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type of exercise training, temperature, cell isolation protocol, regional cardiac
differences or stimulation frequency. However, differences seem to be lesser in
studies using aerobic treadmill controlled-training. Thereby, series of experi-
ments using mouse and rat models highlighted that endurance exercise training
improves cardiomyocytes shortening, time to peak of contraction and time to half
relaxation [ 6 , 7 , 10 , 15 , 34 , 35 ]. Interestingly, the groups of Kemi [ 7 ] and of
Carneiro-Junior [ 36 ] demonstrated in rat ventricular myocytes that improvement
of cardiomyocytes contractility induced by 10 or 8 weeks of endurance exercise
training respectively reversed after 4 weeks of detraining. This demonstrates that
aerobic exercise training induces adaptations of cardiomyocytes including their
contractile characteristics.
At each cardiac cycle, a transient rise in intracellular Ca2+ occurs that will triggercontraction (systole). Immediately thereafter, the decay of intracellular Ca2+ will
cause relaxation (diastole) of cardiomyocytes. Several studies have examined the
effects of exercise training on both cardiomyocytes shortening, and intracellular
Ca2+ transients. Some authors reported a decrease in both systolic and diastolic
intracellular Ca2+ in cardiomyocytes of exercise trained rats [ 10 , 13 , 37 ]. These
results show that improvement of cardiomyocytes shortening by exercise training is
not necessarily associated with an increase in systolic intracellular Ca2+. It can be
also explained by a greater Ca2+ sensibility of myofilaments [ 10 ]. Moreover, if other
studies showed no effect of physical training on both systolic and diastolic intracel-
lular Ca2+, reductions of time to peak and half-time of decay of intracellular Ca2+
transients [ 7 , 15 ] reported in these works confirm the beneficial effect of training.
Indeed, improvement of intracellular Ca2+ transients kinetics, also observed associ-
ated with increase in systolic intracellular Ca2+ in studies by the groups of Kemi [ 34 ]
and Carneiro-Junior [ 6 ], reflect the improvement of Ca2+ cycling induced by exer-
cise training.
2.2 Calcium Homeostasis
2.2.1 Ca2+ Cycling
Cardiomyocytes contraction results from massive Ca2+ release from sarcoplasmic
reticulum (SR), actin-myosin-Ca2+ binding interactions and eventually sarcomere
shortening. The signal for actin-myosin interaction is the binding of intracellular
free Ca2+ on troponin C. Intracellular free Ca2+ is increased due to the known pro-
cess Ca2+ − induced Ca2+ release. The latter takes place as follow: 1/depolarization
of both sarcolemma and T-tubules membrane activates L-type Ca2+ channels current
which allows entry of a small quantity of Ca2+ by L-type Ca2+ channel and by Na+/
Ca2+ exchanger (NCX) which works in the so-called reverse mode. 2/Free Ca2+
stimulates the ryanodine receptor (RyR2) localized on membrane of SR. 3/A rapid
transient of Ca2+- release via RyR2 produces the trigger signal for cardiomyocytes
contraction. During the relaxation, Ca2+ is removed from the cytosol by both the
A. Krzesiak et al.