85
node electrophysiological remodeling. These authors also observed changes in
transcripts of ion channels that participate in cardiac pacemaker activity such as T
and L-type calcium channels. Further studies would therefore be exciting to deci-
pher this electrophysiological remodeling.
3.2 Electrophysiological Effects in Ventricle
Chronic exercise induces cardiac physiological hypertrophy that is observed in ven-
tricular tissue and particularly in left ventricle. As a consequence, different studies
has focused their investigations on the impact of chronic exercise on ventricular
cardiomyocytes electrophysiology. During the plateau of the action potential, a fine
balance exists between inward calcium and sodium currents and outward potassium
currents. This equilibrium controls the action potential duration (APD) and is there-
fore crucial for the excitation/contraction coupling. To date, further studies have
investigated the impact of chronic exercise on different potassium outward currents
remodeling and APD [ 56 – 59 ].
ATP sensitive potassium channels (KATP) are energy sensing channels that areactivated depending on the ATP/ADP ratio [ 60 , 61 ]. They allow to connect meta-
bolic changes to an outward repolarizing potassium current that decrease the APD
[ 61 ]. This characteristic is essential to ensure cardiac acute adaptation to energy
demand increase during exercise. This occurs through APD shortening during heart
rate acceleration that balance cardiac contraction/relaxation function [ 62 , 63 ].
Zingmann and co-workers [ 56 ] have observed that the decrease in APD associated
to rhythm elevation was enhanced in trained mice. This was the consequence of an
increased KATP current density without effects on gating properties or ATP sensitiv-
ity of the channels. Experiments testing the expression of Kir6.2 and SUR2A,
respectively the channel pore subunit and the associated sulfonylurea receptor sub-
unit, indicate a 30–50% increase in both proteins whereas only SUR2A transcripts
increased. A rise in Kir6.2 and SUR protein level (60–75%) were also observed in
trained rats compared to sedentary animals [ 58 ].
Physiological hypertrophy associated to exercise does not necessarily lead to car-diac electrophysiological disorders as observed in pathologic hypertrophy. Indeed,
cardiac pathological hypertrophy is characterized by an increase in myocytes size
associated to a decreased repolarizing potassium current density and an increase in
APD [ 64 , 65 ]. In contrast, using trained mice or a mouse model of physiological
cardiac hypertrophy through PI3Kα expression, a study revealed that left ventricular
cardiomyocytes doesn’t display difference in resting membrane potential, action
potential amplitude or APD [ 57 ]. Trained and PI3Kα animals presented an increase
in left ventricular potassium currents mainly attributed to Ik1, Ito, Ikslow and Iss compo-
nents that were correlated to an increased level of mRNA (e.g.:Kv4.2, KChiP2,
Kv2.1, TASK1, Kir 2.2) and proteins. Interestingly, this rise in potassium current
was at least partially compensated by an increase in membrane capacitance. This
lead to a less important but still significant 10–20% increase in Ik current density and
5 Structural, Contractile and Electrophysiological Adaptations of Cardiomyocytes...