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bobbyjobling

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 #16 
so help  the  rate of change  of tHb  meaning  amplitude  so  from  low  to high or   opposite. Is  that the rate of change. ?  

It's a measurement of how much Thb has changed between sample time ... 

m=\frac{y_2-y_1}{x_2-x_1}.

Rate of Change THb  = (THb(n+1) - THb(n))/(Sample time(n+1)-Sample time(n))

so 

Time SecondsTHbR THb
112 
212.50.5

R THb = 0.5 = (12.5 - 12) / (2 -1)

if we add SmO2, O2Hb and HHb we can then calculate the ROC 

Time SecondsSmO2THbO2HbHHbR THbR O2HbR HHb
1501266   
25012.56.256.250.50.250.25
35012.56.256.25000
45512.56.8755.62500.625-0.625

from this info we might be able to then graphically show when THb moves before SmO2 during the rest period of 5-1-5.

I do this by formulating a logic condition which will give me a TRUE or FALSE answer for example using excel formula : =IF(AND(R THB>R O2HB, R THB> R HHb),1,0)
1 = TRUE and 0 = FALSE

I also added a second logic condition opposite to the above and the output is 0,-1

Logic.png 

From this 1,0,-1 output we can then use the average trend line in the excel chart option to construct a possible trend of disscurve on rest periods. This is how Pulse With Modulation works.

Dissc .jpg 
 

However, I am still optimising the logic condition as I need to test it more with theoretical SmO2 and THb conditions. We can also include Power and HR data in the logic conditions.


It could all be pie in the sky, but it keeps me out of trouble [smile]

juergfeldmann

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 #17 
one section  people  can look is an interesting part . Last  not complete load look at outside  the SmO2  and Thb   feedback. What  can you see there  and it is  interesting  to see.? Thna  o back  to his first load  an see, what  the trend in that feedback is there. ?
juergfeldmann

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 #18 
hmm the logic  conditions look very interesting.  So here a  question for that  try out. Lets  say  I have a  very  fast increasing tHB  and a  same time fast dropping  SmO2. 
 Than I have a very fast increasing  tHb  and an increasing SmO2.
So  how  do I  now, whether   one of this  conditions may change  the  O2  disscurve as there is  one additional  ( more really ) but one important   part in that    " duration .   so as so often  time  to react on the  change in  energy demand  and energy utilization.  So I  can  make a  workout , where  tHb  and SmO2 trends  look  basically he  same, but I  can manipulate one of them  so the O2  disscurve  shift  and one where it does not shift  or I  can  do a third  version, same Hb  trend and sam  SmO  trend and I can decide  , to what   direction I like to shift the 2  diss  curve..
 The result   I see  can  be looked  by actual blood tests or by gas exchange  like  Capnometers  or by cardiac feedback   and so on. BUT  when I  only  look at the NIRS (  weakness of  NIRS )  I  can not see  a different outcome  at least not as I  do it in the rest period  .  So  will need   much more time  to   think through this fascinating option. 
ryinc

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 #19 
I want to come back to this case, as we have still not discussed the "interesting" part. This athlete has an atrial fibrilation (see the unusual HR data) so you can imagine that i was surprised to see a respiratory limiter emerge as would have suspected cardiac system. On discussion with the athlete and his daughter who is a doctor - the athlete mentioned that his cardiologist previously mentioned the respirorimeter results were weak and his daughter also mentioned that she has suspected respiratory problems might be present. So the respiratory system as limiter seems plausible. I am wondering whether the atrial fibrilation may have been brought on as a result of cardiac system compensating for respiratory system for many years (athlete did long distance running for many years) or the opposite weak respiratory system because it has been compensating for cardiac system.

Further thoughts welcome.
bobbyjobling

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 #20 
I was going to ask about HR and if the athlete during the test was on some sort of medication. Perhaps having atrial fibrillation will reduce gas exchange efficiency and other body mechanisms to balance pH. Maybe if we hade a moxy on non involved muscle might show a Cardiac limitation. Is atrial fibrillation always present or can it be intermittent?
juergfeldmann

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 #21 
AF  is a  very common  result of  long distance running  and   endurance athletes.
 The  question is  whether the AF  is  created under load  or only at rest  and  may disappears under load.  The  HR  reaction can be a  hint on  AF  but   to be sure   he needs as  they did  for sure a  ECG

Respiratory  chronic  overload  can create different cardiac  compensatory reactions but as well AF  creates some confusing  partnership  with respiration and vice verca. 

