Post Number: 993
|Posted on Monday, December 08, 2008 - 01:08 pm: |
Here a very nice summary from:
Sue Hopkins MD PhD. University of California at San Diego
" Twenty five years of exercise and pulmonary gas exchange research: Still more questions than answers. "
Forty years ago, the conventiobal view of the pulmonary system was, that it did not (NOT) constrain maximal exercise performance in healthy humans.
However by the late 1970's there was increasing recognition that this view was incorrect, especially in highly aerobic humans and animals. Several studies were published documenting a fall in arterial partial pressure of oxygen (paO2) with exercise, with an associated worsening of gas exchange effieciency, manifest by an increase in alveolar-arterial difference for oxygen (AaDO2). This condition referred to as exercise induced arterial hypoxemia.(EIAH)
EIAH, has fascinated researchers in exercise physiology for the last quarter century. EIAH has been shown to impair VO2max and aerobic performance in some athletes. However despite some twenty five years of study, the underlying mechanisms of the increased AaDO2 are unresolved.. ."
So Sue hopkins showed a very interesting point:
A possible reason could be a rapid pulmonary capillary transit time as a cause of pulmonary diffusion limitation..
Woo how about the idea we have druing a VO2 FaCT CLR test to "force" the client to breath slower and deeper and the reaction we se immediatly of the FeO2 dynamic and the SpO2 levels.
The above idea is what we try to use as an explanation since many years.
A very high heart rate combined with a very high respiratory frequency and often a very low tidal volume may just simply be a very inefficient way of the body for an optimal gas exchange but mainly for an optimal O2 exchange from the lungs to the blood.
a) high blood flow speed
b) high air flow speed
c) low O2 pressure due to low tidal volume.
d) high % of dead space due to high respiration rate and low tidal volume.
We just testsed this weekend in the NOC of Biran Kozak some icehockey player.
VC 5.5 liter.
RF at the LBP 55- 60
TV at LBP 2.1 liter.
dead space calclated 250 - 300 ml.
VE 120 - 130 liter but 18 - 20 liter is "dead air"
By improving tehm to 30 breath / min and 3.5 - 4 L Tidal volume they would have only 9 liter dead air in the same VE and a much lower FeO2 %.
They FeO2 % is above 17 in the cases we tested, compared to respiratory trained people with FeO2 in the 15 + % range.
. I will show a very interesting research from UBC on differences in respiratory work between female and male athletes.
So come back and enjoy.
PS. For the critical reader. Check on the forum the 3 hour research work and look closer the last 5 min at the 3 hour mark. Check the change in RF. TV. and FeO2.
The idea was to see, whether the respiratory system still could change the FeO2 situation or not.
Post Number: 1920
|Posted on Saturday, September 19, 2009 - 06:35 am: |
Here an add on for discussion.
Well in fact the discussion should be over.
I wrote some questions a few month back to a very accepted institution for Education and research. After no answer over many weeks ( not unusual so actually very pleased with the answer) the discussion should be over. Short summary of the answer.
Respiration is never a limiting factor in performance sport.
We can't manipulate FeO2 as it is controlled over the bodies own reactions.
Hmmm so I did after that a simple test on the treadmill. Running by 5 % incline and 5 mph speed for 45 min.
After about 15 minutes I decided to drop my FeO2 % blow 15 % from a stable around 16 % during a relaxed run. So by 15 min my goal was to drop FeO2 % to 15 and or below and than back to "normal" and than reduce FeO2 above 16
I hope some people ( readers ) with VO2 equipment go and try the same.
Or our VO2 equipment does not work properly.
At least my goal was set and here the real print of the session.( Fit Mate print out from the company Cosmed ).
Just some thoughts for your self once you go through the info's.
Post Number: 303
|Posted on Saturday, September 19, 2009 - 12:13 pm: |
The ability to volitionally change the FeO2 should not come as any surprise to those who use VO2 instruments regularly. This is because the FeO2 is simply a measurement of how much oxygen is blown off during exhalation. The longer you hold your breath, the more oxygen will be taken up by the hemoglobin passing the alveoli in the lungs, and the less will be blown back off. If the resp rate is dropped significantly, as Juerg did in his case study, the FeO2 will show a dramatic drop.
Every one of our High Performance athletes, who have each done at least some respiratory training, are able to show the same pattern, with good control of FeO2 for at least a few minutes, before they are forced to return to their "normal" breathing pattern.
We have been able to demonstrate FeO2 of lower than 15% for over 20 minutes using three different breathing patterns. And the only requirement needed to keep FeO2 below a certain level, is to slow the respirations down significantly.
The Fitmate measures FeO2 each breath, and gives an average over a given time period that can be set in the parameters guide when setting up the machine. I believe it is an accurate measurement, but just poorly understood by most traditional test centres.
Post Number: 1926
|Posted on Sunday, September 20, 2009 - 02:14 pm: |
Now here a fun try out based on the above information.
As you can see, as I dropped the RF to about 20 my VE as well dropped. The TV in the slow breathing part was about 3.5 L
and in the normal TV was about 2.8 l and in the fast RF 40 about 2.2 L.
Now here for all VO2 tester.
Okay if the FeO2 is dropping as we breath slower let's do that.
Breath slower again at 20 RF , but keep the TV at 2.8 L and or lower.
Check the test results and see what the FeO2 is doing ,as you breath the same RF as above but a lower TV.
Will be interesting to see the information from the small practical approach.
Post Number: 1929
|Posted on Monday, September 21, 2009 - 06:52 am: |
As we discuss the above ideas.
a) Is it the respiratory frequency, which changes the FeO2 %
b) is it the Tidal volume which changes the FeO2 %
c ) is it a combination of both and if, which one may have the bigger influence
d) is it , that in some athletes the RF is the bigger influence and in others the TV.
