Could rowers benefit from Inspiratory Muscle Strength Training ?

[Mortie31]

An interesting read
https://evanpeikon.medium.com/performan ... 2263c57a37

[Tsnor]

Yeah the whole subject is interesting, I’ve read similar things also that our panting type expiration is due to not only C02 levels but also due to lactate breaking down into hydrogen ions that we then exhale, leading to the burning throat sometime experienced after really hard sessions..

Neat. I'd naively assumed some "drying out" phenomenon for that sore throat after very intense work because the breathing air flow was too large for the normal warming, humidification and and filtering done to inhaled air before it goes into the lung. "..lactate breaking down into hydrogen ions that we then exhale, leading to the burning throat .." seems more interesting.

A google search for <lactate hydrogen ions "throat" exercise> found nothing specific to the throat. If you have any links please post.

[frankencrank]

This is all pretty basic physiology. breathing under normal circumstances is controlled to keep arterial PCO2 constant around 40, which also keeps pH constant. "Breathing" seems to fail when muscles go anaerobic and lactic acid is produced because lactic acid gets buffered by the bicarbonate system. This buffering produces way more CO2 per ATP, which overwhelms the ability of the lungs to get rid of the CO2 so the pH gradually changes (it changes gradually because CO2 is distributed evenly in the entire body whereas O2 is not) and enzymes stop working optimally. After stopping exercise it takes a minute or so (1-2 circulation times) to return CO2 and pH to "normal" which is when breathing returns to normal.

The reason the lungs can't just breath more to expel the excess CO2 is high flow rates cause turbulent flow in the trachea. Once turbulent flow starts it is essentially impossible to increase minute volume regardless of how strong the breathing muscles are.

While it seems like breathing and the lungs limit exercise the real limiter is oxygen delivery to the muscles causing anaerobic metabolism in the muscles.

[Nomath]

@ frankencrank & mortie31
I can't stand such uncurious, lazy attitudes. A simple internet search shows various examples of decreased oxygen saturation with exercise.

LOL

Just read Exercise-Induced Arterial Oxygen Hypoxaemia in Athletes - A Review by Christian Prefaut and others in Sports Medicine (2000)
The figure below is from this article.

Simple pulse oxiometers in which you insert a finger tip use a pair of LEDs at different wavelengths, usually 660 and 940 nm. I definitely see a decreased oxygen saturation in my finger immediately after ending a high intensity training.

That is easily explained and has nothing to do with breathing

The saturation recovers in a few seconds. The device is not suitable for measuring while rowing.

Why not?

I guess the Iwatch is just a show-me-off device.

The watch uses the same technology as the finger pulse oximeter.

Possibly the Iwatch technology is the same, but the wrist is a bad place to measure pulse, let alone oxygen saturation. It is well-known that optical heart-rate sensors perform much inferior to chest sensors when rowing. In a common pulse oximeter you need a stable position of the finger in the sensor to measure oxygen saturation accurately. This is difficult when pulling a handle. Moreover, such a sensor will compromise your grip of the handle.

There may be some better devices like this one, but I don't have them and haven't seen results in vibrating conditions. It is typically made for monitoring your sleep.

[Mortie31]

Yeah the whole subject is interesting, I’ve read similar things also that our panting type expiration is due to not only C02 levels but also due to lactate breaking down into hydrogen ions that we then exhale, leading to the burning throat sometime experienced after really hard sessions..

Neat. I'd naively assumed some "drying out" phenomenon for that sore throat after very intense work because the breathing air flow was too large for the normal warming, humidification and and filtering done to inhaled air before it goes into the lung. "..lactate breaking down into hydrogen ions that we then exhale, leading to the burning throat .." seems more interesting.

A google search for <lactate hydrogen ions "throat" exercise> found nothing specific to the throat. If you have any links please post.

Here’s one, it’s not the one I wanted to add, if I find it later I’ll post..
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133870/

[frankencrank]

Just read Exercise-Induced Arterial Oxygen Hypoxaemia in Athletes - A Review by Christian Prefaut and others in Sports Medicine (2000)
The figure below is from this article.

Does anything strike you as strange about that data, like O2 going up with wattage in the control group and dropping in the athlete group? I will check out that paper and comment more if warranted.

Anyhow, I might point out that PaO2 is not the same as oxygen saturation. Checkout the oxyhemoglobin saturation curve.
Note that oxygen saturation doesn't fall below 90% until PO2 is less than about 70. Such levels of "desaturation" are clinically insignificant. Further, one needs to understand the mechanism of those drops. If PCO2 is normal it has nothing to do with the breathing muscles. There are other explanations.

https://en.wikipedia.org/wiki/Oxygen–he ... tion_curve

[frankencrank]

Just read Exercise-Induced Arterial Oxygen Hypoxaemia in Athletes - A Review by Christian Prefaut and others in Sports Medicine (2000)

I will check out that paper and comment more if warranted.

