25
Recent studies demonstrated a significant reduction of RV fractional area change of
12–32% and of the TAPSE of 4–22% during this phase [ 10 ]. Because these param-
eters could be influenced by the load conditions, it has been studied the RV free wall
strain and the strain rate after exercise because they may be less influenced by load
conditions. As a result, a reduction of 15% has been reported in post exercise RV
strain, while changes in RV strain rate are more variable, probably because the strain
rate is more dependent by the load condition [ 10 – 14 ]. The fact that RV strain rate
has been observed to reduce in some studies but not in others may due to the vari-
ability of this measure. If it is real that RV strain rate is modified by load condition,
also the LV strain rate should be modified by load condition. However, some studies
have reported that the RV strain rate reduces while LV strain is preserved [ 10 – 13 ].
Previously, 20 years ago, Douglas et al. have just demonstrated that after an ultra-
endurance triathlon, RV dilatation appears immediately whereas the LV dimensions
did not change [ 15 ]. During the phase of diastolic overload of RV the interventricu-
lar septum is pushed towards the LV determining an increase of the LV eccentricity
index [ 10 , 12 ]. These observations are also demonstrated with the CMR performed
post-exercise [ 16 , 17 ]. The RV is the cardiac chamber that disproportionately suffers
the fatigue during an intense endurance exercise. The explanation of this work over-
load on the RV can be found in the fact that endurance exercise is an aerob work that
requires greater oxygen supply to the muscle tissue and, so cardiac output have to
increase five to eightfold. This is obtained with an enhanced venous return, increase
of myocardial contractility and dilatation of pulmonary arteries. During exercise,
PASP increases proportionally with the cardiac output. La Gerche et al. performed
echocardiography monitoring during exercise and found a greater increase in PASP
than in invasively measured systolic blood pressure. They demonstrated that RV
wall stress and work is much more high than the LV work during endurance exercise
[ 18 , 19 ]. This analysis is conducted with a non-invasive method to estimate the
PASP. Other studies have evaluated the invasive measure of PASP with catheteriza-
tion of the pulmonary arthery, demonstrating the same linear relationship between
cardiac output and PASP and the marked increase of PASP during exercise in ath-
letes. Moreover, La Gerche et al. demonstrate that the increase of PASP during
exercise is associated with the enhancement of pulmonary vascular reserve, evalu-
ated through the study of the pulmonary transit of agitated contrast (PTAC) to [ 20 ].
At rest, agitated echicardiographic contrast does not significantly pass through the
pulmonary circulation at rest, but may do so during exercise. The researchers dem-
onstrated that, during exercise, the PTAC was higher in the subjects with higher
PASP and lower pulmonary vascular resistance and that this result did not depend
by training status. During intense exercise of short duration, there is an increased
RV function and volume work overload, but it is able to recovery completely at the
end of training. It remains to be determined whether recovery of intense exercise-
induced RV dysfunction is complete in all athletes from repeated bouts.
2 Acute and Chronic Response to Exercise in Athletes: The “Supernormal Heart”