Depending on which question we may find an answer we can than perhaps design a much more effective respiratory training and integrate this in some of the workouts.
Last but not least we than can assess, how much the respiratory change may have an influence on the cardiac work as well.
Here the fitmate printout of TV and FeO2
So the question is, is it really the slower breathing or is it the TV.
Try to play with same respiratory frequency and change TV.
Than play with same TV and change respiratory frequency and compare.
If you work with the same frequency take a metronome or a Spiro Tiger.
The maintaining of the same TV is somewhat harder, but after a few workouts you will get pretty close as you develop a very good feeling.
Once you have the respiration rate and the TV under control you can use them really will as bio markers.
Now assess , which of both frequency or TV will change:
1. FeO2 %
4. metabolic shifts at LBP with lactate
5. SpO2 situation
Post Number: 1930
|Posted on Monday, September 21, 2009 - 08:04 am: |
Thanks , here an abstract i received on my mail.
The question is , whether there may be a difference in rest and in action, where the body may actually "look " for O2. Here to enjoy .
" The Effects of Tidal Volume and Respiratory Rate on Oxygenation and Respiratory Mechanics During Laparoscopy in Morbidly Obese Patients
Juraj Sprung, MD PhD*, David G. Whalley, MB ChB, Tommaso Falcone, MD,, William Wilks, RT, James E. Navratil, MD, and Denis L. Bourke, MD||
*Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota; Department of Anesthesiology, The Cleveland Clinic Foundation, Naples, Florida; Department of Obstetrics and Gynecology, Minimally Invasive Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio; and ||Department of Anesthesiology, University of Maryland, and Veterans Administration Medical Center, Baltimore, Maryland
Address correspondence to Denis L. Bourke, MD, University of Maryland, Anesthesiology Service, Baltimore VA Medical Center, 10 North Greene St., Baltimore, MD 21201. Address e-mail to email@example.com. Address reprint requests to Juraj Sprung, MD, PhD, Mayo Medical School, Department of Anesthesiology, Saint Mary’s Hospital, MB 2-752, 200 First St. SW, Rochester, MN 55905.
Morbidly obese (MO) patients undergoing laparoscopy have lower PaO2 compared with normal-weight (NW) patients. We hypothesized that increases in tidal volume (VT) or respiratory rate (RR) would improve oxygenation. All measurements were performed at: 1) baseline: VT 600–700 mL and 10 breaths/min, 2) double VT: VT 1200–1400 mL and 10 breaths/min, and 3) double rate: VT 600–700 mL and 20 breaths/min. We calculated static respiratory system compliance (Cst,rs) and inspiratory resistance (RI,rs). End-tidal CO2 was measured with a mass spectrometer, and PaO2 and PaCO2 with a continuous blood gas monitor. Supine anesthetized MO patients had 29% lower Cst,rs than the NW patients (P <0.05).> 0.7). Before pneumoperitoneum, RI,rs was higher in the MO patients compared with the NW patients regardless of body position (P = 0.01). Doubling either RR or VT before pneumoperitoneum did not change RI,rs in either group. After pneumoperitoneum, RI,rs increased in both the head-down and head-up positions (P < 0.05), but not in the supine position. Regardless of the conditions studied, alveolar-arterial difference in oxygen tension was always significantly higher in MO patients (P < 0.05). The alveolar-arterial difference in oxygen tension was not affected by body position, pneumoperitoneum, or the mode of ventilation. Arterial oxygenation during laparoscopy was affected only by body weight and could not be improved by increasing either the VT or RR.
IMPLICATIONS: Morbid obesity decreases arterial oxygenation and respiratory system compliance. During laparoscopy, arterial oxygenation is affected only by the patient’s body weight. Increases in tidal volume or respiratory rate do not improve arterial oxygenation."
Post Number: 1935
|Posted on Tuesday, September 22, 2009 - 06:29 am: |
This is an interesting summary of a nice study.
Look carefully on the SpO2 values.
- TRADITIONALLY they will tell us , that SpO2 in healthy people will not drop.
- look at the respiratory rate and the Tidal volume.
- Next step is to see, what is happening in the cardiac system comparing this too sports.
As well you can see, that a respiratory training may look different for each sport and it would be interesting to see, whether the limitation in both sports is caused by the same system or whether there are different limitation in the 2 sports by the same person.
Again teh question here remains:
Is the drop in SpO2 and PaO2 caused by the higher or slower respiration rate or by the higher or lower Tidal volume.
They are closely related to each other in non respiratory trained athletes, because as soon you breath faster you often breath less deep.
The question or task would be to "overrule " this reaction and try to keep the tidal volume despite a higher respiration rate and visa versa and see the results.
Post Number: 1936
|Posted on Tuesday, September 22, 2009 - 06:30 am: |
here the study
Is exercise-induced arterial hypoxemia in triathletes dependent on exercise modality?Galy O, Le Gallais D, Hue O, Boussana A, Préfaut C.
