The question I keep coming back to after reading some of the aspirin-for-gym discourse: the inflammation literature on NSAIDs and muscle protein synthesis was mostly done in young healthy subjects. The Trappe group’s COX-2 work showed blunted satellite cell activation after ibuprofen and paracetamol, but those participants didn’t have chronic systemic inflammation to begin with. For those of us with T2D, the picture is different. We’re not starting from a zero-inflammation baseline. Whether acute, exercise-induced prostaglandin activity matters the same way in that metabolic context is genuinely unclear to me, and I went looking for papers that address it specifically and came up mostly empty.
The aspirin-insulin sensitivity thread adds another layer entirely. There’s older literature on high-dose aspirin improving insulin sensitivity through NF-kB inhibition, which is a separate mechanism from the muscle adaptation question. The two threads get conflated in the TikTok discourse and I’m not sure they should be. Has anyone here raised this with their consultant, particularly if you’re already on something like tirzepatide where the metabolic baseline is shifting anyway?
eta: one more thing