To start with, I would like to briefly explain a few physiologic parameters of interest.
This is simply the amount of oxygen the tissue is utilizing. VO2 max would be the maximum O2 usage attainable.
The classic definition is derived from the Fick equation:
VO2 = Q × (CaO2 − CvO2)
Q is the cardiac output which is (heart rate x stroke volume). The stroke volume is the amount of blood pumped per beat. As exercise intensity rises, the stroke volume rises, but plateaus well below the max heart rate. At high work rates, we can assume stroke volume as a relative constant (technically it could even drop at very high HR from inadequate atrial filling). That would mean cardiac output (at high work loads) is very proportional to heart rate.
(CaO2 − CvO2)
This refers to the difference in arterial and venous O2 content. Although not a direct measurement of such, the NIRS O2 saturation is related to this somewhat, discussed next.
Locomotor muscle O2 saturation
Both oxygen delivery and consumption are able to affect the measurement of SmO2. The balance between delivery increase (vasodilitation) and higher consumption (motor activity) may yield a variety of final results. The net balance between the delivery and consumption is reflected as the amount of extraction. For example if the delivery stays constant, a higher consumption (exercise) will cause a larger O2 desaturation (and a higher net extraction). On the other hand, a decrease in delivery (heart failure) with stable consumption can lead to higher extraction and lower measured tissue O2 as well. Both conditions lead to higher extraction though different mechanisms.
It has been shown that at moderate exercise intensities both HR and ventilation are related to the VO2. Certainly at work rates above the MLSS, ventilation will be boosted from acidosis compensation. This is a figure from a study looking at this relationship.
The end result is that looking at the early ventilation rise in either Fast or Slow starts may be a reflection of VO2 on kinetics.
Does tHb indicate blood flow?
Although it is tempting to use this as a measure of flow, it just does not work out.
There are some sophisticated methods to estimate flow (without cuff occlusion), but the simple tHb tracing can be misleading.
From the quoted paper:
With exercise the flow is up (L panel), SmO2 is down (R panel) but tHb is flat. This would be the general situation in most of our tracings, except for the consequence of external compressive forces.
With Cuff occlusion:
The tHb is relatively flat in cuff occlusion, but does show a tiny rise with cuff release and compensatory hyperemia. The cuff is not surrounding the area of measurement so no compressive effects are seen.
Given the above background, several physiologic differences will be looked at in the Fast vs Slow start routines.
- Is there better O2 extraction in locomotor muscles?
- Is there a difference in cardiac output as reflected by heart rates (assuming constant stroke volume)?
- Is there a difference in early ventilation increase (as a potential indirect look at VO2)
- Is the end interval ventilation rate different?
- Is the post interval ventilation recovery faster in FS?
- Re examination of the costal O2 desaturation pattern in view of now having ventilation data.
- Can a Fast start prime the "system" resulting in faster recovery than otherwise seen in an Even pace
VL desaturation patterns
Slow vs Fast start 3 min at 320 watt average total.
- Both intervals started at the same O2 saturation (65-66%) and since this was done on the same ride, assume the position did not change.
- The end O2 sat was about the same (53-54%)
- There was a faster and deeper drop in saturation in the Fast start. At 20 seconds into the effort, the Fast start was down a net 5% over the Slow start effort (62 vs 57%). The maximal desaturation was lower in FS (51 vs 53%).
- A slightly faster re oxygenation to a similar peak post interval in FS (55 vs 50 sec).
For instance the following is a total Hb tracing of the latissimus muscle during a heavy load pulldown. The prompt reduction in tHb (blue down arrow) is the start of muscle contraction and the blue arrow up is the end of the exercise set.
Does this occur during the Fast or Slow starts?
Here is the Slow start VL tHb (in purple):
And the Fast start VL tHb (in purple):
There does not appear to be a compressive blood volume reduction.
Therefore it does appear that the O2 extraction is faster and more complete in the initial part of the Fast start interval unrelated to external compressive flow restriction.
Does the RF have a similar pattern?
Here is the Slow start RF O2 tracing:
The Fast start:
- The O2 saturation drop is faster and deeper in the Fast start than the slow start (50 vs 42 % at 20 sec). Similar to the VL.
- The end interval saturation is similar in both
Is the tHb pattern different?
This is a graphic of the zoomed out ride (power in gray). Both tHb patterns look similar (red color).
The RF patterns are similar in both intervals, as in the VL monitor tracings.
- Both the RF and VL desaturate faster as well as reaching lower total values in the Fast start interval
- There is no notable difference in tHb measurements between Fast and Slow starts
- Although this is not meant as a flow measurement, it does seem that there is at least a more rapid O2 extraction (with higher peak extraction) with a more significant hypoxic stimulus for metabolic change in the Fast start. One of the hypothesized mechanisms for FS superiority is a more rapid buildup (or loss) of biochemical factors associated with muscle hypoxia.
The Hexoskin shirt has been shown to give accurate measurements of breathing rate, index of minute ventilation (when not calibrated to the individual) and heart rate.
Is there a difference in any of these parameters?