Laboratoire ACTES, UFR-STAPS Antilles-Guyane, Pointe à Pitre Cedex, France. firstname.lastname@example.org
To determine whether exercise modality affects arterial hypoxemia (EIAH) during training-intensity exercise, 13 triathletes performed 20 min of cycling (C) followed by 20 min of running (R): C-R, and two weeks later, 20 min of R followed by 20 min of C:R-C. Each trial was performed at an intensity slightly above the ventilatory threshold and close to the daily training intensity (75 % of VO2max). Ventilatory data were collected continuously using an automated breath-by-breath system. Partial pressure of oxygen in arterial blood (PaO2) was measured after each C and R segment and arterial oxyhemoglobin saturation (SpO2) was monitored continuously via pulse oximetry. The metabolic rate was similar across modalities and trials, i.e., C-R (53.8 +/- 3.8 vs. 51.1 +/- 5.3 ml.min(-1).kg(-1)) and R-C (52.2 +/- 4.5 vs. 53.2 +/- 4.6 ml.min(-1).kg (-1)). EIAH showed significantly greater severity for R compared to C irrespective of the order (p < 0.05 for both trials). R values of PaO2 (and SpO2) for C-R and R-C were 88.7 +/- 6.0 mm Hg (93.0 +/- 0.6 % SpO2) and 86.6 +/- 7.3 mm Hg (93.5 +/- 0.6 % SpO2) and C values were 93.7 +/- 8.4 mm Hg (95.4 +/- 0.4 % SpO2) and 91.4 +/- 5.4 mm Hg (94.8 +/- 0.3 % SpO2). R ventilatory data described a significantly different breathing pattern than C, with higher respiratory rate (35.9 b.min(-1) vs. 51.1 b.min(-1) for C-R, p < 0.01; and 50.0 b.min(-1) vs. 41.5 b.min(-1) for R-C, p < 0.01) and lower tidal volume (2636 ml vs. 2282 ml for C-R, p < 0.02 and 2272 ml vs. 2472 ml for R-C, p < 0.05). We concluded that EIAH was greater during running than cycling for a similar metabolic rate corresponding to training intensity and that EIAH could thus be considered dependent on exercise modality.
Post Number: 304
|Posted on Tuesday, September 22, 2009 - 08:32 am: |
I will start by admitting that I have not had time this week to play with the Fitmate to see what changes occur in FeO2 numbers occur, with the different breathing patterns Juerg has suggested we investigate. However, lets talk about the FeO2 data, and what it really means, and we should be able to make some good predictions.
FeO2 is simply the per cent oxygen in the expired gases. It is a end product of a series of steps that begins with inhalation of oxygen containing air (approximately 21% if brething room air), continues through the process of supplying some of that inspired oxygen to the alveoli for delivery to the pulmonary capillaries,and diffusion of a portion of the oxygen contained in the alveoli to the vascular bed through a process of diffusion. The unused portion of oxygen is expired. The higher the oxygen dependent metabolic demands on the system, the more oxygen will diffuse across the membrane due to the concentration gradient, and the less will be available for expiration.
To examine the changes as Juerg suggests, means we must best attempt to control the other variables that will affect FeO2. That is, we need to control the metabolic demands, by stabilizing the work being done by the body, as in holding a steady wattage on a bike, or running a constant speed on a treadmill, ans assuming the change in breathing patterns does NOT change the oxygen requirements of the exercise itself, which in fact, it might do. By controlling the intensity, and ensuring we are working a constant VO2, we can then examine whether the FeO2 changes with Tidal Volumes (TV) or Respiration Rate (RR).
Here are some thoughts...a constant energy demand in terms of wattage or speed, should yield a constant VO2 demand (if the work is done below LBP). If the volume of oxygen consumed by the body is constant, then the FeO2 will also be constant, until the Ve (minute ventilation) is changed in some manner. That is, the amount of oxygen drawn from the inspired air will remain the same, whether it is provided in big slow breaths, or short fast breaths. The Ve is simply a product of the TV and the RR. For example, one can get to a Ve of 100l/min, by breathing 50x2 or by breathing 25x4.
There is a problem with using the simple numbers from the Fitmate, and that is the factor of dead space, that we have talked about before, which increases with increased RR. So, even though the Ve on a Fitmate will yeild 100 l/min in the above examples, the higher RR will have twice the dead space (approximately 50x0.2=10 compared with 25x0.2=5). This means there is less air available for diffusion of oxygen. In the high RR group, only 90l will be available for oxygen diffusion, whereas in the low RR group 95l will be available.
If the same amount of total oxygen is consumed, then in fact, the higher RR group will actually need to extract a greater percentage of the oxygen available. Have I sufficiently confused everyone?
However, if the lower resp rate, also results in lower total ventilation, then the body will be forced to be more efficient at extracting the oxygen form the inhaled air, and drop the FeO2.
As Juerg mentioned. In most cases, the slowing of the resp rate results in lower total Ve, which means a greater percentage of oxygen is extracted from the available pool, and results in a lower FeO2.
In the tests I reviewed, it is fairly obvious that as the minute ventilation increases, so does the FeO2 value, and this can be reversed by dropping Ve through either slowing the respirations, or by dropping the tidal volumes.
In fact, I think these numbers are even more connected in the Fitmate than all this round about way of describing it that I have attempted today. And that is because, I believe the Fitmate calculates the VO2, by taking the measurement of FeO2, subtracting this value from the standardized oxygen in room air, and multipying this times the minute ventilation, to yield a calculated volume of oxygen utilized per minute. I think any discrepancies in numbers are the result of not taking into account dead space changes with regards to the impact of resp rate on the actual amount of air available for oxygen exchange.
Is that confusing enough?
Please correct me if I am wrong.
Post Number: 1937
|Posted on Tuesday, September 22, 2009 - 10:43 am: |
Here is another link to some more reading into this area:
Here a question to all the people , who tried the idea of stable RR and change of TV and stable TV and change of RR.
" Ventilation/perfusion mismatch"
In a 'perfect lung' all alveoli would receive an equal share of alveolar ventilation and the pulmonary capillaries that surround different alveoli would receive an equal share of cardiac output ie.ventilation and perfusion would be perfectly matched.
