MitoQ is 2-3 orders of magnitude more potent than
idebenone, for scavenging reactive oxygen species (ROS) in mitochondria.
advantages of MitoQ, may turn out to be that it can do a very good job
protecting mitochondria, w/o disrupting ROS signaling in the cytoplasm.
Additionally, MitoQ looks to be an inhibitor of the mitochondrial
permeability transition pore (MPTP), while idebenone seems capable of
inducing it (as does ALA). The significance of this at concentrations in
vivo is anyone's guess. MPTP opening, is a critical step in apoptosis, but
may also play a role in other forms of Ca2+ signaling.
Now, for exercise.. in response to endurance exercise there is generally an
increase in mitochondria, beyond what is necessary to achieve
circulatory-limited VO2 max. One theory behind this excess in mitochondria,
is that additional mitochondria are needed due to high amounts of ROS
mediated damage done to mitochondria during exercise. If this is a
significant contributor to fatigue, MitoQ might do a nice job extending the
time till fatigue. What I do not know, is how dependent muscle adaptations
are on ROS originating from mitochondria. Determining the best way to use
MitoQ, for enhancing exercise, will probably require some careful
experimentation. I'm excited to hear your observations.
Dose timing doesn't appear to be critical. I suspect that the half life of
MitoQ will be similar to that of the attached cation. This puts the half
life somewhere around 1.5 days, w/ steady state concentrations being reached
after 7-10 days of dosing