Briefly:
Stroke volume is influenced by the volumetric space of the left ventricle and the strength of systolic contraction (ergo myofibril density of ventricular wall)
Strength of systolic/concentric contraction is related to volume of blood remaining afterward (ejection fraction)
Ventricular size (hypertrophy of cavity volume) is associated with training at lower sub-maximal HR intensities relative to the anaerobic threshold
thickening/hypertrophy of the wall at higher, yet still sub-maximal intensities of AT
Regarding diastolic/eccentric contraction, interesting things happen at HR intensities above the AT as the hypoxic conditions created at the level of the cardiac muscle via anaerobic-glycolytic loads yield adaptations which improve aerobic capacity of the cardiac muscle itself via increased hypertrophy of the muscle, increased myofibrils, increased mitochondrial density. The hypoxic conditions induce the ‘diastolic defect’ at the level of the heart in which the relaxation/expansion of the cardiac muscle during diastole is inhibited and is unable to ‘loosen’.
Interesting that these anerobic-glycolytic conditions influence mitochondrial biogenesis at the myocardium yet destroy mitochondria at the level of the skeletal muscle fibers.
Thus different protocols must be used to influence mitochondrial biogenesis at the level of the I, IIa, and IIb(x) fibers respectively
This information is reflective of the work of Zhelyazkov and Dasheva
Regarding the morpho-functional adaptations of sprint training one may consider the heart rate intensity ranges associated with different sprint distances/intensities as well as the associated blood lactate concentrations.