Diseased lungs may have marked mismatch between ventilation and perfusion. Some alveoli are relatively overventilated while others are relatively overperfused (the most extreme form of this is shunt where blood flows past alveoli with no gas exchange taking place (figure 1). Well ventilated alveoli (high PO2 in capillary blood) cannot make up for the oxygen not transferred in the underventilated alveoli with a low PO2 in the capillary blood. This is because there is a maximum amount of oxygen which can combine with haemoglobin (see haemoglobin-oxygen dissociation curve figure 2a). The pulmonary venous blood (mixture of pulmonary capillary blood from all alveoli) will therefore have a lower PO2 than the PO2 in the alveoli (PAO2). Even normal lungs have some degree of ventilation/perfusion mismatch; the upper zones are relatively overventilated while the lower zones are relatively overperfused and underventilated."
In areas where we not breath regular we seem to "loose" some ability to exchange O2.
"In order to decrease the detrimental effect that shunt and ventilation/perfusion mismatch have on oxygenation, the blood vessels in the lung are adapted to vasoconstrict and therefore reduce blood flow to areas which are underventilated. This is termed hypoxic pulmonary vasoconstriction and reduces the effect of shunt. "
Now what we see in sport is often a very "underdeveloped" ability to really breath with the diaphragm.
Many Athletes under severe performance breath with a lot of so called auxilliary muscles ( neck ) and by moving their shoulders up reduce the ability to breath with the diaphragm
This you can see in one of the articles where you can compare running TV and cycling TV.
This leads to the fact , that in many athletes the SpO2 drops further in running than in cycling and the FeO2 is higher in running than in cycling.
In both cases again we see a difference in the way that higher RR goes together with lower TV.
So if we move the breathing to the "higher area , where we have an over ventilated area, but a lower perfusion rate.
The main reason some believe is, that in the night , where we mainly breath with the diaphragm the lower area is mainly used and we have a perfect perfusion.
So this may lead to :
"In order to decrease the detrimental effect that shunt and ventilation/perfusion mismatch have on oxygenation, the blood vessels in the lung are adapted to vasoconstrict and therefore reduce blood flow to areas which are underventilated. This is termed hypoxic pulmonary vasoconstriction and reduces the effect of shunt. "
As with so many reactions, we will change from optimal situation to work or training adapted situations.
Many athletes , who don't breath properly during a workout will therefor move air in a lungs area ( upper area ), where there may be a great ventilation but not a great perfusion and visa versa.
Now when you try to maintain the Respiration rate , but you try to increase the Tidal volume you may see very individual reactions of FeO2, which some use to find out the difference between ventilation and perfusion.
Based on this info we than design a different respiratory training.
There are different respiratory measurement with tape measure existing to actually see some of this trends.
We are talking of: Clavicular diameter,
costo sternal diameter, xyphoid diameter,
Some older respiratory schools used this information even for diagnositical tools of some diseases and they where surprisingly accurate just from observation of the respiratory breathing pattern.
Nose breathing will move the air different in the lungs , than mouth breathing and some go so far , that they will explain , that if you breath in with one side of the nose you attract one side of the diaphragm more than the other.
There is a very fun practical approach in the school to feel something .
Okay let's try .
Close one nose side with a finger and breath deep in , all you can . Than once you feel that is it , close immediatly the side your where breathing in and open the other side and try to breath in a again.
What do you feel ?
Could a missmatch of ventilation and or perfusion exist in many "healthy " athletes, which may help to explain some very individual reactions of FeO2 trends, where some react different based on respiratory frequency and some react different when playing with Tidal volume.
Try it out and show on here the different infos you may find or not find.
Post Number: 1938
|Posted on Tuesday, September 22, 2009 - 12:10 pm: |
now here for all who have fun so far a few more "exercise" with bio feedback n the screen
1. Run or bike or row on where you consider is teh change from the STF to the FTF intensity.
Now try there to breath a fixed respiration rate lets' say 20 on the bike and rowing and perhaps 30 in running.
Now breath a big TV and a small Tidal volume for example 3 liter and 2 liter and check FeO2 and SpO2.
1.2. Now repeat the same intensity but you breath a fixed TV ( 2.5 ) and you change respiration rate from 20 to 40 for example.
2. Now repeat a day later the same but at LBP
If that is too hard try the following .
Sit first and breath with your diaphragm deep in and out and you will see the abdominal area going in and out.
start for 3 min with 20 RR than for 3 min with 30 RR and than for 3 min with 40 and if you can three minute with 50 RR.
Watch where you "loose " the RPM for abdominal and diaphragm pattern and you start popping up and down on the saddle ( resp. your chest and shoulder start to go up and down.)
Keep the same TV. Now repeat this ideas in sitting bending forward like on a bike and in standing upright.
Than do the same but use a step in TV.
Start with 30 RR and 2 L TV and go to 2.5 3 . 3.5 L and again watch what happens to the "coordination " pattern in your respiratory motion.
Once you have a individual reaction on yourself go back and think about the "miss-match of ventilation and perfusion" assume one or the other scenario and than think what may happen.
This are very common Spiro Tiger exercises for patients and athletes alike.
Post Number: 1945
|Posted on Thursday, September 24, 2009 - 01:29 am: |
What we are doing today and tomorrow.
1. Assessing the influence of dead space size on FeO2 and actuall work ( LCWindex ) on the heart as well as on O2 use ( VO2 ) I build a home testing "entrapment yesterday and see whether it works.
The question is, whether the dead space has an influence on FeO2 % so that different type of breathing with different volume of dead space may influence the O2 and CO2 movements.
What I did yesterday after "construction is the testing of the influence of respiratory frequency on FeO2 % compared with the influence of TV to the FeO2 as theories and practical testing may have different outcomes,.
Here the practical datas from this case study.
What I produced is a miss match of ventilation and perfusion areas by breathing in some cases with the diaphragm and than more apical.( by choosing different endurance activity like running and biking )
The goal was to get the respiratory frequency as close as possible or the Tidal volume as close as possible.
Case 1 . Stable respiratory frequency but change in Tidal volume:
Here the results as average.
