Mitochondria are organelles responsible for oxidative (O2 using) generation of ATP through carbohydrate metabolism, so having excellent function and abundance of these would certainly make sense from an endurance exercise perspective. Changes in either the quantity (total volume) and/or quality (peak function per volume) are important factors to consider in any training intervention. Additionally, enhancing mitochondrial function and volume may improve O2 extraction at the level of the exercising muscle thereby boosting VO2 max. The following post is a exploration of these concepts.
An excellent review to get a better understanding of this situation:
Observational data suggest that both mitochondrial function and volume improve with greater levels of fitness:
However it appears that the relation is not so simple. Although there are relatively few studies, there is general agreement that mitochondrial volume is more influenced by total training volume and not intensity. In other words, those junk miles that you are piling on are actually doing something, they are increasing total mitochondrial volume/mass:
The left graph is a relation of intensity of training versus the right, which is volume. It seems pretty clear that training volume is associated with mitochondrial enzyme activity (an index of mass). In regards to intense training, one could argue that there may even be a negative association.
How can we improve peak mitochondrial respiratory ability? Here it seems that intensity is the answer:
Unfortunately the study numbers are small but the association seems real.
De-training reversal of function and volume:
What happens to all the hard won changes in structure and function we have worked for after a period of rest or de-training? As one would expect there is a reversal in diverse parameters, but of somewhat different time frames.
Peak function reversal:
Enzyme activity which is generally used as an index of volume/mass:
There is a significant drop in both mass and function with lack of continued training. There is probably some sort of genetic variation in how each individual parameter behaves. I suspect some athletes will be more or less affected by this. From an evolutionary standpoint, the rapid loss of machinery that no longer is needed was probably a survival benefit in times of starvation/stress (less diversion of scarce nutritional components to less essential body functions). Not desirable in modern times, especially for endurance sports, but that is the legacy we are left with.
Finally the studies conclusion:
In other words
- Training volume = mitochondrial mass
- Training intensity = mitochondrial function
Can mitochondrial function help increase VO2 max through enhanced O2 extraction?
Although cardiac output plays the major role in VO2, part of the Fick equation is the A-V O2 difference (extraction). A recent study examined the relationship between mitochondrial O2 affinity and muscle O2 extraction.
As noted above, VO2 of the mitochondria is related to respiratory capacity (OXPHOS) but inversely to p50mito. p50mito is related to mitochondrial O2 affinity, so as affinity drops, VO2 rises.
The authors reasoned that high oxidative mitochondrial capacity resulted in lower p50mito, higher O2 diffusion and O2 extraction (which is a good thing).
Indeed, the lowest p50mito values (resulting in higher O2 extraction) were in the group doing cycling exercise in normal O2 inspired air:
In an attempt to isolate out the effects of blood flow, the following was shown:
- There was no relation (in this model) with O2 extraction % and change in flow.
- However the extraction % was very related to OXPHOS (respiratory capacity), especially at the high levels
Finally, it was felt that mitochondrial oxidative function influences O2 extraction, making the mitochondrial function an integral part of the VO2 calculation:
Lastly, since this is muscle O2 blog, a comment on training and muscle O2 extraction:
The study looked at NIRS measurements using the Portamon sensor on the dominant VL of Olympic class women hockey players before and after a cycling HIT intervention:
- Post HIT desaturation was more pronounced in subjects but not uniformly, some had more or less of an effect.
- In particular, lets look at subject 3 and 4. Both had good improvement in TSI but little change in power.
- In fact, most of the group average effect in power was from subject 1 who had minimal change in TSI.
The individual tracings as follows for those interested:
I put this in as a caution about over relying on a muscle O2 sensor as an index of training improvement. Although attractive as a response marker, the lack of TSI, or O2 desat changes over a course of training should not in itself be a warning sign, indicating lack of response.
- Training volume is a stimulus for mitochondrial volume/mass. Junk miles are not really wasted, they are a potent enhancer of mitochondrial mass.
- Training intensity is a stimulus for mitochondrial function, higher respiratory ability.
- Improving the ability of mitochondrial OXPHOS and mitochondrial O2 affinity may improve O2 extraction, hence VO2. This should be trainable.
- High intensity interval exercise can enhance muscle O2 desaturation and this may in some people be related to improvements in power.
- However some athletes may train with intensity, improve power parameters but with minimal TSI/O2 desaturation.
- De training effects on mitochondrial function occur quickly, within a matter of days or weeks. When peak form is needed, don't take too much time off.