One of the attributes of successful endurance performance is the presence of a large proportion of "slow twitch", type 1 muscle fibers. Baseline genetic endowment is advantageous but aggressive endurance training is potentially helpful. To that end, multiple studies have shown that both short high intensity as well as long moderate intensity exercise can lead to fiber transformation. Many of the interventions have shown that if there is not a true fiber type switch, at least there will be a change of the type 2x (strength, fatigable, glycolytic) to type 2a (strength, fatigue resistant, oxidative). In a previous post we looked at genetic SNP markers that correlate to muscle fiber type. In particular if you have ACTN3, ACE DD positivity, chances are you will have a relative low proportion of type 1 and a higher amount of type 2 fibers. Therefore if you are born with this genetic pattern it would not be advantageous to train with a protocol that tends to increase type 2 fibers even further. You would want to employ a method that would best make your type 2 fibers fatigue resistant/oxidative (type 2a) and hopefully some conversion to a true type 1 over the years. On the other hand, lets say you have homozygous markers for all endurance parameters (ACTN3 neg, ACE II) and have noted that your long distance performance is fine but sprint power is lacking. Then it may be helpful to convert some of your type 1 fibers to the stronger, fast twitch variety to improve that issue. So the question becomes what is the best type of HIT method to either cause a fiber shift if wanted, as well as what to avoid if endurance enhancement is your goal.
A study was just published looking at a high intensity sprint training method that indeed will lead to a slow to fast fiber transformation. This post will discuss the study, training method and a look at NIRS tracings in RF, VL and costal areas.
All training sessions started with 5min at rest on the cycle
ergometer, followed by a running-in for 2min at 10 Watt (W),
a 10min warm-up at 50% maximum power (Pmax), a 45min
interval phase with 90 intervals of 6 s at 250% Pmax, each followed
by a 24 s pause at 10W, and a cool-down of 5min at 50%
Pmax. Subjects were asked to keep cadence at 70-90 min−1.
Subjects performed three training sessions per week, resulting
in 18 training sessions in 6 weeks
To start with I was a bit confused by the Pmax parameter. Is this the maximum power reached in 1 revolution (Cycling Peaks definition) or related to power at VO2 max, steady state lactate levels etc? Well, it appears to be defined as the last 1 min stable power on a VO2 max ramp test. This value can vary according to the ramp protocol but you get the idea. It is not your 1 min max average power(would be very hard or impossible to do 2.5x that number). The study used (2.5) x (the ramp 1 min peak power). Given that I have no way of knowing what that value would be for myself, I decided that I would just do an almost all out 6 sec sprint.
The training sessions were split into 2 x 3 weeks periods, each week having 3 interval days, each session consisting of 45 mins, which translates to 90 intervals. So, 270 intervals in 1 week!
Testing was done at various times including pre, post and during the intervention. Muscle biopsies were done of the VL, enzymes involved in fat and carbohydrate oxidation assessed and various exercise tests done (lactate levels at various power outputs, VO2 max).
Without getting too detail oriented lets look at some of the results.
Despite no difference in VO2 max pre and post, the ability to handle lactate was markedly improved. This was felt to be possibly related to improved whole body lactate clearance (liver and non involved muscles).
Time to exhaustion at both 65 and 80% of the Pmax was improved:
However, the proportion of Type 1 fibers dropped significantly during the study:
Consistent with the fiber type shift, oxidative enzyme levels dropped as well:
In the discussion, other studies were reviewed that either were consistent or not with the findings. One study of note done many years ago found the opposite, a fast to slow fiber transformation but used a training protocol much different (fewer sprints and longer rests).
This is data from that paper:
It is strange that the slow twitch area dropped while the % slow twitch fibers increased. That said, the two studies are not comparable given the very significant difference in training volume (we will see my NIRS data in a bit to elaborate).
From the paper:
Sprint training. The sprint training programme lasted for 7 weeks
at the rate of four sessions each week. Each session consisted of
two series of maximal intermittent sprint cycling (5-s sprint, 55-s
rest) at 80% Fmax (i.e. 130-140 rpm). The rest period between the
two series was 15 min. The first week sessions included 8 sprints
in each series (see Fig. 1). This number was increased by 1 sprint
every week so that each series of the last weeks sessions included
As noted the rest interval is 55 seconds, number of sprints was much less as well.
I was curious as to see what behavior both leg and costal O2 would display during the 6/24 sec training method. My guess was that we would see little in the way of costal hypoxia but profound intermittent changes in working leg muscles since the interval time was so short. If so, the short intense intervals may not be a good stimulus for cardiac output, contractility, venous return. Therefore, for folks with problems in cardiac output distribution from lower stroke volumes, it may pay to avoid this type of training. Conversely, in those who don't have a good peak power, sprint capability, transforming fibers to type 2 could be quite helpful.
