Daniel Plotkin

@dhood_york Hmm, review seems to make that conclusion with quality assessments that aren’t fair to the context; can we blind a participant to cuff condition? Given the volume of literature it’s pretty fair to say that hypertrophy is similar when looking at reasonable protocols, BFR vs Trad.

Looks like more research is required to establish blood flow restriction training as an effective tool for adaptation in older adults. sciencedirect.com/science/articl…

@BradSchoenfeld Nice, congrats! Good to see this out… there’s one particularly odd study in this area… 👀

Preprint of our new study posted. We show that palm cooling does not enhance resistance training performance during moderate rep protocols. Lots of data, no additive benefits sportrxiv.org/index.php/serv…

Ok. I’ve not been running. In the gym 3–4 times a week. And eating 1.5x my body weight in grams of protein per day. Still not jacked. What am I doing wrong?

@gerdy_mac I’ll play! 1. Exercises aren’t always for one muscle so assumption all MU are recruited at ~3 RIR not true across exercises. 2. Granting reps after full MU recruitment are less hypertrophic they are still likely hypertrophic. Thus decision making would be in context of session

For all the "train to failure" folk there is only only one question.. ..what do you think is happening between failure & 0-3 RIR that will specifically enhance hypertrophy? Please provide an explanation in terms of %MVC/ MUR & MUFR? + evidence #hypertrophy #muscle

@rruetigger @AviBittMD @MattWalshBlog I think all that is being said is that you can run a trial and observe side effects over time without knowing or finding a mechanism.

@AviBittMD @MattWalshBlog Fair enough. Perhaps another time. I'm a neuropsychologist, would be interested in hearing your position - all in good faith.

Here is an example of why those engaging in scientific discourse would be immensely helped by having a basic level of phil/logic/semantic analysis. @MattWalshBlog says that the chemical imbalance theory of depression has been debunked. And he's right! It has. That's simply not what causes depression. @Bathcat8 says that they are clinically depressed and SSRIs were life-saving. This statement is also probably correct. So what's the issue? Well, neither of these statements even contradict each other in the first place. It can both be true that the chemical imbalance as a theory of depression is false and SSRIs are still life-saving medications to many people with depression. There are many cases where a medication works, a theory is developed as to why it works, and it turns out that theory is wrong and the medication works for a completely different reason. In the case of SSRIs, they change the serotonin concentrations in the synaptic cleft rather quickly, and yet patients do not respond to SSRIs until 2-4 weeks and often do not reach complete response until several months. So the mere concentration of serotonin is not underpins the depression response - thus the "chemical imbalance" theory is indeed incorrect. However, what does coincide with the treatment effect onset of SSRIs is down-regulation of the 5HT1A receptor, which just so happens to coincide at 2-4 weeks treatment time. Thus, it is more likely that many cases of depression are not caused by a chemical imbalance in the brain, but by differences in how our receptors in our brain respond and process those chemicals, even if those chemicals are at normal levels. And so yes, SSRIs still end up working for many people with depression even if the change in concentration of serotonin levels isn't fixing any imbalance as they modulate the effect by a different mechanism. But of course, there's still room for improvement with this technology. Learning about the actual differences that underly depression and how to effectively modulate them will help us understand depression further and develop even more effective treatments.

@DanielPlotkin_ (@AuburnKINES) et al. look at the effects of exercise stressors and disuse, and how these impact skeletal muscle myosin heavy chain fragmentation! 📜buff.ly/4eOGSPI

@DrAndyGalpin At first I thought you were underlining your disagreement by changing causal to casual 😂 would’ve been a savage move

CASUAL association between low grip strength and sleep duration, sleep-wake disorders, & napping. Perfect paper? No. However, the bidirectional Mendelian randomization approach used here makes an excellent case. pubmed.ncbi.nlm.nih.gov/39464515/

@JuanSAMUDI57306 @RogerEnoka @avigotsky It’s possible but probably not given within subject design and untrained individuals who have a lot of room for type 1 growth.

@DanielPlotkin_ @RogerEnoka @avigotsky Would you say that because the soleus is composed primarily of slow twitch fibers the difference of 2.1 and 2.9 is possibly meaningful therefore showing more soleus growth in the seated than standing?

