It's so much harder to put lean mass on than it is to lose it isn't it. Strength training can be a great help. On the other hand eating badly and putting bodyfat on seems quite straightforward.
After an incident I had a superb cardiologist who diagnosed an aortic heart valve condition that they would leave unless a ct scan showed anything. I had the scan then they wanted an angiogram immediatley. I was 95th percentile and they got me in quickly during covid for a valve replacement and a quadruple bypass. I was a strength coach, I'd been sprinting and strength training for years at high intensity. Had no idea that my arteries were more bony than my bones. Going in to that surgery, any surgery I guess, with as much muscle mass as possible and in best health as possible is smart because there is so much time spent horizontal and it takes some time to rehab and get moving again.
I understand that CT scans for dudes over 40 would be ridiculously expensive but it's a big silent thing.
Forgive the unsolicited advice but do try to keep your diet clean and eat plenty, especially protein.
My cardio laid out the plan for me at the start: even though asymptomatic, because of my PAD/diabetes/smoking history the idea was to progressively try to "rule in" with first step echo study; if nothing from that then exercise stress test; and if nothing from that then CTCA.
I kind of wonderd why not go straight to CTCA, given that I'm pretty active and have zero symptoms (except for some fatigue which up til now has seemed to me to be a leg thing, not heart). Part of the reason, maybe not an important part, seems to have been that he actually needed to cite symptoms like shortness of breath or angina to get through CTCA triage, and in the end he faked a shortness of breath cite, nothing else having turned up from the stress test etc. Anyway, kudos to him for successfully wrangling the situation.
My angiogram is booked for Firday. I hope they can check for coronary collaterals. A big reason why I can be active despite having a completely occluded left femoral artery is because I have a whole lot of leg collaterals, grown as a result of constant aerobic exercise over the last 5+ years. That can also promote coronary collateral development, which is maybe a reason why eg I could pull 12+ METs on the exercise stress test in spite of the gammy leg and apparent three-vessel occlusive heart disease. Maybe it would change the risk/benefit go/no-go analysis for the bypass op? Anyway it's going to be really interesting to see how things pan out.
If I do need a bypass, I'm really hoping it's not needed very urgently. Just started a new project and I'd rather not have to tell the client, "Oops sorry, have to put things on hold while I have heart surgery" if I can avoid it
🙂 I'd also like to have some time to bulk up a bit, as you say.
EDIT: Just to geek out a bit on collaterals ...
This is the EXCITE study from 2016, looking at coronary collateral development in response to exercise, pulished in the American Heart Association's journal
Circulation:
https://www.ahajournals.org/doi/epub/10.1161/CIRCULATIONAHA.115.016442
Background—
A well-developed coronary collateral circulation provides a potential source of blood supply in coronary artery disease. However, the prognostic importance and functional relevance of coronary collaterals is controversial with the association between exercise training and collateral growth still unclear.
Methods and Results—
This prospective, open-label study randomly assigned 60 patients with significant coronary artery disease (fractional flow reserve ≤0.75) to high-intensity exercise (group A, 20 patients) or moderate-intensity exercise (group B, 20 patients) for 4 weeks or to a control group (group C, 20 patients). The primary end point was the change of the coronary collateral flow index (CFI) after 4 weeks. Analysis was based on the intention to treat. After 4 weeks, baseline CFI increased significantly by 39.4% in group A (from 0.142±0.07 at beginning to 0.198±0.09 at 4 weeks) in comparison with 41.3% in group B (from 0.143±0.06 to 0.202±0.09), whereas CFI in the control group remained unchanged (0.7%, from 0.149±0.09 to 0.150±0.08). High-intensity exercise did not lead to a greater CFI than moderate-intensity training. After 4 weeks, exercise capacity, Vo2 peak and ischemic threshold increased significantly in group A and group B in comparison with group C with no difference between group A and group B.
Conclusions—
A significant improvement in CFI was demonstrated in response to moderate- and high-intensity exercise performed for 10 hours per week.
On the other hand, the accompanying editorial
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.116.022037 criticizes the study, essentially saying that the trial design did not support the conclusion that improvements were due to collateral development.
Nevertheless, the EXCITE study continues to be cited. Which IMO is a nice illustration of the murky status of collaterals as treatment targets and risk modifiers in general - wide-spread feeling that they are probably pretty good for preserving & restoring function coupled with apparent lack of high-quality studies, a robust evidence base and well-accepted mechanisms.
My personal experience is that leg collaterals have been really powerful for preserving and restoring function and so I'm hoping something similar applies to my heart and that the angiogram will deliver some insights.
