Does anyone know of any work looking at cardiac muscle adaptations to sprint training specifically?
I’m curious if the adaptations are more like those from strength training, endurance training or a mix of the two looking at factors like stroke volume, ejection fraction, systolic and diastolic function (and the accompanying ventricular hypertrophy or dilation).
Thanks.
My experience when looking at sprinters has been that they have the capacity to accelerate the HR rapidly up to high numbers and to recover back down rapidly as well, verses the distance adaptation of bigger stroke vol
This is what I was thinking, based on the demands. Thanks for the responses.
Any other input is welcome.
The common thinking amounst the cardiac community is that resistance training can result in Left Ventricular (LV) Hypertrophy, and that prolonged endurance training results in a larger LV cavity (due in some part from increased venous return), both of which can result in increased cardiac output.
A collegue of mine performs echocardiography for the British Olympic Association, and has found amoungst all the athletes he has scanned, those with the biggest hearts were rowers. He found there LV’s hearts were hypertrophied and had bigger cavities. This is probably explained by their cross training ie weights and prolonged endurance training.
That seems to concur with this:The Athlete’s Heart
I do cardiopulmonary testing and I’m fortunate enough to be able to have an echo just about anytime I want, but we don’t test very many athletes.
Hi where are you based? I also do CPET but mainly on Heart Failure patients.
Sorry, just saw this. I work in the Poconos (East Stroudsburg, Pennsylvania).
What are their resting heart rates (on average)?
They ranged from mid 40s to high 50s generally in a group including males and females with the lowest rate male at 46 and the lowest rate female at 48. I really only kept track till 1982 and never looked after that as I didn’t see what I could do with the info anyway.
I also found that my better sprinters had lower Heart Rate Variability than the slower sprinters when we sampled them at rest. I think this was confirmed by Val Nasedkin based on the Omega Wave sample of track and field athletes from what I remember.
Interesting. That means there’s not much hope for me then, as my range is from 36 to about 220.
Miguel Indurain had a herat rate range from 28bpm to 220bpm, so your prowess could lie in other events/sports 
N2,
Heart rate variability in regards to R-R interval variability, or pulse rate variability? I ask since individuals on this tread have been discussing pulse rate.
If you are speaking in regards to R-R intervals, why do you suspect a lower HRV with your better athletes?
HRV using analysis of R-R intervals.
Not exactly sure why, but I remember hearing that the “health” and strength of the vagal response had something to do with it. I assume it had something to do with their abilities to recuperate. Not sure if it directly related to general fitness and conditioning.
HRV using analysis of R-R intervals.
Not exactly sure why, but I remember hearing that the “health” and strength of the vagal response had something to do with it. I assume it had something to do with their abilities to recuperate. Not sure if it directly related to general fitness and conditioning.
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.