Interesting

NWlifter

Active Member
https://www.mdpi.com/1422-0067/19/11/3649/htm

Abstract
:
Lactate is a metabolic substrate mainly produced in muscles, especially during exercise. Recently, it was reported that lactate affects myoblast differentiation; however, the obtained results are inconsistent and the in vivo effect of lactate remains unclear. Our study thus aimed to evaluate the effects of lactate on myogenic differentiation and its underlying mechanism. The differentiation of C2C12 murine myogenic cells was accelerated in the presence of lactate and, consequently, myotube hypertrophy was achieved. Gene expression analysis of myogenic regulatory factors showed significantly increased myogenic determination protein (MyoD) gene expression in lactate-treated cells compared with that in untreated ones. Moreover, lactate enhanced gene and protein expression of myosin heavy chain (MHC). In particular, lactate increased gene expression of specific MHC isotypes, MHCIIb and IId/x, in a dose-dependent manner. Using a reporter assay, we showed that lactate increased promoter activity of the MHCIIb gene and that a MyoD binding site in the promoter region was necessary for the lactate-induced increase in activity. Finally, peritoneal injection of lactate in mice resulted in enhanced regeneration and fiber hypertrophy in glycerol-induced regenerating muscles. In conclusion, physiologically high lactate concentrations modulated muscle differentiation by regulating MyoD-associated networks, thereby enhancing MHC expression and myotube hypertrophy in vitro and, potentially, in vivo.
 
https://www.mdpi.com/1422-0067/19/11/3649/htm

Abstract
:
Lactate is a metabolic substrate mainly produced in muscles, especially during exercise. Recently, it was reported that lactate affects myoblast differentiation; however, the obtained results are inconsistent and the in vivo effect of lactate remains unclear. Our study thus aimed to evaluate the effects of lactate on myogenic differentiation and its underlying mechanism. The differentiation of C2C12 murine myogenic cells was accelerated in the presence of lactate and, consequently, myotube hypertrophy was achieved. Gene expression analysis of myogenic regulatory factors showed significantly increased myogenic determination protein (MyoD) gene expression in lactate-treated cells compared with that in untreated ones. Moreover, lactate enhanced gene and protein expression of myosin heavy chain (MHC). In particular, lactate increased gene expression of specific MHC isotypes, MHCIIb and IId/x, in a dose-dependent manner. Using a reporter assay, we showed that lactate increased promoter activity of the MHCIIb gene and that a MyoD binding site in the promoter region was necessary for the lactate-induced increase in activity. Finally, peritoneal injection of lactate in mice resulted in enhanced regeneration and fiber hypertrophy in glycerol-induced regenerating muscles. In conclusion, physiologically high lactate concentrations modulated muscle differentiation by regulating MyoD-associated networks, thereby enhancing MHC expression and myotube hypertrophy in vitro and, potentially, in vivo.

Ok. I put it through Google translate.... is it a recipe for chicken fried noodles?
 
:) ok - and hopefully keeping this in simple terms - how - or even, can - that be applied practically? I understand, again very basically, lactic acid that builds up during intense exercise. Is this a way of identifying hypertrophy has been stimulated?

Please don't reply in Latin. Us Brits really don't learn that anymore....:D:D:D:D
 
LOL
I'd say, there is more benefit to the 15's than we thought.... low reps take the tension path, where higher reps with a 'burn' might stimulate hypertrophy via this path.
 
Ok. Yes, that is very interesting.

I have followed HST since the early 2000s, and I always felt that the 15s were underrated.
I came from years of HIT style training (blame Dorian Yates!! We only have one legend!) and so I was used to heavy sets of 5-10 reps, not 15s, and I really felt it, and, tbh, struggled with the 15s.

I noticed on here, over time, that people were often talking about skipping the 15s and just going straight to 10s and 5s and extended 5s.
But I always stuck with them.

The problem is, is that 15s, and above, were orginally mis-associated with fat burning and endurance, whereas the 5s and 10s were the 'heavy-duty' stuff. That's what us macho guys - and gals - wanted. So it was at least partly psychological.
But I always committed to the 15s. I still do.

More so now, as I got into myo reps - which as Blade points out - are pretty much optimal at the 15 rep range.

