Anatomically, evidence suggests that while consistent dynamic and static exercise may lead to eccentric and concentric hypertrophy (respectively), most athletes will fall within left ventricular normal limits. One study I read (Pellicia) notes that LV size, thickness, and mass decreased after a deconditioning period of about 5.5 years. And wall thickness returned back to normal in each athlete. Physiologically, evidence LV systolic function is normal at rest and during exercise, while LV diastolic function is enhanced during exercise (Fagard). Of course, this finding is welcomed, as we know that exercise increases both demand and cardiac output. Enhanced LV diastolic function occurs because adequate blood filling demands it. Electrophysiologically, understanding what’s going on becomes more challenging. And your video was helpful here. I’ve long noticed that athletic heart physiology can mimic heart pathophysiology. What troubled me was the knowledge that there are many people who are the embodiment of both. And so it follows, what are we to make of these realizations? How many people are running this weekend with stenotic coronary pipes, while convinced that they are living healthy? How many athletes are playing a deadly game of hot potato? How many physicians don’t understand the athletic heart and are incorrectly diagnosing and treating it? How many physicians fail to identify something pathological in their patients who are athletic because the lines can be blurred? A helpful video. It begs for more. Thank you for you time and teaching.
Will have to watch your repolarisation abnormality section again to compare to my slightly better than novice understanding of the matter. If I had the opportunity, I’d ask you several questions regarding axis orientation, fascicular blocks, AV block progression, QRS voltage progression and limit, T wave inversion, LVH, atrial enlargement, SCD, and asymptomatic bradycardia low normal rates that raise concern.
