together with tHb.
closer look hhb o2hb same step.jpg

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