Here is the abstract:

During exercise, healthy individuals are able to maintain arterial oxygenation, whereas highly-trained endurance athletes may exhibit an exercise-induced arterial hypoxaemia (EIAH) that seems to reflect a gas exchange abnormality. The effects of EIAH are currently debated, and different hypotheses have been proposed to explain its pathophysiology. For moderate exercise, it appears that a relative hypoventilation induced by endurance training is involved. For high-intensity exercise, ventilation/perfusion (V̇A/Q̇) mismatching and/or diffusion limitation are thought to occur. The causes of this diffusion limitation are still under debate, with hypotheses being capillary blood volume changes and interstitial pulmonary oedema. Moreover, histamine is released during exercise in individuals exhibiting EIAH, and questions persist as to its relationship with EIAH and its contribution to interstitial pulmonary oedema. Further investigations are needed to better understand the mechanisms involved and to determine the long term consequences of repetitive hypoxaemia in highly trained endurance athletes.

Nowhere is anyone hypothesizing that the phenomenon (which doesn't cause clinically significant arterial desaturation) is due to failure of the inspiratory muscles.

[Mortie31]

An interesting read
https://evanpeikon.medium.com/performan ... 2263c57a37

Having reread this article, 3 factors seem to predominantly limit performance 1) limited respiratory system which can be either, or both inspiration/ expiration 2) delivery system limitations (cardiovascular) 3) muscular utilisation limitations.
If we can train or improve a limited respiratory system? How do we know whether we have inspiration or expiration deficiencies? Then which devices do what?, powerbreathe as being discussed in this thread only trains inspiration muscles. Aerofit supposedly trains both inspiration and expiration.
For me there is a potential benefit from theses devices if you have a defined limited respiratory system, but this applies to most prescribed training, of any description; fit the prescribed training solution to best meet the desired improvement…

[frankencrank]

An interesting read
https://evanpeikon.medium.com/performan ... 2263c57a37

Having reread this article, 3 factors seem to predominantly limit performance 1) limited respiratory system which can be either, or both inspiration/ expiration 2) delivery system limitations (cardiovascular) 3) muscular utilisation limitations.
If we can train or improve a limited respiratory system? How do we know whether we have inspiration or expiration deficiencies? Then which devices do what?, powerbreathe as being discussed in this thread only trains inspiration muscles. Aerofit supposedly trains both inspiration and expiration.
For me there is a potential benefit from theses devices if you have a defined limited respiratory system, but this applies to most prescribed training, of any description; fit the prescribed training solution to best meet the desired improvement…

That article is so bogus. Hardly anything in it makes any real physiological sense. In most healthy people oxygen delivery to the exercising muscles is limited by the mean diffusion distance from capillary to mitochondria (the article doesn't mention this issue). Contraction frequency can also be an issue. I discuss this contraction rate issue as the second physiological issue affecting performance in this slideshow. https://youtu.be/f9g9zZDy3T0

There is zero evidence that respiratory muscles are limiting in normal athletes.

[Mortie31]

An interesting read
https://evanpeikon.medium.com/performan ... 2263c57a37

Having reread this article, 3 factors seem to predominantly limit performance 1) limited respiratory system which can be either, or both inspiration/ expiration 2) delivery system limitations (cardiovascular) 3) muscular utilisation limitations.
If we can train or improve a limited respiratory system? How do we know whether we have inspiration or expiration deficiencies? Then which devices do what?, powerbreathe as being discussed in this thread only trains inspiration muscles. Aerofit supposedly trains both inspiration and expiration.
For me there is a potential benefit from theses devices if you have a defined limited respiratory system, but this applies to most prescribed training, of any description; fit the prescribed training solution to best meet the desired improvement…

That article is so bogus. Hardly anything in it makes any real physiological sense. In most healthy people oxygen delivery to the exercising muscles is limited by the mean diffusion distance from capillary to mitochondria (the article doesn't mention this issue). Contraction frequency can also be an issue. I discuss this contraction rate issue as the second physiological issue affecting performance in this slideshow. https://youtu.be/f9g9zZDy3T0

There is zero evidence that respiratory muscles are limiting in normal athletes.

Is the oxygen delivery not covered by the muscle utilisation deficiencies? I kind of agree about respiratory muscles in normal athletes, but who fits into that category? Would some not benefit from a fitter diaphragm for instance or are you saying all well trained athletes will already have this? I don’t know the answer, just throwing it out there for discussion/ clarification. In my experience there are very few athletes without some weaknesses is this one of them I don’t know. Having tried this device without researching thoroughly about what it actually did and did I actually need it? Out of all the weaknesses I have it seems inspiration isn’t one of them, hence why I found it did nothing for me.

