Detailed Topic Index

Sunday, October 1, 2017

Strength Training, effects of rep speed, rep number

To round out the discussion on strength training variables and their influence on muscle O2 we should address how repetition speed and number influence muscle O2 changes.  

In some of the earliest low load studies, it was implied that a relatively slow movement speed was superior in regards to O2 drop.  From the standpoint of injury rehab, we basically have little choice, and a slow movement speed is a safe method.  However, there have been many opinions that in older populations is particular, high rate of force development is quite helpful.  In aging there is a loss of type 2 fibers responsible for peak strength and fast contractions.  By training at higher speed and force, this hopefully is mitigated.  Explosive type training is also another heavily researched subject with data showing enhancement in peak force.  In addition to fiber type change, optimal neurological firing strategy occurs with faster repetition speed.  By training at slow speeds we may be neglecting this aspect.

Potential downsides to fast contractions are several.  Obviously there is the potential for injury.  In addition there may be some stress shielding both in the tendon and muscle.  This concept is not often discussed.  If there is a very rapid force change in the tendon muscle unit, the force is not necessarily transmitted equally along the tissue.  So some areas get more or less strain.  The higher strain area could become damaged, the lower strain area may not get loaded enough to stimulate positive cellular change.  Coupled to this idea is the tension on the muscle through the range of motion.  In a very fast contraction, the initial training force is highest at the beginning of the motion, but as you approach the end, you are minimally using the muscles as momentum has taken over.  Another issue is the large metabolic consequence regarding the increase in work (physics wise) when you are doing faster contractions over the same time period. In other words the energy used is higher with faster rep speed over the same time duration (net more repetitions).  We may not be able to sustain this amount of net work so a shorter training time may result but don't really want to short change the time the tissue is subjected to hypoxia.  So there needs to be some compromise.  Most studies doing comparisons in fast vs slow velocity try to equate work done.  The last possible issue is what happens to intra muscular pressure during fast contractions(not much data on this).  As mentioned above, it may be that not enough continuous compressive force is exerted on the muscle, sabotaging our low load theoretical rational (avoid cuffs by relying on intra muscular pressure to occlude vascular flow).  So although the initial force is high, there could be a major intra muscular pressure reduction toward the middle to end of the given motion.

So the question is, what is the net effect of higher movement speed and what do the tracings look like.  Is there some issue with blood inflow leakage during the set (preventing desat), is the higher work needed impossible to actually do?  

The first attempt at doing this definitely showed me the difficulty in going from about 8 reps to 20.  This is a tracing of 3 sets of chest press, sensor on the chest with a weight 15% below my usual low load.  The first set the usual slow/moderate speed of about 8 reps.  The next 2 sets were done fast on both the concentric and eccentric phases, with no pause at transition.  Despite the O2 drop looking similar, the fast sets were very taxing.

Notice the red line, the total hemoglobin.  The slow first set captures the variation in compressive force, but I suspect there would be more of this pattern in the fast sets if the time resolution was higher.  The sensor only measures every 1 second.  However despite this, the average hemoglobin drop was similar
Note as well the very typical O2 desat, no better nor worse. 
In conclusion, with fast reps there is no penalty in regards to hemoglobin drop nor reduction in O2 desaturation.  The only issue is the severe fatigue and possible over training if this is done too often.  The other observation is the lack of lower O2 reached with much higher "work" done and presumably high lactate generation.

Another potential variation that may combine the benefits of rapid motion with less overall fatigue is doing a fast concentric phase then a slow eccentric (in order to limit the total reps over the same time).

Here are some examples:

This is a tracing of the pulldown, low load weight, 45 sec sets sensor on the lats.
The concentric phase is fast (<1 sec) but the eccentric is about 6 sec making the rep count in line with what has been done previously.  Desaturation is also similar to previous protocols. 

Here is the dip, sensor on chest, modified reverse drop set (start 15% below then set 2 and 3 at usual low load).  The first set was done at the usual pace - about 7-8 reps over 45 sec.
There does not appear to be any deterioration of O2 drop with the change in contraction speed and fatigue was manageable.

Finally, this is the chest press with sensor on chest, modified reverse drop set (first set -15% then next two at usual low load).  All three sets were done with fast concentric and slow eccentric.  Excellent desat and hemoglobin drops.

Saturday, September 16, 2017

Cycling Intervals Part 2

After the last discussion about cycling interval desaturation observations and conjectures, I was asked several questions.
  • The oxygenation trends through a ride session including warmup, intervals and cooldowns.
  • Possible use of this technology to help alert for over train and over reach conditions. 
  • More elaboration about the fluctuation of muscle O2 during a typical ride, making the absolute numerical reliability problematic.