The  fact that he  "pushed "  relative hard  and had  no  cardiac limitation sign  is because we have a brainless protocol. So  he  decided  that it is  now  the end. If we  suspect a cardiac limitation (  and in his case it was documented)we  never tell the load  and  look whether   the  cardiac protection CG  will simply reduce  motorunits recruitment  and  the client believes  he still pushes  harder.
  So they in fact keep going but lower load  by the  same HR or  CO.  I assume  you had a ECG  support in this assessment including a medical person ( Daughter )  there   with a defibrillator.
juergfeldmann

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 #22 
Here a  small add on  to  support  the idea of limiter and compensator.

Reduced lung function and risk of atrial fibrillation in The Copenhagen City Heart Study

P. Buch, J. Friberg, H. Scharling, P. Lange, E. Prescott

European Respiratory Journal 2003 21: 1012-1016; DOI: 10.1183/09031936.03.00051502

Abstract

Chronic obstructive pulmonary disease has been associated with a high frequency of arrhythmias. Few studies have analysed the role of reduced lung function in predicting atrial fibrillation (AF). The aim of the present study was to investigate the relationship between forced expiratory volume in one second (FEV1) and risk of first episode of AF in a prospective study.

Data from 13,430 males and females without previous myocardial infarction, who participated in the Copenhagen City Heart Study, were analysed. New AF was assessed at re-examination after 5 yrs and by hospital admission for AF during a period of 13 yrs. Multivariate analyses were used with adjustment for cardiopulmonary risk factors. There were 62 new cases of AF at 5-yr follow-up (0.58%) and 290 cases (2.20%) diagnosed at hospitalisations.

Risk of new AF at re-examination was 1.8-times higher for FEV1 between 60–80% of predicted compared with FEV1 ≥80% after adjustment for sex, age, smoking, blood pressure, diabetes and body mass index. The risk of AF hospitalisation was 1.3-times higher for FEV1 between 60–80% and 1.8-times higher for FEV1 <60% compared with FEV1 ≥80%, when additional adjustment was made for education, treatment with diuretics and chest pain at activity.

The authors conclude that reduced lung function is an independent predictor for incident atrial fibrillation.

 
juergfeldmann

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 #23 

I was not sure, whether I like to go that far  but s we discuss the limiter and compensator in sport  you can see how unplanned  due to disease  situation create  certain remodeling. Now  the key in physiological guided training is  to do this under control instead   uncontrolled  without  any  idea, that this is happening.

This s where we  learn the  reactions and how we  than  go and control the situation as we know  what we do versus  taking any  %  of what ever  and hope something may happening and not even understanding, that we may have a limiter already  which is  chronically overloaded.




Abstract

COPD is one of the leading causes of Mortality & Morbidity in the US and is associated with a wide variety of cardiovascular diseases especially arrhythmias, angina, myocardial infarction and congestive heart failure and is directly associated with the severity of COPD described in the GOLD initiative. COPD is an independent risk factor for AF/AFL. Smoking, hypoxia and inflammation all contribute to AF in COPD patients mainly via atrial remodeling while hypercapnia contributes to it via increasing refractoriness of the atrial musculature and a delay in the return of the refractoriness to normal after resolution of the hypercapnia. The most common EKG abnormality found in patients with COPD is P pulmonale and the PQ interval is the strongest predictor of developing AF. The P wave Dispersion (PwD) was also an independent risk factor for the development of AF and was found to be more in the acute phase than in the stable phase.

The BODE index, an important prognostic score among patients hospitalized with a COPD exacerbation has a direct co relation with the prevalence of AF/AFL while the DECAF score, which was found to be superior to the CURB 65 score as a mortality predictor for hospitalized patients, includes AF as one of the criteria. Chronic hypoxemia is one of the main reasons for altered pulmonary vein anatomy and hence the presence of COPD was identified as an independent risk factor for the recurrence of atrial tachyarrhythmias after catheter ablation in patients with COPD and the absence of COPD was also found to be an independent predictor for a successful electro-cardioversion. These patients were also found to have an increased incidence of non-PV foci for the arrhythmias. Oral glucocorticoids were associated with an increased risk of developing AF especially high dose steroids. It is recommended to correct the underlying respiratory decompensation while treating patients with AF as they render the treatment of AF ineffective. Non-dihydropyridine calcium channel blockers should be used as first line rate control agents for AF in patients with concomitant COPD while the β-blockers, sotalol, propafenone can be used in patients with obstructive lung disease who do not have bronchospasm.

juergfeldmann

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Posts: 1,501
 #24 
A  nice  part of this discussion is  to show  the  need in the future  to be able to   understand  that  any training  is  specific  and  as long we  use  %  of  a  max  and not  understanding current limiter and the question , whether they recovered or not  so we    use sport as it suppose to be, for health  and not  for short  term bragging rights  of   ???

