Are you familiar with myocardial bridging? I suffered a cardiac arrest while running March 2025 at age 62. I was born with 2 childhood heart defects. While most die undiagnosed I somehow lived due to over 40 years of running and such a strong heart. Over 9 min of CPR Saved my life and my mind. Prior to open heart surgery my surgeon told me I would be able to run better than ever once he unroofed my heart to allow my arteries to lay on top and I would finally have a full breath. 7 months after my cardiac arrest i ran 3:42 in New York and 5 months later 3:27 in the Boston Marathon April 26.
2:47 is best at age 46 and I ran sub 3 at age 61. The heart and body are so amazing. Thanks for reading
Cardiology is one of my favorite topics in medicine. This work looks at structural changes that enable athletes to adapt to the demands of training, but I'd be interested to see how electrical changes are coupled to this. The ACC updated their guidelines for interpretation of EKGs in athletes last year (https://www.jacc.org/doi/10.1016/j.jacc.2024.12.025). LVH has a clear signature on EKG, but first and second-degree AV blocks, early repolarization, and incomplete RBBB are also common and non-pathological in the absence of other findings. Some of these changes make sense and align with structural changes (ex. early repolarization to shorten refractory time). Of course, this is all taken at rest, but some of it can be extrapolated to exercise
The low resting heart rate point deserves more attention than it gets. Everyone obsesses over training zones and heart rate variability, but the real signal is what your resting heart rate tells you about your filling dynamics. At 33 bpm you're not 'unfit' — you're operating with fundamentally different cardiac architecture. The question isn't whether your heart rate goes high enough during exercise, it's whether your stroke volume can keep up when the filling window gets compressed. The athlete's heart doesn't ignore the clock — it learns to negotiate with it.
This topic always interests me. In addition to your information, another factor that makes athletes' hearts unique is the hypertrophy of the supraventricular crest with endurance training. It decreases in size when the athlete does less training. When I did my master's thesis, I found the EKGs showed an Rsr' with hypertrophy and the r' disappeared with decreased training. This happened in both male and female endurance athletes.
It is a muscular ridge within the right ventricle of the heart. It is located between the tricuspid and pulmonic valves, at the junction of the right ventricular anterior (free) wall and the interventricular septum. It has a "U-shaped" morphology, which serves as a "trough" for the proximal right coronary artery. It guides blood flow from the inflow tract into the outflow tract, ensuring a smoother transition between the trabeculated ventricular wall and the conus. The Rsr' can be mistaken for right bundle branch block.
Are you familiar with myocardial bridging? I suffered a cardiac arrest while running March 2025 at age 62. I was born with 2 childhood heart defects. While most die undiagnosed I somehow lived due to over 40 years of running and such a strong heart. Over 9 min of CPR Saved my life and my mind. Prior to open heart surgery my surgeon told me I would be able to run better than ever once he unroofed my heart to allow my arteries to lay on top and I would finally have a full breath. 7 months after my cardiac arrest i ran 3:42 in New York and 5 months later 3:27 in the Boston Marathon April 26.
2:47 is best at age 46 and I ran sub 3 at age 61. The heart and body are so amazing. Thanks for reading
Incredible! Thanks so much for sharing... that's a condition I've not heard of. Glad to see you are kicking ass!
Cardiology is one of my favorite topics in medicine. This work looks at structural changes that enable athletes to adapt to the demands of training, but I'd be interested to see how electrical changes are coupled to this. The ACC updated their guidelines for interpretation of EKGs in athletes last year (https://www.jacc.org/doi/10.1016/j.jacc.2024.12.025). LVH has a clear signature on EKG, but first and second-degree AV blocks, early repolarization, and incomplete RBBB are also common and non-pathological in the absence of other findings. Some of these changes make sense and align with structural changes (ex. early repolarization to shorten refractory time). Of course, this is all taken at rest, but some of it can be extrapolated to exercise
So good.
Thanks Josh!
The low resting heart rate point deserves more attention than it gets. Everyone obsesses over training zones and heart rate variability, but the real signal is what your resting heart rate tells you about your filling dynamics. At 33 bpm you're not 'unfit' — you're operating with fundamentally different cardiac architecture. The question isn't whether your heart rate goes high enough during exercise, it's whether your stroke volume can keep up when the filling window gets compressed. The athlete's heart doesn't ignore the clock — it learns to negotiate with it.
This topic always interests me. In addition to your information, another factor that makes athletes' hearts unique is the hypertrophy of the supraventricular crest with endurance training. It decreases in size when the athlete does less training. When I did my master's thesis, I found the EKGs showed an Rsr' with hypertrophy and the r' disappeared with decreased training. This happened in both male and female endurance athletes.
It is a muscular ridge within the right ventricle of the heart. It is located between the tricuspid and pulmonic valves, at the junction of the right ventricular anterior (free) wall and the interventricular septum. It has a "U-shaped" morphology, which serves as a "trough" for the proximal right coronary artery. It guides blood flow from the inflow tract into the outflow tract, ensuring a smoother transition between the trabeculated ventricular wall and the conus. The Rsr' can be mistaken for right bundle branch block.
Thanks for sharing. That’s super neat!