Oxygenation trends:
Some representative tracings of the L RF of a typical cycling session.
First up is a baseline after 15 min stabilization.  There have been observations made by some that some time may be needed to lead to stable readings (few minutes).  As can be seen the O2 is quite steady.

The value of 56% is actually pretty reliable as a baseline for me at that particular site, +- 2%.

Now things get interesting:
What happens after a max interval of 60 sec, but instead of resting, you continue at a lower level (just barely hanging on since you just did a max effort)?
Here are 2 examples:

The yellow is muscle O2, excellent drop on the L RF(all readings done on this page) for the 1 min max, then despite still riding at 170 watts, the re oxygenation still dramatically occurs (as does THb).  Perhaps a physiologist could mathematically model some parameter from this data, but from a practical standpoint not much can be gleaned(except reperfusion).  

Here is a similar interval, same 1 min max, then 180 watts for 1 min then 300 watts for 1 min.
My take home lesson here is that muscle O2 is not very useful for assessment of fatigue.
Despite being about as exhausted as physically possible (in the name of science), my muscle O2 was near the preinterval value.  So claims that O2 monitoring can help to guide when you are ready to train hard again just don't make sense to me. The published data on using O2 to detect fatigue are mixed as well.  Most report fatigue as an effort is done and O2 drops as a result.  But that possibly is just coincident association since they are normal physiological results that should occur together.  A better study did not find fatigue to be associated:
Our results indicate that for modest submaximal contractions, regional differences in oxygenation are not associated with differences in muscle activation or with fatigue development

Also note that the O2 drop at 300 watts was only to 62%.  This is above my baseline (at 170 it's 56%), and nowhere near what a typical 300 watt session will reach.  It does make one wonder if it was worth it from a training perspective to do that last sprint in view of the perceived stress I felt.

So by the end of the ride, do the sats look much different.  Yes, at a similar power the muscle O2 is higher than when I started.

These observations lead me to conclude that the absolute muscle O2 at any particular time is highly dependent on the time spent cycling, the intervals done as well as "micro environments" within the interval.
On a personal level, subjective feelings and heart rate are better clues as to when to nail an interval again, not muscle O2.

That leads to the issue with overtaining detection.  I did do a pubmed search and found nothing mentioning muscle O2 in regards to overtraining.  There was a nice review and summary of factors that have been looked at in this subject.  Interestingly, they concluded that subjective feelings were the best monitor!
I have looked at my muscle O2 during weeks of performance fluctuation (over reaching) and could not find anything meaningful.  That is not to say that the changes were not there, but since it is hard to get the exact same site every day, the O2 will always be a bit different day to day.  This is not the sensors fault, but an intrinsic limitation of the process.  

Interval Optimization

I am more intrigued with using the sensor for getting an O2 drop with the most efficient way, one that can help in doing more quality work with less subjective fatigue.

Here is another 3 min interval with a ramp up protocol, to equal the usual net average watts I would do. This is similar to the previous post.

What I am starting to look at now is what happens if you start with even lower power.  This was my first attempt.  The 3 min average is much lower than usual, the end power is close to the usual average.  Although it is not as significant a desaturation as usual, this type of interval is not as taxing.  I did this after the multiple ones shown above (including the 1 min max) and I am not sure I was even capable of getting a profound desaturation (from residual hyperemia).  More to follow...

Take away points:
  • Depending on the previously performed exercise, the muscle O2 can be quite different.  Even the pattern can be different- rising O2 when it should normally be dropping (seen after a max effort, then doing a sub max effort immediately).
  • Muscle O2 has limited use with indicating readiness for the next effort.  Practically, heart rate and subjective feelings are better indexes.
  • Muscle O2 has not been looked at in regards to over training.  Subjective feelings are very useful in this regards.
  • More investigation into using O2 sensor technology to modulate interval training is needed.  Optimizing the way an interval is done seems the most logical use of this technology from my observations thus far.  It may turn out to be a valuable tool in proper training program design


Tuesday, September 12, 2017

Optimal cycling interval investigation

Despite my initial conclusion that muscle O2 sensor tech may not be an important part to make one a better cyclist, I have continued to think about how this intriguing physiological metric can be better utilized.  The post below is my first(maybe more to follow) of a possible way to do so.

