Genetics, cardiac output redistribution and personalized training/racing

Various criticisms and issues have been brought to bear in using muscle O2 for lactate testing, training zone prediction, recovery dynamics.  The specific factors relate to which muscle is tested, site on the muscle, deep vs shallow differences in fiber type, recruitment patterns, overlying skin/fat thickness, temperature etc.  One property that has not been explored relating to O2 desat is the exercise related SNP pattern (single nucleotide polymorphism) of the tested individual.  Namely do they have endurance or strength genetics. 
There are two major SNP types recognized as associated with either strength versus endurance abilities.  Historically the I/D (insertion/deletion) genotype of the ACE enzyme was the first major single nucleotide polymorphism noted to be somewhat correlated with either a propensity to excel at either strength or endurance. The newest SNP and more predictive is the ACTN3 marker.  



Multiple studies have looked at both markers and while overlap exists, having endurance alleles in both will statically favor that particular individual in endurance activity. Conversely, having strength markers in both will statistically favor that individual in sports requiring strength like football, power lifting and short sprints.
Also of note, the proportion of type 1 muscle (endurance) progressively diminishes as the strength markers "pile up".  This chart below shows the situation nicely.


Interestingly, the study did not show a correlation in fiber type and SNP status in women.  The subject population was Japanese, whether the data holds in other groups is not known.

Getting back to muscle desaturation patterns, it is also known that athletes with higher proportions of Type 1 fibers desaturate less than average in a ramp test.  Therefore it is certainly possible that between muscle type (1 vs 2), endurance SNP's, that the net pattern/degree of hypoxia could vary based on these parameters alone.
Here is a figure from the study:
 
So athletes with endurance profiles will just not be able to desat as well as strength oriented subjects.  The authors went on to suggest that this lack of desaturation could be used to actually measure fiber type on a relative basis.


Examples:
In previous posts I have presented data on strength trained upper body during weight lifting, and costal/leg muscle desaturation during cycling exercise in one individual, namely myself.  I recently had the opportunity to look at another individuals pattern using my sensor.  The following findings are not only good proof of concept of costal O2 monitoring but perhaps even more interesting, highlight the strategies employed by the cardiovascular system in redistributing O2 to handle differences in stoke volume and muscle type at similar relative loads in a strength versus and endurance SNP perspective.  In further testing to come over the next several weeks, I plan on looking at leg muscle desat in the same person.

Thanks to low cost mass throughput testing, you can find out what SNP markers you have.  As background info, we are born with a marker from each parent, and have 2 total markers.  So if each parent lets say had hybrid markers, Stren/Endur, each child could have SS, SE, or EE.  According to the 23 and me panel, I have both strength markers in the ACE and 1 strength marker in ACTN3 (one marker seems equivalent to both in regards to strength at that site).  So I represent the extreme strength case individual.  But through many years of intense training(and powercranks), my cycling stats are reasonable.
My friend on the other hand has pure endurance markers at all sites, both copies.  He has no problem riding 100 miles day after day and rarely gets winded with an intense interval.  On the other hand, I can put out high power for a short time, need days to recover and have difficulty with more than 50 miles.  We have similar resting heart rates, my max is about 10 beats higher but I am younger.
We have seen how the cardiovascular system can re allocate resources to deal with high demand to the legs but limited supply from lower (relative) stroke volumes. I was curious to see what my endurance friend's pattern would be.  According to the literature, the endurance SNPs confer a greater percentage of type 1 slow twitch endurance muscle.  However, little is know about stroke volume with exercise and SNP type.  However, the ACE gene is associated with hypertension, vascular disease in the strength variety so it's certainly plausible that stroke volume/venous return are affected by this genetic pattern.

My prediction was that he would not nearly desat the costal muscles as much as I do, even though I can outpace him for short and moderate distance.  Long distance, especially in the heat is a major for me issue since I am not going to perfuse the gut well and have trouble hydrating ( I know this all too well in Florida).  He does not have this problem presumably because of better stroke volume and less cardiac redistribution.

Findings: Here is a tracing of costal O2 during a 10 minute freely chosen pace that my friend felt he could sustain for 30 minutes or so.  He has never used a power meter but feels from experience that he can pace himself optimally.
 
He started with a costal sat of near 88% as baseline, and dropped to about 70%.  

Here is a 1 min max tracing with a start O2 of 82% and a nadir of 64%:


So we know his lowest reachable O2 is near 64% and baseline above 80%.

Here is my tracing done riding next to (not drafting) up the same hill:


I started at 71% and dropped to about 40% (which is far from my potential nadir), but I was not going at a max effort.


Result Summary:
The magnitude of costal desaturation is significantly less than mine.  When asked what is hindering further exertion at max effort, it is not shortness of breath, but just lack of leg muscle ability to maintain that pace.  That is in contrast to my "feelings" at the end of a max effort or ramp which are severe breathlessness.  Other observations of a retrospective nature now make sense, my friend does not have issues with fluid replacement since cardiac redistribution away from the gut is presumably not a factor, endurance recovery is faster since a greater proportion of type 1 muscle is present (inferred from SNP data).  

Another interesting conclusion we both came up with was that his "race pace" was well below what he was capable of when trying to achieve maximum hypoxia.  It seems that he was using heart rate as a guide, and was in effect cheating himself of additional watts since max heart rate with costal O2 pacing almost equaled his previous race pace HR.


In summary we have a tale of 2 very different cyclists.  

• Strength vs Endurance SNP markers
• Type 1 vs 2 muscle
• Very different cardiac output redistribution strategies(mild vs severe costal drop)

This knowledge may help us train and race better as well.  For training, perhaps incorporating strength exercise of the legs would be helpful to the "endurance" type but actually harmful (from a performance perspective) to the strength athlete.  In a race or long training bout, nutrition/hydration could be a major issue to the strength folks who may not perfuse their gut as well during continued high intensity efforts.  The strength subject could potentially power past the endurance type either at the end of a race or to get a "gap".

True Limiters
Much is discussed in various forums in terms of identifying and training "limiters" (whatever that means), but perhaps looking at physiology as noted above could prove more helpful.  The literature indicates that HIT, SIT training of various types will improve VO2 max, capillary density, oxidative enzymes, power output etc.  But although we know how to get faster, stronger in general, a more nuanced approach based on individual genetics(SNP markers) and physiology(patterns of cardiac output redistribution) may yield even better results in training, recovery and race conditions. 
 
This was taken from the above outlined paper:
 
Although I do not personally agree with their rational, I just wanted to show that the field of genetic testing, innate exercise ability and how best to train/race is just beginning.  From my standpoint, I would have recommended strength training to the endurance group since that is what they would have had a genetic weakness in.  On the other hand, for a strength favored individual like myself, avoiding strength training, and exclusively using HIT, SIT and plenty of low level aerobic miles seems most appropriate.  Anecdotally, every time I attempted to add strength training to my regime, the endurance ability worsened (but leg strength improved). 


Future thoughts:

• The next step planned is to see if costal O2 monitoring can help him pace more effectively(without looking at a power display).  There is a costal desaturation taking place and finding a practical cutoff to stay above will be investigated.  One test we may do is to use a power meter (but with no visual display) to measure average 10 min power with and without costal O2 optimization.
• Another idea could be a "crowd sourced" study looking at SNP markers(strength vs endurance), pattern of costal O2 desat(severe vs mild hypoxia) during a ramp test.  The above observations on just 2 individuals may or may not be valid and more data is needed.  There are many muscle O2 sensor enthusiasts and a collaborative study of this nature would be simple to do.