Respiratory muscle O2, a better tool?

The ability to perform both strength and endurance exercise has been honed through many years of evolution.  Each endeavor relies upon different biochemical specificity and trade offs, so it may be not only difficult but contradictory to have maximal ability in both.  An analogous comparison is the competition for resources between exercising locomotor muscle and the pulmonary musculature.

During intense aerobic physical activity there is an increase in blood flow into the locomotor muscles which are doing the active task.  Obviously, if you are running there will be very little need to perfuse/oxygenate the forearms. However as you need to increase the fuel supply(O2), the respiratory system needs to work harder to provide it.  The rate of respiration, and volume of each breath will increase.  Since this respiratory boost is accomplished by muscular effort,  the body needs to make some choices in what to focus on, the exercising muscles versus the pulmonary musculature involved in the work of breathing.  

This is not an easy choice on first glance.  Obviously if we neglect the lung muscle function(more to the legs for example), the oxygen and CO2 transport will suffer leading to issues with locomotor muscle performance and systemic hypoxia.  On the other hand being too generous toward the respiratory system could take away resources to the working muscles preventing a faster run/bike/swim.  This interplay between pulmonary and locomotor blood flow and substrate use has been investigated with some fascinating results.  For example, a study was done comparing the muscle O2 drop(vastus lateralis and intercostal) from forced hyperpnea (rapid breathing attempting to make the resp muscle work harder) vs the O2 drop with a cycling ramp test.  As seen below, the O2 did decrease as expected in the VL, but actually did an even greater drop in the intercostal area.  There was no real change with forced breathing.


In summary, the intercostal muscle O2 drop was profound and even larger than the typically measured leg muscle in cycling.  


Another way to look at the situation between competing muscle groups is to either load or unload one group and see how the other group performs.  This is what was done by this study that looked at quadriceps force after a 300 watt cycling interval under three conditions.  The subjects were either breathing through a resistive load (increase work of breathing), a respiratory unloading device (less work of breathing) and control.  As imagined the quad peak force was diminished by the resistive load (and time for interval completion reduced).  However, the unloading device actually improved the post exercise quad force from control.  From the paper:
 
Another key finding was that perceived exertion in the legs as well as dyspnea (short of breath) was less with the unloading trial and higher during the respiratory load:

Finally, the next study looked at blood flow through the quad muscles, neck muscles (sternocleidomastoid) during cycling exertion with various respiratory loaded and unloaded states.  They found that the neck muscles had higher blood flow as the respiratory resistance was increased (and reduced with unloading).  More importantly the blood flow to the leg muscles was reduced with the increased work of breathing, and boosted with reduced work of breathing.  This may partly explain beneficial effects on endurance exercise after inspiratory muscle training.


So in summary, there does appear to be a real competition between respiratory and locomotor muscles for fuel supply and the body has choices to make as to which organ is favored in allocation.  Now that we are aware of this situation, is there any utility in looking at the O2 sat in muscles involved in the work of breathing.  If a reproducible result could be obtained, we may have a clue as to when our locomotor muscle engine is starting to decompensate(by the excessive respiratory muscle hypoxia) especially in a race case situation.  Going back to my original criticisms of the use of muscle O2 in cycling, running, perhaps there is a viable advantage to using O2 senor tech.  As seen in previous posts and multiple studies, the measurement of muscle O2 for cycling performance, training and testing is of dubious value.  Again, I will not rehash the issues involved but much of the criticism is related to which muscle group is measured, as well as the depth of O2 sensor penetration both leading to difficult to interpret data.  It would be nice to have a legitimate physiological marker when we really are in the red zone.  Looking at costal muscle O2 may be a better surrogate for the reciprocal changes happening in the legs during intense efforts.

The first issue is whether measuring the respiratory muscle O2 is possible from a technical standpoint - can a commercially available sensor actually get meaningful and consistent data.  The studies in the literature generally place a small sensor along the anterior axillary line near the border of the lower rib area.  Many use a tracer dye to enhance the measurement accuracy.  On a personal note, I have struggled with sensor placement, ambient light interference (outdoors) and simply getting the sensor to stay flat and not move.  After trial and much error, I have gotten a pretty good handle on technique and consistent data.  Over the next few posts I will present some of my findings.  From my preliminary observations, this type of measurement may have some real utility in time trial/race power modulation, training zone prediction, recovery time to next interval/effort, and perhaps if there is a need for specific inspiratory muscle training to improve pulmonary efficiency.

Let's look at 2 examples of O2 sensor data, sensor placed on the R anterior axillary line, about 1 inch above the lower rib margin.  On the next post I will go over some more details on sensor placement, consistent readings and practical aspects.

This is a 7 min steady state interval at about 270 watts, baseline O2 was about 62% with a steady 48% the last third.  There is a mild costal O2 drop but it remains pretty steady and perceived effort was high but bearable.  Shortness of breath was mild at the end.

 

Contrast the above to a near maximum 60 sec at 530 watts, followed by 60 sec of 240 watts
There is a major costal O2 drop and perceived effort was extreme.  Shortness of breath was quite severe at the end.
 

Several interesting observations can be seen.  First is the magnitude of the muscle O2 drop between a difficult but sustainable 270 watts versus a 1 min max of over 500 watt average.  Clearly the 10% muscle O2 is not sufficient to sustain normal motor function/efficiency.  Second, although there is a slight improvement in O2 during the next 60s of 230 watts it is still clearly in a functional hypoxic range that could still hamper normal respiratory motor function.  Lastly, there is no rebound past the initial baseline in recovery as seen in the locomotor tracing below(rectus femoris) of similar watt pacing:

 

The rebound of the total Hb also is different from the tracings in both endurance and strength training.  Here is a rectus femoris total Hb plot with a 1 min max, showing the initial drop(muscle compression), then rebound with vasodilation:
 

However, the costal/respiratory muscle does not show the typical pattern as above.

Perhaps the lack of sustained muscle compression(inspiration vs expiration) does not cause the Hb drop but it is a useful marker for proper placement and delineation from typical motor contraction patterns.


Conclusions:

• There is a well established literature in regards to the competition between respiratory and locomotor muscle needs during intense exercise.
• It is possible to measure costal muscle O2 drop with (at least the BSX) sensor tech.
• The typical patterns of total hemoglobin drop from muscular compression and rebound hyperemia are not present in costal muscle tracings.
• The measured muscle O2 range is large making real time tracking with effort/power modulation potentially practical.  With very redistricted O2 ranges in some athletes, using the data in a race situation would be difficult given the "noise" in the system.
• Anecdotal data (above) indicates the possibility of using the costal O2 for: 
• optimal time trialing, 
• avoiding red zone decompensation, 
• purposeful supra maximal efforts,  
• return to physiologic baseline before another stressful interval of effort.

The next post will deal with sensor placement, practical measurement issues and how to get this up and running
Further data on non locomotor muscle monitoring advantages.