Anastasios Makris

Do metabolic “thresholds”/ sudden breakpoints exist? Is there an on/off switch in glycolysis or the LD enzyme? Is there an on/off switch on La diffusion or a “passage” from aerobic to anaerobic metabolism in the muscle fiber? Is this what blood La behaviour tells us?

@BradSchoenfeld Logical is not physiological 😏

A common bodybuilding strategy is to perform a single-joint exercise for a given muscle group immediately before a multi-joint exercise that targets the same muscle group. The rationale is that pre-fatiguing the target muscle may allow it to receive greater stimulation during the subsequent compound movement before fatigue in assisting muscles limits the set. For example, during the squat the spinal erectors often become the limiting factor, fatiguing before the quadriceps. By first performing leg extensions to pre-fatigue the quads, the quadriceps may be pushed closer to their limit during the squat before the erectors fatigue and terminate the set. Our recently published study put this theory to the test. We randomized 41 resistance-trained individuals to perform either a pre-exhaust protocol (leg extension → squat and leg curl → RDL) or a traditional straight-set protocol using the same exercises over 8 weeks. Results showed similar improvements in strength and muscle power between groups. Interestingly, hypertrophy was slightly greater with the traditional protocol, possibly due to the substantially higher volume load accumulated during traditional training. On the other hand, the pre-exhaust approach was more time-efficient, reducing workout duration by about 36%. Bottom line: Contrary to popular belief, pre-exhaust training does not enhance muscle growth and may even slightly compromise results. It’s a good reminder that what seems logical in theory doesn’t always translate into better outcomes in practice. 💪 intjexersci.com/ijes/vol19/iss…

@the_hough “…neither impair, nor increase skeletal muscle hypertrophy…0” would be more accurate…

Large increases in resistance training volume do not impair skeletal muscle hypertrophy or anabolic–catabolic molecular signalling in trained individuals scholar.google.co.uk/scholar_url?ur…

More intriguing research coming from our Lab!

Excited to see our lab in Athens share these new and intriguing results!

@BradSchoenfeld physoc.onlinelibrary.wiley.com/doi/full/10.11…

"Not statistically significant" does not necessarily mean "no differences." The two terms are commonly conflated in exercise science research, which confuses messaging to the general public. We need to do better...

@Nyborger_Nybo @JasonFitz1 And what about the term “Anaerobic fitness”?

@JasonFitz1 IMO "aerobic fitness" is a quite broad/vague term -> VO2-max (will plateau after some years), but you may still improve slowly and steady via improved RE, higher % utilization and increased phys-resilience (durability of all the three factors)

For most runners, there's nearly unlimited potential to develop your aerobic fitness. If you're consistent, you can keep building endurance for more than a decade. Now compare that to anaerobic fitness, which can plateau after a few months. I know where I'm focusing.

@cleiton_libardi @DrMikeRoberts @maxmichel_ Very interesting study! By “one-time 120% increase in weekly set volume” do you mean they increased the volume by 120% only for 1 week? Or for the whole training period of 8weeks? And if this is true, it kinda contradicts the commonly believed theory that volume is the driver.

NEW PREPRINT (bioRxiv) A one-time 120% increase in weekly set volume did not promote greater hypertrophy than a 20% increase. First authors: Júlio Camargo & Diego Bittencourt Great collab with @DrMikeRoberts and the Auburn team (@maxmichel_ et al.) biorxiv.org/content/10.648…

@GregLehman @Brady_H What about people with low VO2max that can’t improve it much with training (e.g. from 32 to 40ml/kg/min). Are they genetically doomed? Don’t health indices improve with exercise (Despite no large increase in VO2max)? Too much hype for VO2max as a surrogate for everything?

@Brady_H If someone is already exercising what value does the VO2max test bring? It doesn't guide your intervention. If it's low you keep training. If it's high you keep training.