Here some interesting Reading  and many more paper  exist.

This  first one shows   what is overloaded  and  therefor  lie in our discussion   the question shows up. Overloaded with not optimal planned recovery times in between loads, or overloaded  due to another limiter  so this  part had  to compensate.

Author information

Abstract

AIMS:

The aim of this study is to determine the incidence of lone atrial fibrillation (LAF) in males according to sport practice and to identify possible clinical markers related to LAF among marathon runners.

METHODS AND RESULTS:

A retrospective cohort study was designed. A group of marathon runners (n = 252) and a population-based sample of sedentary men (n = 305) recruited in 1990-92 and 1994-96, respectively, were contacted in 2002-03 and invited to attend an outpatient clinic to identify suggestive symptoms of having experienced an arrhythmia requiring medical attention. In those with suggestive symptoms of atrial fibrillation, medical records were reviewed. Finally, LAF was diagnosed on the basis of the presence of atrial fibrillation in an electrocardiographic recording. In the group of marathon runners, an echocardiogram was performed at inclusion and at the end of the study. The annual incidence rate of LAF among marathon runners and sedentary men was 0.43/100 and 0.11/100, respectively. Endurance sport practice was associated with a higher risk of incident LAF in the multivariate age- and blood pressure-adjusted Cox regression models (hazard ratio = 8.80; 95% confidence interval: 1.26-61.29). In the group of marathon runners, left atrial inferosuperior diameter and left atrial volume were both associated with a higher risk of incident LAF.

CONCLUSION:

Long-term endurance sport practice is associated with a higher risk of symptomatic LAF in men. This risk is associated with a larger left atrial inferosuperior diameter and volume in physically active subjects.

 

And here one of the many  studies in this interesting direction

Europace. 2009 Jan;11(1):11-7. doi: 10.1093/europace/eun289. Epub 2008 Nov 6.

Endurance sport practice as a risk factor for atrial fibrillation and atrial flutter.

Mont L1Elosua RBrugada J.

Author information

Abstract

Although the benefits of regular exercise in controlling cardiovascular risk factors have been extensively proven, little is known about the long-term cardiovascular effects of regular and extreme endurance sport practice, such as jogging, cycling, rowing, swimming, etc. Recent data from a small series suggest a relationship between regular, long-term endurance sport practice and atrial fibrillation (AF) and flutter. Reported case control studies included less than 300 athletes, with mean age between 40 and 50. Most series recruited only male patients, or more than 70% males, who had been involved in intense training for many years. Endurance sport practice increases between 2 and 10 times the probability of suffering AF, after adjusting for other risk factors. The possible mechanisms explaining the association remain speculative. Atrial ectopic beats, inflammatory changes, and atrial size have been suggested. Some of the published studies found that atrial size was larger in athletes than in controls, and this was a predictor for AF. It has also been shown that the left atrium may be enlarged in as many as 20% of competitive athletes. Other proposed mechanisms are increased vagal tone and bradycardia, affecting the atrial refractory period; however, this may facilitate rather than cause the arrhythmia. In summary, recent data suggest an association between endurance sport practice and atrial fibrillation and flutter. The underlying mechanism explaining this association is unclear, although structural atrial changes (dilatation and fibrosis) are probably present. Larger longitudinal studies and mechanistic studies are needed to further characterize the association to clarify whether a threshold limit for the intensity and duration of physical activity may prevent AF, without limiting the cardiovascular benefits of exercise.

 

 

ryinc

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Posts: 369
 #25 
Juerg, Bobby thanks for the papers and additional info. To confirm a few points
1. The athlete did use to do long distance running for 20+ years. I agree that it is likely AF is coonected to the running - i know a few runners that were diagnosed.
2. The athlete cycles regularly and in the assessment did not push the hardest load possible so did not feel concerned about the asessment but based on your comments about having defibrillators ready etc i will not repeat the assessment
3. Bobby, the athlete HRs is consistently out
4. The athlete was a smoker, but for a relatively short time and many many years ago.
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