There appears to be several differences between intervals
- The heart rate rose faster in the Fast start. The 30 sec HR was higher in the Fast start (149 vs 141) supporting the concept of a faster rise in cardiac output using that technique.
- The peak heart rate (at the end) was higher in the slow start (170 vs 166).
- Minute ventilation also rose faster in the Fast start (98 vs 86 at 30 sec), but the end of interval value was similar (208). If ventilation is a valid marker of VO2, the higher rise in the Fast start supports the concept of faster VO2 on kinetics
- Post interval ventilation (one minute after 170 vs 118 while coasting) is markedly higher in SS. Since ventilation more quickly returns toward "normal" in FS, readiness for another heavy load occurs sooner. This may be related to the higher overall oxidative metabolism in the FS with less O2 debt.
What about average heart rate?
Unfortunately, this was not easily obtainable given the problems in parsing the Hexoskin data (I did not record it as usual on Ipbike - see last post) but it was approximately 4 BPM higher in the Fast start.
For a better look, here are two intervals (on different days) with solid average HR data:
- The average heart rate on the Fast start interval was 6 BPM higher.
- The pattern of faster HR rise was also seen again
The costal O2 potentially reflects both cardiac output redistribution effects, as well as increased respiratory muscle work rates (higher O2 usage by those muscles) from ventilation rise (normal O2 needs as well as lactate buffering). This paper was reviewed awhile back but is an important theme for the data below.
Slow start costal tHb:
Fast start tHb:
- The tHb patterns of both Fast and Slow starts are very similar at the costal muscle location.
Costal O2 desaturation tracings:
Slow start costal O2
Fast start costal O2
- Although the initial desaturation rate is faster in the FS, the ultimate final value is lower in the SS (25 vs 30%).
- More importantly, the O2 sat curve is relatively flat/stable in the FS, but steadily dropping into historic minimal values in the SS. This occurs despite the similar ventilation rates at the end, (seen with the Hexoskin above). The end interval costal hypoxic pattern in the SS is associated with shortened time to fatigue (seen in other intervals like a 1 min max).
- The similar ventilation rates (at the end) should equate to similar muscular work loads of the respiratory muscles. Therefore, the lower costal O2 values end interval may be more reflective of redistribution effects. Since power to the legs is higher at end interval SS, the redistribution of cardiac output may be further diverted away from the costal muscles. It could also be possible that the "efficiency" of these muscles become impaired with hypoxia (in SS) leading to reduced respiratory function and respiratory fatigue (leading to severe overall decompensation with continued effort).
- Recovery time (black arrows) is shortened in FS. Return to a more stable baseline takes longer with the SS. This may be related to the higher ventilation rate seen post interval in the SS (higher costal muscle O2 consumption/extraction).
- The above potentially could hamper re oxygenation kinetics of the locomotor muscles as well (metobo-reflex - sympathetic vasoconstriction of the leg vasculature).
A look at longer intervals:
Given the observation that both HR, ventilation volume and presumably VO2 on kinetics are improved with the initial FS pace, does starting a longer interval this way adversely impact the remainder. For instance, in a hypothetical race, are we worse off with starting with a 30 second effort at a higher power before dialing back to about MLSS vs just keeping at the MLSS from the start? Does that initial 30 sec power burst "cost" us later, or does it create the optimal exercise physiology environment for the upcoming interval?
The best Hexoskin equipped intervals that I have to compare are as follows (not perfectly matched):
This is a 7 min Even start at 251 watts:
And the respiratory data:
Compare it to a 10 min 253 watt interval after an initial 30 sec at 400 watts:
- Baseline HR about the same
- HR at 30 sec higher in FS (148 vs 134)
- Steady state HR about the same
- Baseline ventilation was the same
- Ventilation at 30 sec higher in FS (95 vs 72)
- Steady state ventilation toward the end about the same in FS vs ES
- One min post interval ventilation lower in FS despite an extra 3 minutes and the higher initial power (however the coast time was shorter in ES)
- Costal O2 pattern similar (given that the baseline values and interval length were different)
Some final thoughts (open to corrections)
Is there better locomotor muscle O2 extraction in either condition?
- Yes, it's higher in FS
- Yes - It appears that both average and 30 second heart rates are higher in FS. Final HR generally is not.
- Yes, it's higher in FS
- Both conditions are very close
- Costal O2 at the end of interval is higher in FS despite similar ventilation rates. This raises the question of cardiac output redistribution(with lower costal flow and higher extraction) and resultant changes in respiratory muscle efficiency/fatigue.
- Possibly (quicker ventilation recovery)
- Not very much - end HR, end ventilation, end costal O2 are all equivilant
As an end comment, these observations were done on one person, older than the usual test subject, and genetically more of a strength than endurance athlete. Whether or not younger, more elite endurance folks would show this pattern is unknown. However, with relatively simple gear, these same test intervals could be done by anyone to see if they would benefit from a Fast start strategy.
VO2 max related posts
- VO2 max/peak estimation
- VO2 max training and trainability
- The Wingate 60, a measure of VO2 max status
- Firstbeat VO2 estimation - valid or voodoo?
- Exercise in the heat and VO2 max estimation