Apparently the big thing on X today was the “debunk” of VO2 max as a longevity metric. Unfortunately, the arguments are flimsy. Point #1: Most studies showing a beneficial association w/ mortality are measuring cardiorespiratory fitness (CRF) using metabolic equivalent of task (MET) units, *not* objectively measuring oxygen uptake. This is true. But guess what? Do you know what a MET is? It’s equivalent to 3.5 ml/kg/min oxygen consumption. So take someone’s maximal CRF x 3.5 and you derive (albeit an estimate) of their maximal oxygen consumption. A max CRF test is a VO2 max test without gas exchange data. You’re still measuring maximal aerobic function, and those MET values were derived from somewhere (using gas exchange, most likely). There are also more than a few studies showing higher *objectively* measured VO2 max correlates with lower ACM, among other outcomes. But I digress… Point #2: VO2 max from wearables is not accurate, people should stop obsessing about it, and nobody needs a VO2 max test. Au contraire. The fact that most people are using their (inaccurate) wearable device-estimated fitness level actually strengthens the assertion that it’s probably a good idea to GO GET YOUR VO2 MAX MEASURED IN A LAB! If your maximal CRF/VO2 max is valuable to know (it is, providing risk stratification and, as we’ve seen, predicting ACM risk), then getting an accurate lab-grade assessment for $150 might just one of the best health investments you can make. That actually costs *less* than your smartwatch and takes ~15 minutes. Point #3: (What they don’t discuss) This is equally important for “longevity” but not often discussed in this debate on whether VO2 max is useful. We know that there is a fitness level (maximal oxygen consumption) below which activities of daily living become hard or impossible—it’s about 15 ml/kg/min of oxygen consumption. If you near that frailty threshold, you lose functional independence. We also know generally how fit you want to be at age [X] if you want to perform activity [Y]. And most of us want to DO stuff into old age, not just exist. So if you know that you want to be able to perform an activity requiring 30 ml/kg/min of O2 at age 60, you damn well better have a VO2 max higher than that. And the only way to know that—and to tell if you’re on the right path—is to measure your oxygen consumption. … I do NOT think a laboratory VO2 max test is necessary for everyone. But it’s accessible to many, relatively inexpensive, and valuable if you’re truly invested in health and fitness. I see so many people using their watch-derived VO2 max, which is generally next to useless other than (maybe) identifying trends. I find this whole “let’s debunk aerobic fitness” thing kind of odd. Particularly because the data are generally strong and nobody is *really* benefitting from propagating fitness as a longevity metric (ok, yeah, I wrote a book about it once, but…) And does anyone really believe being aerobically fitter (to a point) will NOT likely improve lifespan or health span to some degree? I find that hard to believe.

@JuanSAMUDI57306 The “capillary-to-mitochondria distance” theory (diffusion constraint) is quite interesting but very speculative. How can the muscle fiber “sense” the distance? And how is this then controlled? (What’s the detectable change and what’s the adaptive response at the molecular level?

@AnastasiosMakr4 2) or the “principle of striated muscle”, diffusion constraintes, physical constrained of capillaries, etc. So it’s clear that with aerobic exercise we are signaling a different stimulus but I can’t say much more of the mechanistic signaling that is occurring.

Dear Professor @mackinprof , what a great read! I would like to ask you something regarding mechanical tension. It is mentioned in this paper that “Mechanical tension refers to the force generated by muscle fibers during active contraction or passive stretch —>

@JuanSAMUDI57306 And yes there are a few studies on sprint exercise and the contribution of energy systems. They have used biopsies and found drops in intramuscular ATP levels.

@AnastasiosMakr4 Do you know research showing that? I haven’t been caught up with endurance work. My reasoning came from data showing that there are some specific fibers that do get depleted to critical levels: pubmed.ncbi.nlm.nih.gov/2289498/ To be fair these were type II fibers though

@JuanSAMUDI57306 Ca+2 levels in muscle fibers can be rapidly pumped back into the SR. If we compare the pattern of contractions during running (Rhythmic contract/relax.) and during lifting (continuous/longer contractions with minimal relax.) this would have a greater effect during strength ex?

@AnastasiosMakr4 2) I think there is also the possibility that protein synthesis is negatively regulated by calcium-dependent kinases, which in turn are influenced by fluctuations in intracellular Ca2+ concentration (amplitude and frequency).

@JuanSAMUDI57306 And ATP levels in muscle fibers have been observed to drop after a 200m or 400m sprint… during a marathon, ATP doesn’t really drop…

@AnastasiosMakr4 1) Sure ATP levels don’t fall to critical levels but it is possible that local ATP levels in key parts of the muscle cell may become limiting for crucial ATP-dependent processes that are fundamental for skeletal muscle contraction would you say?

@JuanSAMUDI57306 It’s hard to test this cause metabolites in muscle fibers (including ADP) are moving randomly in the cytoplasm colliding with one another. They usually take muscle specimens before and after an activity and measure ATP concentration (not local to a specific area).

@JuanSAMUDI57306 I see your point. You are sort of talking about an interference effect between endurance and strength type of training. Most recent studies, however show no interference effect on hypertrophy. Also, during endurance exercise, ATP levels don’t really drop to activate AMPK…

@AnastasiosMakr4 1) Good question! It’s reasonable to assume an interaction between mechanical signaling and metabolic or energetic signaling, where pathways like AMP kinase, NAD-signaling, or sirtuin signaling might counteract hypertrophic signaling.

You replied: “signalling mechanisms arising from mechanical tension are 'sensed' very differently between exercise subtypes”. Do we have any updates or papers on this since then?

“Type 1 fibers in marathon runners are overloaded for long periods of time. Type 1 fibers in bodybuilders are overloaded for way shorter periods of time. How is it that these muscle fibers grow in bodybuilders but not in marathon runners?” —>