From previous observations in strength training, it appears that the first initial effort will produce the best O2 desaturation per given load.  So on further exercise sets, a higher weight is needed to equal the one previous at least in respect to muscle O2 drop.  Hence my proposal to do reverse drop sets (with low load weights).  Can this type of approach be useful in endurance training interval work?
I have briefly touched on the problematic nature of using muscle O2 in cycling, with significant variation in results depending on sensor position, temperature, skin thickness etc.  But, the sensor is accurate by itself with the same position, and the temp range should not change too much on a given ride.  The other issue also touched on is the major difference in desat curve shape and magnitude.  So one muscle may start at 75% and only drop to 65% with max effort, but another may drop to 20% with the same effort.  This may partly relate to muscle type and current level of fitness
Given the above constraints in day to day reproducible results (not device accuracy), are there ways we can use the muscle O2 knowledge to help us train.  Before answering this, a couple of foundational principles should be kept in mind.  First, always training with a max effort is not felt to be good for the athlete or the outcome in fitness.  Overtraining, and excess physical stress is harmful to immune function, mental status, and the parameters we are training for (muscle growth, endurance etc).  So there is a sweet spot (or spots) of suitable high intensity zones in which to work out.  These high intensity efforts are generally short (10-300 seconds), with the longer ones at slightly lower intensity.  Common HIT workouts would be 30 sec near max, or 2-3 min submaximal power, with a few repeats.
Another principle of training would be in relation to what do you want to accomplish.  For instance, peak power would be better trained by short, intense muscular bursts.  Most of endurance athletes are more interested in things like mitochondrial density of muscle, capillary growth for better blood supply, improvement of aerobic metabolism chemical machinery.  Hypoxia been shown to improve the mechanism for capillary growth, so perhaps prolonging the time the interval is done under hypoxic conditions could be useful.  In other words, alter the way we do an interval to maximize the time of hypoxia with the least "effort".  

Let's look at some muscle O2 curves (my personal data) to show an example of the above.

One of my typical training interval protocols is to ride at 3 min with a power that I could sustain for about 4 min at max effort. This ends up with my heart rate at max, my muscle O2 at minimum (no matter the muscle).
For example:
3 min effort at 330 watts, sensor on rectus femoris, start O2 63, minimum 19%:


The problem is that this takes a bit out of me and I generally just do 2 on a given day.  Now, in the spirit of perhaps less pain but just as much gain, can we get the same curve with less fatigue.  I decided to do a reverse drop set, start easier but end with more intensity to equal the same net average watts.  Subjectively, this is easier for me to do and I had no problems doing three that day.

This is the same muscle group, average power, but the first 2 min were at 300 watts and the last min at 360 watt avg.

I wonder if there was a slight plateau at the end of the first 2 min, then a resumption of hypoxic response with more power (reminiscent of weight training patterns).

Second set of the above about 10 minutes later:

Note that the start and end muscle O2 were both about 10% higher than the first effort.  Presumably this relates to vasodilitation effects, I don't think acid base shifts in O2 sat would relate since I was reasonably rested.  This type of observation also reinforces my view that muscle O2 is not a totally consistent parameter to follow since it can vary over the ride, with no change in temp, hydration or location change.
But, the pattern is similar with a good initial drop, slight plateau then resuming the drop with higher muscular power.   

Possible conclusion, one can achieve similar muscle hypoxia with a lower starting load, but using a bit higher load for the last segment (same average overall).

After the above 2 intervals, I moved the sensor to my left vastus lateralis for comparison.
The following trace is the result, 300 watts for 2 min then 360 for 1 min:

What about 350 watts all the way through?  This is the vastus lateralis on another day (so slight location change probable):

On this muscle the pattern and magnitude of desaturation is quite different.  There is an initial drop with a nadir at 1 min, but no real further drop occurs at higher power.  Does this mean that there is no further hypoxic stimulus above the initial 300 watts?  Or, is the prevention of the slight rise effect a significant advantage of higher power at the end?  Could doing the lower power (first 2 min) for longer (5 min) lead to better mitochondrial and capillary density effects?
These questions are impossible to answer at this point, but clearly outcome studies are needed comparing the two training modalities.  

In my view, less emphasis on VO2 max/lactate testing is needed and more in this type of area looking for actual performance benefits, or lack of benefit from overtraining.

  • The pattern and magnitude of muscle O2 drop can drastically differ both in different muscle groups as well as the exact same spot (after intense efforts).  This makes day to day result comparison difficult as well as outcome studies.  Looking to see if you have a "better" curve may be misleading as a result.
  • Utilizing the muscle O2 sensor can help craft different interval workouts to minimize fatigue, help one do more interval sets, optimize hypoxic conditions.  This will hopefully lead to enhanced physiological outcomes in capillary growth, mitochondrial density and quality.
  • Outcome studies and biochemical investigation are needed to look at these ideas.