A principle is taking over social media in that we should train muscles where they have the greatest internal moment arm because that’s where they would be recruited and hence grow best but is this principle ready to be extrapolated to hypertrophy? pubmed.ncbi.nlm.nih.gov/30985474/

@JuanSAMUDI57306 @RogerEnoka @avigotsky pubmed.ncbi.nlm.nih.gov/38156065/ and link.springer.com/article/10.100… trained and untrained populations.

@DanielPlotkin_ @RogerEnoka @avigotsky Yes! Ive seen research like that where just because muscles aren’t as active that doenst mean they’ll grow less. Could you link the paper where they showed similar soleus growth?

@JuanSAMUDI57306 @RogerEnoka @avigotsky For example one that comes readily to mind is why does soleus get same growth from seated and standing calf raise if there’s less contribution/growth in the gastroc in seated wouldnt we expect more from the soleus?

@JuanSAMUDI57306 @RogerEnoka @avigotsky Yeah to be clear I do think mechanical variables matter I just don’t like the reductionism. The extent to which each matters how they interact with hypertrophic stimulus I think will be unpacked with coming work(mine included). But there’s already head scratchers that cast doubt.

@JuanSAMUDI57306 @RogerEnoka @avigotsky More energy demanding would be dependent on the extent of diff. for whatever parameter right? Not sure how to ascertain that without some sort of modeling. Also do we know where a muscle would be on the length tension relationship in vivo with high force dynamic contractions?

@DanielPlotkin_ @RogerEnoka @avigotsky And while I also think the LTR is a factor I’ve had someone tell me that the LTR isn’t as efficient compared to a larger IMA because it’s more energy demanding? But I’m terms of pCSA I have seen data of muscles with larger pCSA be preferentially recruited.

@JuanSAMUDI57306 @RogerEnoka @avigotsky As you have seen there’s tons of debate about motor control and it’s far from a done deal 😂 so reducing things to one factor and then overlaying hypertrophy prediction on top I don’t think is appropriate. Particularly in light of some non-intuitive findings with hypertrophy.

@JuanSAMUDI57306 @RogerEnoka @avigotsky I think there’s a reason why biomechanists use optimization models and simulations because there’s a lot of factors that can be considered, muscle length(velocity of shortening), pCSA, length tension, if a muscle has multiple actions, history effects, etc.

@Nick_Christian2 @BradSchoenfeld Yeah it’s interesting cause it depends on the type, for example given that with training interventions of all types we see an exclusive shift away from IIx it would surprise me if there wasn’t a large genetic contribution/higher baseline amount in unique individuals.

@BradSchoenfeld What are your thoughts on fiber type in relation to genetics? Do genetics dictate how many fast twitch you will have?

It has been proposed that muscles should be trained based on fiber type %, with heavier loads for type 2 dominant muscles and lighter loads for type 1 dominant. Our study refuted this theory, showing similar changes regardless of load.physoc.onlinelibrary.wiley.com/doi/10.14814/p…

@WardWriting Associated does not (always) imply causation 😎

If association does not imply causation, what does?

@brady_h @WardWriting To my knowledge benefits were modest to non-existent in humans. I assume Shaun meant in humans 🤷🏻‍♂️

@WardWriting Weight loss is the example I had in mind. Lean/healthy BMI transplant to an obese individual (or rodent) leads to weight loss/improved metabolic health.

What is the most convincing evidence that a certain change in the gut microbiome has caused a positive health outcome?

@HornbergerLab @JuanSAMUDI57306 @Geoff_A_Power Yeah it’s definitely possible, always harder with humans 😂 but many of the papers state they took great care to try to prevent isometrics, do you think something neurological independent of that possibility (GTO perhaps) could be getting ~20% increases in peak force?

@DanielPlotkin_ @JuanSAMUDI57306 @Geoff_A_Power Hard to know whether the increase force with stretching was due to neurological adaptations or true improvements in peak force.

Exploratory physiological experiments are not clinical trials sciencedirect.com/science/articl… "We have received endorsement from 95 colleagues in the field showing their support for this initiative" .... Well you can make that at least 96, and I'm sure MANY MANY more agree.

@JuanSAMUDI57306 @HornbergerLab @Geoff_A_Power We were talking about stretching interventions in humans, not immobilization. Table 3 ncbi.nlm.nih.gov/pmc/articles/P…

@HornbergerLab @Geoff_A_Power I’ve also spoke with @DanielPlotkin_ on this about the force increase seems to be a bit too much for just serial sarcomere addition. Maybe he knows some papers off the top of his head.