RF 19.7 / 19.6 / 32 / 32
TV 3.0 / 3.4 / 3.6 / 2.7
FeO2 15.84 / 15.35 / 16.75 /16.26
VE 59.2 / 65.5 / 117.7/ 85.1
VO2/kg 28 / 32 / 43.8 / 34.8
Now here fixed Tidal volume
TV 3.4 / 3.4 / 3.14 / 3.18
RF 19.7 / 28.4 / 18.8 /25.5
FeO2 15.35 / 16.4 / 16.26 / 16.14
Ve 65.5 / 97.9 / 59.1 / 81.8
Now the next step is to go through this case and see, whether TV and or RF or both together have a trend info on FeO2 or whether there are other factors we don't take into consideration if using respiration as a bio marker for feedback on physiological reactions.
Questions like :
Is a higher TV more important or not for FeO2 results ?
Is a higher respiratory rate and advantage and or a disadvantage for performance and so on.
Does a higher respiration rate always goes together with a lower Tidal volume.
Does a mismatch in ventilation and perfusion can be corrected with specific training .
Does in different sport the miss match have an influence on O2 and CO2 trends.
And last but not least do this intervention actually change performance and how much does the cardiac trend like higher HR with lower or higher stroke volume and therefor perfusion changes can as well influence O2 extraction at teh lungs / blood area, as well at the cellular area.
As you can go though the above numbers you will see many "oh see " followed by "oh no" .
Now here an easy solution for people too confused on the above thoughts.
If you stick to wattage and % of FTP and or HR based on 220 - age and % of that or on Speed and maximal speed and % of that you avoid headache and have a very easy way of planning for your clients a great looking exercise and training program.
\ No discussion no questions just clear and straight forward answer caused by your calculator.
It may even save some of your head ache medications. ( Smile )
Post Number: 1946
|Posted on Thursday, September 24, 2009 - 02:00 am: |
wowww some readers must be 24 h on this Forum . Thanks for teh fast email. here to "unpuzzle" some of the confusion.
1. Does a lower or slower Respiration frequency leads to a lower FeO2 ?
RF 18.8 vs 25.5 so clear RF difference.
Here the FeO2 numbers
FeO2 for 18.8 16.26 vs 16.14
Now look at TV Does a bigger TV has always a lower FeO2
TV 2.7 vs 3.6
Fe O2 16.26 vs 16.75
TV 3.4 vs 2.7
FeO2 15.35 vs 16.26
Sue Hopkins research comes in mind and the old idea of Miescher from the last century, that the situation at the O2 exchange are can be influenced by speed of the blood ( HR ) , the pulmonary vascular resistance ( depending on pCO2 ) the tidal volume as an influence of miss match on ventilation and perfusion areas. The "speed" or contact time of the air on the exchange area and so on.
So what we look as well is , whether a higher HR has a direct influence on O2 exchange as well.
remember that the O2 "stickiness" (affinity ) to Hb is much higher than the release ability of CO2 from plasma so the exchange of O2 may be somewhat harder for the system than the release of CO2.
Here a practical application:
In a hilly run or bike or ski try to think as a coach what may be needed at the current moment :
Intake of O2 or release of CO2. Taking a chance of short deficit of ATP versus reloading of ATP?
Using a higher PCO2 to decrease SVR and therefor unload some cardiac work ?
Now in a training session this can be lot's of fun and has to be practiced like any other technique, so that under race conditions the body is doing that on its own.
Problem that you need a thinking coach with a thinking and great feedback client versus a good computer technician with a good mathematician
Post Number: 487
|Posted on Thursday, September 24, 2009 - 03:21 am: |
Juerg wrote :-
"If you stick to wattage and % of FTP and or HR based on 220 - age and % of that or on Speed and maximal speed and % of that you avoid headache and have a very easy way of planning for your clients a great looking exercise and training program."
"Problem that you need a thinking coach with a thinking and great feedback client versus a good computer technician with a good mathematician"
I think some of those coaches will probably feel insulted.
Only today I posted sum of your data you wrote a few months ago about how different cadences affected the body in terms of VO2, HR, VE and RF ( TV ) and FeO2 %.
The reply i got from a coach who uses power mostly to coach his clients :-
"If you can make sense of Jeurg, you're a better man than me
that's all very nice but what matters is speed (& power), not efficiency"
Post Number: 1947
|Posted on Thursday, September 24, 2009 - 03:38 am: |
He makes a good point.
" The only thing which matters is speed and power. ".
My question back would be:
Who produces this speed and power.
Why is an old fart still biking or cross country ski much better , than a young storng athelets or beginner.
Could there be some connection with efficiency.
Could it be that even a believer of Watt FTP may see, that some cyclist can bike by 80 % of the max power and the FTP is by that 80 %. And other bikers can only go by 65 % of the max power at FTP.
hmmm may be it is effciency on how they can use their physiological systems ?
So many questions.
Again I am clear in that way and agree with teh above info on speed and wattage . It is all what matters when you like to stop thinking and have a great day out on teh bike.
Post Number: 1948
|Posted on Thursday, September 24, 2009 - 04:36 am: |
Hmm it may be a bit "insulting" to all cycling coaches to tell them , that it is only power and speed and NOT efficiency.
Nevertheless if you google cycling and efficiency you will be surprised on how many coaches believe efficiency may be important. So if you can make sense out of this coaches answer you are better man than me ( Smile )
here one of many great examples from a coach, who is working on efficiency . "
Smooth Strokes - Improving Your Cycling Efficiency
by Seiji Ishii
»» Jump to the drills!
