1 Mariannick Marcil, Karine Bourduas, Alexis Ascah, Yan Burelle ...

increase in ROS production, had similar effects in both experimental groups. These results
would thus suggest that altered ROS production is not responsible for the increased CRC
observed in mitochondria following training. However, ROS production could not be accurately
measured during the Ca 2+ challenge due to artifactual changes in the fluorescence of HVA in
these conditions (5). Therefore, the present data cannot rule out the possibility that during the
Ca 2+ challenge, ROS production was lower in trained mitochondria due to a reduced ability of
Ca 2+ to increase ROS production through its action on the TCA cycle and/or on several
components of the respiratory chain (12).
Taken together, results from the present study indicate that mitochondria isolated from
trained hearts are more resistant to Ca 2+ -induced PTP opening when energized with succinate.
This adaptation could potentially be beneficial to the heart in the setting of ischemia-reperfusion,
a situation where exercise was shown to be protective (9, 10, 13). The mechanisms underlying
this increased resistance remain obscure(6, 22, 40) but are apparently not related to changes in
endogenous adenylates content, alterations in respiratory chain function, redox state of PN’s, or
ROS production. One possibility is that this phenomenon is caused by changes in the
expression of anti- and pro-apoptotic members of the Bcl-2 family of proteins known to modulate
Ca 2+ sensitivity of the PTP. Indeed, the balance between Bcl-2 and BclXL on the one hand and
Bax on the other hand was recently shown to be increased following training (34, 54). However,
this hypothesis remains to be ascertained.
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