Here is the usual 1 min maximum effort interval with sensors on the VL and costal:
Note that at about 12 seconds, the VL has it's nadir O2, while the costal takes far longer to drop. Remember, the intense muscular contraction is also going to cause external compression (as in the weight training tracings) limiting blood flow making local muscular hypoxia even more pronounced. Since this has been my usual pattern, I certainly did not believe that 6 seconds followed by a rest would lead to systemic costal hypoxia.
In relation the above study, one could almost compare this to doing a weight training session with heavy loads, few sets but short rests of 24 sec.
Now to the 6/24 protocol.
This was done with sensors on the L RF, R VL and R costal areas. Warm up was about 1 hour, ambient temp was a bit high, near 90 F.
The first tracing is that of the VL, with no real surprises, there is a desaturation on each 6 sec interval and a return to baseline quickly during the rest:
If we magnify a few of the 6 second bouts, the total Hb also drops nicely (purple curve) with each effort. This certainly makes sense as there is significant external muscular compression (as in weight training).
The Rectus femoris also behaves as the VL, but with much deeper desaturations:
Although power is not shown in this plot, the RF/VL are essentially identical in time course. However, the RF has nadir O2 values of near 15% and an exaggerated rebound.
To see how these values compare to a 1 min max effort (which usually produces the best nadirs) this was done later in the same ride session:
And all three sensors without showing power:
Now for the surprise. I originally thought that brief 6 sec bouts with 24 sec rest would not produce much systemic effect. Well, I was very wrong. As noted below, the costal drops from a baseline of 60% to 12%. This was after just 12 intervals, not 90. In fact, I was fairly winded at 6 minutes and decided to call it quits.
The VL does desaturate during the 6 seconds, with a return to baseline during the rest. However, the costal area has a notable delay and the actual nadir is well into the rest period. In addition, as the intervals progressed, there was a downsloping of both the recovery and nadir costal O2 that was not seen in the VL.
A close up of the costal O2 also is interesting, the nadir is well into the rest and the O2 actually rises for the 6 sec effort. I can't explain the initial rise, but that pattern is also present on the 1 min max above and on other high intensity tracings. In regards to the O2 drop during "rest", several factors could be causing this. The rebound blood flow rise into the legs needs to come from somewhere. As the legs seem higher priority than the respiratory muscles, the costal area may be getting a perfusion drop. This does not seem to be the case. The following tracing (data points only every 5 sec, a Garmin quirk) shows the costal tot Hb rising during the rest phase (even as O2 drops):
The pattern is the same for each cycle. Other potential reasons for the drop could be two complimentary effects. There is both an acidosis leading to respiratory rate increase and therefore costal muscle activity may be even higher than the first few seconds. Although there does not appear to be a drop in costal flow, these muscle are still a lower priority.
Looking at the above, the 6/24 study results now makes more sense. The leg muscles are challenged by a "resistance training like effort" repeatedly but at the same time there appears to be significant systemic lactate elevation, acidosis and respiratory threshold effects (high resp rate, work of breathing related to the acidosis). This is certainly a major training stimulus.
On a practical level, I have concerns of possible overtraining, as well as knee strain. I don't think I could do the study protocol as written but perhaps if I was 25 again I could.
Where does this leave us from a practical standpoint?Should we use this training modality or not?
On one hand it improves lactate clearance, time to exhaustion parameters but on the other we convert type 1 fibers to type 2, as well as lose oxidative enzyme effect.
Training based on SNP markers and historical demographics?
Previously, I have shared some of my data and genetic markers, all clearly in line with strength rather than endurance. Interestingly, my Cyclinganalytics.com data also agrees with that assessment. Over the years I have amassed a large database on that site and a graph exists that compares your best times with other athletes who use the site. Here is what my curve looks like:
Everything less than 10 min is valid (I don't do longer intervals than that). Note my ranking is proportionally much better at 30 to 60 seconds versus the 8 or 10 min times. Even at 3 min, I fall off the curve despite doing my best efforts at those interval times.
Back to the study....
One important point about the study is it did not compare how other training modalities affect lactate clearance, fiber type and time to exhaustion. This is not a criticism in any way, but for those of us who either can't tolerate such intervals (bad knees), or who are concerned with fiber shifts (that they do not want) there could be alternate interval types that may produce even the same or even more benefit.
The other question to ask, is whether or not there was a difference in training effect in each individual (good and poor responders to this method within the whole group). If there were, it would be interesting to stratify them according to SNP markers, VO2 max, stroke volume, etc.
I think the decision to employ this training modality should be based on personal strengths and weakness.
- For those with genetic strength markers, evidence of limited stroke volume, performance characteristics more in line with sprinting, the above type of training may not be appropriate. In this case longer intervals of 30 to 300 seconds, different ramp intensities may work to better enhance their deficiencies.
- However, individuals with great genetic endurance markers, limited sprint strength, a performance curve that does not look like mine(better rating at longer duration), then taking advantage of the study technique is potentially of benefit.
- The concept of limiters based on local muscle O2 desaturation curves continues to have no support in the literature.
- A better view of ones limitations should be based on genetics, systemic (costal, deltoid) desaturation as a surrogate of cardiac output limitation, demographic comparisons in power vs time.