We have all seen it at our local club ride or on TV, athletes with a seemingly effortless pedal stroke, turning an incredible cadence, power flowing to the pedals without any wasted motion or energy. Smooth and efficient transfer of energy from body to bike that results in quicker times in the bike leg and leaving more reserves for the run leg. Armstrong harnessed a quicker and more efficient pedal stroke to help in his domination of the last five Tours. Competitors could not overlook his obviously quicker and more efficient pedaling style. Yes, we have seen it, read it, and heard it but have we practiced what is seemingly a key to success in the cycling discipline?
Triathletes spend incredible amounts of time and energy into refining swim stroke technique and an energy saving running style. The pedaling stroke is often overlooked; after all we have all been riding bikes since childhood. This is akin to saying you won't drown and that's good enough. And since the bike leg is always proportionally longer in time than the other legs of a triathlon, it starts to make sense that efficiency on the bike may warrant some serious thought and effort in your training regime.
Where do you start on your quest for that energy efficient smoothness? First off has to be bike fit. All talk about pedaling dynamics doesn't matter if your bike fit doesn't allow you to use your muscles in an effective manner. Correct fit makes learning and utilizing good pedaling mechanics much easier and will keep you more efficient (and injury free) in the long run. Proper bicycle fit will allow you to use the most of the correct muscle mass to apply force to the pedals.
The next step is to develop an efficient application of force. What this involves is applying force to the pedals during then entire 360 degrees that make up the pedal stroke. You can utilize a simple drill to help teach your nervous system and ready your musculature to apply force all the way around. This one legged pedaling drill will make you aware of deficiencies in pedal stroke and will stress the muscles in your legs that are not being used to their potential. Set your bike up on an indoor trainer and place a chair on each side of your bicycle. After a warm up period, place one foot on a chair, make sure that your hips are still square, and pedal a short interval with one leg only. Concentrate on the top and bottom sections of the pedal stroke, the areas where it is the most difficult to apply force. You should attempt to slide your foot forward inside your shoe as you clear the top of the stroke and slide your foot back inside your shoe across the bottom. As your foot starts to come up again, just try to carry the momentum back to the top. You are not attempting to apply an upwards force here, you are just unloading the weight of your leg from the pedal so that the opposing leg does not have to waste any energy lifting that dead weight. A cue you can use here is to attempt to throw your knee over the handlebar. A visual indicator you can use during this drill is to look at the top run of your chain. If the chain droops momentarily, that is a point within your pedal stroke where you are not applying tension on the chain, which indicates you are not applying the correct force to the pedal. Start this drill at a slow cadence so you can concentrate fully on correct form. Gradually increase your cadence while maintaining this form and continue the interval only a long as this form holds true. You can start with 30 second intervals and work up to one minute per leg. Alternate legs and periodically use both feet concentrating on the form you were using with one leg. More than likely you will feel fatigued in strange muscles that you have been underutilizing, usually the hip flexors (in front of your hip joint) and anterior tibialis (in front of your shin). Remember to only perform this at a cadence and time interval that allows perfect form.
Cadence is the next factor in your quest for efficiency. Practicing and implementing a higher cadence during your cycling will give you a deadly double edged sword: First, the higher your cadence, the less force you must apply at the pedals to generate the same power. Less force applied to the pedals means less stress applied to the musculature of your legs, leaving you more reserves for the run. You can, of course, apply the same force with a higher cadence to achieve a higher speed as well. Second, the higher speed at which your feet move through a pedal cycle results in a smaller time interval during which you have to apply this force. Basically you have less time to apply the force during each crank revolution since you are getting through the cycle faster. The effectiveness of this one-two punch can also be better understood if we think about some physics here. Power is defined as the product of force and velocity. A higher cadence diminishes the force and the length of time you apply this force per pedal stroke. The result is less power produced per pedal stroke. This is what saves your musculature. Just ask Professor Armstrong about that equation. You can use high cadence drills to teach your nervous system to operate in this more efficient manner. Use a low gear that keeps you well in your aerobic HR zones and do 5-10 minute intervals at a cadence between 107 and 130. Relax your upper body and feet, be smooth and supple with your legs. No bouncing in the saddle! Remember that you are specifically stressing foot speed here, not force, so the force you apply to the pedals should be very low. Recover for the same amount of time at a lower cadence of 90 to 100. Use various hand positions during these drills to make sure you can use a fast cadence no matter how your body is positioned on your machine. You can also stress using correct cadence while fatigued by doing these intervals at the end of a long ride. Recovery rides provide another opportunity to do these drills since the muscular stress is so low. The ultimate goal of this drill is that you engrain this fast cadence into your neuromuscular system and employ it in all your rides. The accompanying chart describes a sample workout for both the single leg pedaling drills covered earlier and these high cadence drills. This chart is only a sample of the many variations that you can add to these very effective drills.
The early base building periods are the optimal time to focus on pedaling skills and the described drills. During these periods intensity is low so it is much easier to focus on efficiency. Also, the skills and motor patterns that make up an efficient pedal stroke must be learned at lower force and aerobic intensity levels before you can carry them over at high force and aerobic intensity levels.
Once you have mastered the efficient application of force and adopted a quicker pedaling cadence you will be well on your way to harnessing more power, higher efficiency, and less leg fatigue on the bike leg. You will be able to sustain a higher average speed during the bike and feel less muscle fatigue when you leave T2. Your competitors may notice something different about your pedaling style as you scream past them on the bike leg in all your efficient glory or float past them on the run on your fresh and springy legs. You will definitely notice the improved results brought to you by your newly acquired skills."
Post Number: 1949
|Posted on Thursday, September 24, 2009 - 05:21 am: |
Here another "efficiency idea " vs speed and wattage :
Eur J Appl Physiol. 2007 November; 101(4): 465–471.