[Mortie31]

An interesting read
https://evanpeikon.medium.com/performan ... 2263c57a37

Having reread this article, 3 factors seem to predominantly limit performance 1) limited respiratory system which can be either, or both inspiration/ expiration 2) delivery system limitations (cardiovascular) 3) muscular utilisation limitations.
If we can train or improve a limited respiratory system? How do we know whether we have inspiration or expiration deficiencies? Then which devices do what?, powerbreathe as being discussed in this thread only trains inspiration muscles. Aerofit supposedly trains both inspiration and expiration.
For me there is a potential benefit from theses devices if you have a defined limited respiratory system, but this applies to most prescribed training, of any description; fit the prescribed training solution to best meet the desired improvement…

That article is so bogus. Hardly anything in it makes any real physiological sense. In most healthy people oxygen delivery to the exercising muscles is limited by the mean diffusion distance from capillary to mitochondria (the article doesn't mention this issue). Contraction frequency can also be an issue. I discuss this contraction rate issue as the second physiological issue affecting performance in this slideshow. https://youtu.be/f9g9zZDy3T0

There is zero evidence that respiratory muscles are limiting in normal athletes.

An interesting presentation, not much on actual muscle oxygen delivery efficiency processes and theory, your cranks are cool though… and the erg return stroke idea is interesting..
Muscle fatigue processes are covered in depth in this article written by Allen, Lamb and Westblad…
https://journals.physiology.org/doi/ful ... ossref.org
A lot of this subject goes over my head, but I try to look at what I can do to improve and measure, I’m currently measuring HRV DFA alpha 1 and heart rate to train effectively under my VT1 levels and monitoring my HR vs pace to track improvements, which is similar to your power/ bpm work. I’m abit of a amateur data geek

[frankencrank]

Let me point out a couple of other things related to this. What changes occur in the athlete with aerobic training (strength training is a bit different)? How do the lungs change? More alveoli? No. More blood vessels? No. Bigger bronchi? No. No changes whatsoever is the answer. How about the blood vessels? Aorta bigger? No. More arteries? No. (one exception may be the heart) Bigger arteries? No. There really are only two changes of note. The muscles get more capillaries. The muscles get more mitochondria. More capillaries allow more blood flow to the muscle while reducing the mean diffusion distance to the mitochondria. More mitochondria means the more available oxygen can be better utilized.

breathing muscles will adapt to the training also such that breathing is never the limiter.

[frankencrank]

Would some not benefit from a fitter diaphragm for instance or are you saying all well trained athletes will already have this? I don’t know the answer, just throwing it out there for discussion/ clarification. In my experience there are very few athletes without some weaknesses is this one of them I don’t know.

In normal athletes breathing is never a problem. Every athlete has a weakness. Time is best spent training weaknesses over training strengths. Identifying weaknesses can be a problem though.

[frankencrank]

Here is some data to suggest that breathing exercises should have no benefit to rowing performance. A study showing that increasing inspired oxygen concentration from normal (20%) to supernormal (60%) had a tiny affect on performance (yes there would be a tiny increase in oxygen delivery because of increase oxygen in solution accounting for the difference

https://www.academia.edu/25612405/Effec ... view-paper

[Nomath]

...
There is zero evidence that respiratory muscles are limiting in normal athletes.

At the top of page 2 I listed 6 publications in scientific journals about the effects of training the respiratory muscles. Two papers found significant improvements in the range of 2-4% on rowing performance. One paper found significant improvements for women, but not for men. One paper didn't measure rowing performance. Two paper didn't find significant improvements on rowing performance.

You call this zero evidence, because what 3 out of 6 studies found doesn't fit in your dogmatic concept of oxygen transport.

Here is some data to suggest that breathing exercises should have no benefit to rowing performance. A study showing that increasing inspired oxygen concentration from normal (20%) to supernormal (60%) had a tiny affect on performance (yes there would be a tiny increase in oxygen delivery because of increase oxygen in solution accounting for the difference.
https://www.academia.edu/25612405/Effec ... view-paper

The same facile treatment of evidence again. Peltonen, the author you referred to, measured the effect of the oxygen concentration in air on rowing performance in 1995:
In a 2500m all-out test the mean final rowing time was 2.3% shorter in air with 60% oxygen and 5.3% longer in air with 16% oxygen, compared to normal air (21% oxygen). The effects on VO2max were even bigger (11% higher in 60% oxygen ; 15% smaller in 16% oxygen).
You call this "tiny effects"!
Why is it that a decrease from 21% oxygen (standard air) to 16% affects the rowing performance so strongly, if according to you there is an abundance of oxygen in the lungs?