Published online 2007 July 28. doi: 10.1007/s00421-007-0519-3. PMCID: PMC2039810
Copyright © Springer-Verlag 2007
The effect of ambient temperature on gross-efficiency in cycling
Florentina J. Hettinga,1,4 Jos J. De Koning,1,3 Aukje de Vrijer,1 Rob C. I. Wüst,1 Hein A. M. Daanen,1,2 and Carl Foster3
1Research Institute MOVE, Faculty of Human Movement Sciences, VU University, Amsterdam, The Netherlands
2TNO Defence, Security and Safety, Soesterberg, The Netherlands
3Department of Exercise and Sports Science, University of Wisconsin-LaCrosse, La Crosse, USA
4Faculty of Human Movement Sciences, Vrije Universiteit, Van der Boechorststraat 9, 1081 BT Amsterdam, The Netherlands
Florentina J. Hettinga, Phone: +31-20-5988557, Fax: +31-20-5988529, Email: email@example.com.
Accepted June 25, 2007.
Materials and methods
References AbstractTime-trial performance deteriorates in the heat. This might potentially be the result of a temperature-induced decrease in gross-efficiency (GE). The effect of high ambient temperature on GE during cycling will be studied, with the intent of determining if a heat-induced change in GE could account for the performance decrements in time trial exercise found in literature. Ten well-trained male cyclists performed 20-min cycle ergometer exercise at 60% (power output at which VO2max was attained) in a thermo-neutral climate (N) of 15.6 ± 0.3°C, 20.0 ± 10.3% RH and a hot climate (H) of 35.5 ± 0.5°C, 15.5 ± 3.2% RH. GE was calculated based on VO2 and RER. Skin temperature (Tsk), rectal temperature (Tre) and muscle temperature (Tm) (only in H) were measured. GE was 0.9% lower in H compared to N (19.6 ± 1.1% vs. 20.5 ± 1.4%) (P < 0.05). Tsk (33.4 ± 0.6°C vs. 27.7 ± 0.7°C) and Tre (37.4 ± 0.6°C vs. 37.0 ± 0.6°C) were significantly higher in H. Tm was 38.7 ± 1.1°C in H. GE was lower in heat. Tm was not high enough to make mitochondrial leakage a likely explanation for the observed reduced GE. Neither was the increased Tre. Increased skin blood flow might have had a stealing effect on muscular blood flow, and thus impacted GE. Cycling model simulations showed, that the decrease in GE could account for half of the performance decrement. GE decreased in heat to a degree that could explain at least part of the well-established performance decrements in the heat.
Keywords: Heat, Performance, Muscle temperature
ConclusionGE was lower in the heat. Tm was not high enough to make mitochondrial leakage a likely explanation for the observed reduced GE. Neither was the increased Tre. The extra VO2 in the H condition seems to be at least partially attributable to the extra myocardial VO2, since a higher cardiac output has to exist to continue supplying the muscles with the same blood flow, but have to send extra blood to the skin for cooling and thus impacted GE. Based on our findings under the current circumstances, it can be concluded that the temperature-induced change in GE could account for about half of the well-established performance decrements found during time trial exercise in the heat.
Post Number: 1950
|Posted on Thursday, September 24, 2009 - 05:31 am: |
And here to add more discussion to the efficiency a nice study :
Effects of pedal frequency on muscular efficiency during cycling exerciseAccession number;06A0036924
Title;Effects of pedal frequency on muscular efficiency during cycling exercise
Author;TOKUI MASATO(Kyushu Women's Junior Coll.) HIRAKOBA KOHJI(Kyushu Inst. Technol.)
Journal Title;Proceedings of the Symposium on Biological and Physiological Engineering
Figure&Table&Reference;FIG.3, TBL.2, REF.15
Abstract;This study was designed to clarify the effect of pedal frequency on muscular efficiency during cycling exercise with the same total work. Seven healthy male subjects (age; 22.5.+-.0.9 yr, height; 169.+-.4.8 cm, mass; 65.0.+-.7.5 kg) performed three exercise tests with different pedal frequencies (40, 80 and 120 rpm) on a cycle ergometer. The exercise test consisted of 3-min rest and unloaded cycling for 2 min followed by 5-min constant-load exercise. Gas exchange parameters, heart rate and electromyogram of the vastus lateralis were continuously measured throughout the exercise tests. Fingertip capillary blood samples for lactate concentration were taken before and after each exercise test. VO2 during constant-load exercise in 80 rpm was observed to be the lowest value, despite the fact that total work calculated as the sum of internal and external work was the same level in the three trials. Therefore, the true efficiency (.ETA.true) in 80 rpm revealed a significantly higher value (28.9.+-.0.8%) compared to 40 (24.3.+-.0.5%) and 120 rpm (22.3.+-.0.9%). From the results of this study, it is suggested that the lower .ETA.true in 40 and 120 rpm compared to 80 rpm may result from the greater recruitment of low-efficiency type II muscle fibers, presumably owing to higher tension per muscle contraction (40 rpm) and faster contraction velocity (120 rpm). (author abst.)
Post Number: 24
|Posted on Thursday, September 24, 2009 - 06:42 am: |
Back to the TV vs FeO2 subject, I can add some data from a test that we did a while ago where we were trying to establish the extra "work" required by breathing at a faster rate but controlling for tidal volume. We attempted to test at a breathing frequency of 15 then double that to 30 then back to 15 and maintain a large TV throughout - with the idea being that we were using a high percentage of the vital capacity to maximize the O2 gradient in the lungs. We didn't get the numbers exactly but here's what happened:
8 min blocks of cycling at 20% below LBP power, LBP hr 160. VC 6.5.
VO2 VE RF HR FeO2 TV SpO2 BLa
41.3 78.2 14.6 149 15.81 5.36 94% ??
45.4 141.2 29.5 155 17.79 4.79 98% 3.1
43.9 80.3 13.6 156 15.62 5.90 94% 1.6
The heart rate during the last run steadily increased from 152 to 159.
End result: with TV relatively close, big difference in FeO2. Cost of increased RF approx 10% VO2 (LCWi?). Of course this was only one test, unfortunately our Fitmate was damaged before we could try again. There seems to be lots of other possible interactions so I don't know if you can draw any conclusions?
It will be interesting when we can repeat this test with the Fitmate and the Physio Flow.
Post Number: 1951
|Posted on Thursday, September 24, 2009 - 09:47 am: |
Here a study with the argumentation , that change in respiratory frequenzy may not influence O2 uptake.
Unfortunately they did not assessed the situation of stable RF or stable TV.
Charles D. Kennard1, Bruce J. Martin2 and Physiology Section/Medical Sciences Program
(1) School of Basic Medical Sciences, University of Illinois, 61801 Urbana, IL
(2) 256A Myers Hall, Indiana University, 47405 Bloomington, IN, USA
Accepted: 15 November 1983
Summary Although many studies indicate that the spontaneous breathing frequency minimizes breathing work, the consequences of this for exercise energetics have never been investigated. To see if the spontaneous exercise breathing frequency minimizes oxygen uptake, we compared during treadmill walking (2/3 max) at several alternative frequencies. The alternative frequencies ranged from the lowest sustainable to a frequency twice the spontaneous value. All eight subjects adjusted tidal volume to comfort. Exercise oxygen uptake was constant, independent of breathing frequency. At the same time, minute ventilation rose to be 65% greater at the highest frequency than at the lowest (P<0.01). We then reproduced the various exercise frequencies, tidal volumes, and ventilations during seated isocapnic hyperpnea to measure with locomotory muscles at rest. Once again, oxygen uptake was constant, independent of breathing frequency. We conclude that the spontaneous exercise breathing frequency fails to minimize during either exercise or resting reproduction of exercise ventilation.
Post Number: 1952
|Posted on Thursday, September 24, 2009 - 10:29 am: |
Hey Duncan , here an interesting study on the cardiac reactions if we change FeO2 and with it potentially the cardiac reactions.
This can be one of our test ideas in the next week camp where we can produce a hypoxic hypercapnic reaction by using either different respiration rate and a fixed TV or visa versa by using the new one piece spiro tiger and we can control the TV with that , as well as the respiratory rate and at the same time look at changes in FeO2 and as well cardiac reactions .
For all readers not able to be in our camp we will post results on here.
Cardiovasc Ultrasound. 2004; 2: 22.
Published online 2004 November 2. doi: 10.1186/1476-7120-2-22. PMCID: PMC529306
Influence of oxygen tension on myocardial performance. Evaluation by tissue Doppler imaging
Ole Frøbert,1,2 Jacob Moesgaard,1 Egon Toft,3 Steen Hvitfeldt Poulsen,4 and Peter Søgaard1
1Department of Cardiology, Center for Cardiovascular Research, Aalborg Hospital, Aarhus University Hospital, Denmark
2Institute of Pharmacology, University of Aarhus, Denmark
3Center for Model-based Medical Decision Support Systems, Department of Health Science and Technology, Aalborg University, Aalborg, Denmark
4Skejby University Hospital, Aarhus, Denmark
Ole Frøbert: firstname.lastname@example.org; Jacob Moesgaard: email@example.com; Egon Toft: ET@healthntech.dk; Steen Hvitfeldt Poulsen: firstname.lastname@example.org; Peter Søgaard: email@example.com
Received August 26, 2004; Accepted November 2, 2004.
Low O2 tension dilates coronary arteries and high O2 tension is a coronary vasoconstrictor but reports on O2-dependent effects on ventricular performance diverge. Yet oxygen supplementation remains first line treatment in cardiovascular disease. We hypothesized that hypoxia improves and hyperoxia worsens myocardial performance.
Seven male volunteers (mean age 38 ± 3 years) were examined with echocardiography at respiratory equilibrium during: 1) normoxia (≈21% O2, 79% N2), 2) while inhaling a hypoxic gas mixture (≈11% O2, 89% N2), and 3) while inhaling 100% O2. Tissue Doppler recordings were acquired in the apical 4-chamber, 2-chamber, and long-axis views. Strain rate and tissue tracking displacement analyses were carried out in each segment of the 16-segment left ventricular model and in the basal, middle and apical portions of the right ventricle.
Heart rate increased with hypoxia (68 ± 4 bpm at normoxia vs. 79 ± 5 bpm, P < 0.001) and decreased with hyperoxia (59 ± 5 bpm, P < 0.001 vs. normoxia). Hypoxia increased strain rate in four left ventricular segments and global systolic contraction amplitude was increased (normoxia: 9.76 ± 0.41 vs hypoxia: 10.87 ± 0.42, P < 0.001). Tissue tracking displacement was reduced in the right ventricular segments and tricuspid regurgitation increased with hypoxia (7.5 ± 1.9 mmHg vs. 33.5 ± 1.8 mmHg, P < 0.001). The TEI index and E/E' did not change with hypoxia. Hyperoxia reduced strain rate in 10 left ventricular segments, global systolic contraction amplitude was decreased (8.83 ± 0.38, P < 0.001 vs. normoxia) while right ventricular function was unchanged. The spectral and tissue Doppler TEI indexes were significantly increased but E/E' did not change with hyperoxia.
Hypoxia improves and hyperoxia worsens systolic myocardial performance in healthy male volunteers. Tissue Doppler measures of diastolic function are unaffected by hypoxia/hyperoxia which support that the changes in myocardial performance are secondary to changes in vascular tone. It remains to be settled whether oxygen therapy to patients with heart disease is a consistent rational treatment