Currently, I do 15s on Mondays, but 1 set as an activation and then myo reps until auto regulation kicks in.
(I then do 5s on Wednesday and 10s on Fridays - DUP)
But I don't do myo reps for squats or deadlifts, so I will do 2 X 15 (cutting, as I am currently) or 3 X 15 for bulking.

Ultimately, it is important to vary the rep ranges anyway, whether linear or DUP, so it never made sense to me to drop the 15s, so I never did.

Thank you for the input and compounding my beliefs.

Brix
 
Ah cool info,
oh wow so you vary load during each week instead of progressive tension like HST? does that seem to work as well?

I agree, I think the 15's could even be extended rather than skipped. People have and do grow from muscle burning muscle frying fatigue...
 
I like the linear progression as originally set out in the vanilla HST program, but DUP also fits in too, and it was something Blade wrote about a few years ago in his "Optimal routine" article somewhere in the wide abandonment of the internet, of varying reps and sets during the week.

Basically, at the beginning of the week, I hit 15s (using myo reps where I can) - this also warms the muscles and tendons up for the heavy/strength day on Wednesday - 5s - and then I finish with a typical hypertrophy range day (10s) on the Friday

A lot of the routines out there - Layne Norton's PHAT for example - start the week with the heavy day, after a weekend rest.
Maybe as I am getting older, I feel the benefits of starting with the 'light day' - 15s - to warm up my joints and tendons etc.. before the heavy session on Wednesday.

That said, I also do still believe in linear progression too, but, now I am older - I do see an advantage in varying the load during the week (light/heavy/medium) rather than struggling with my joints on 2 full weeks of heavy 5s, and usually a further 2 weeks of negatives.
 
The concept of metabolic stress being important for muscle hypertrophy was one of the main ideas in my dissertation. I questioned the consensus idea that blood flow restriction exercise makes muscle grow because you get more recruitment as the muscle begins to suffer from metabolic congestion. I made the argument that it made more sense that it was the metabolic stress itself that was the cause of the muscle growth, and that this metabolic stress was basically a redundant signaling pathway to mechanical stress, both being able to generate muscle hypertrophy but with little additive effects when load is optimized. Here's a spinet:

"While mechanical load alone (e.g. passive stretch, eccentric contractions) is able to stimulate compensatory hypertrophy, in real world conditions mechanical loading is seldom if ever not also accompanied by the production of metabolic by products of muscle contraction (Bangsbo, Johansen, Graham, & Saltin, 1993; Bangsbo, Krustrup, González-Alonso, & Saltin, 2001; Li, King, & Sinoway, 2003; Mohr, et al., 2007). Anaerobic metabolism in working muscle leads to the accumulation of metabolic byproducts such as lactate, H+, inorganic phosphate (Pi), adenosine diphosphate (ADP), H2PO4-, and generates reactive oxygen and nitrogen species. This metabolic disturbance of the internal milieu of working muscle may serve as a coactivator of anabolic signaling. It has been proposed that increased levels of metabolic stress can affect several downstream mechanisms to facilitate muscular hypertrophy (Toigo & Boutellier, 2006; Takada, et al., 2012; Wadley, 2013; Ito, Ruegg, Kudo, Miyagoe-Suzuki, & Takeda, 2013; Schoenfeld, 2013; Scott, Slattery, Sculley, & Dascombe, 2014; Feriche, García-Ramos, Morales-Artacho, & Padial, 2017; de Freitas, Gerosa-Neto, Zanchi, Lira, & Rossi, 2017; Popov, et al., 2015).

lactate.

Most research to date has focused on lactate’s metabolic role during exercise. More recently, lactate has been recognized as playing a role in anabolic signaling as well (Oishi, et al., 2015; Nalbandian & Takeda, 2016). In support of an anabolic role for lactate, a recent study reported that lactate promotes differentiation in satellite cells (Oishi, et al., 2015). Lactate also significantly increased myogenin protein content and P70S6K phosphorylation. While not reaching significance, lactate also showed a trend for increasing Pax7, MyoD, and mTOR phosphorylation. Interestingly, lactate also significantly increased follistatin levels and decreased levels of myostatin in C2C12 cells, both factors associated with the conditions necessary for myofiber hypertrophy. In vivo, oral lactate with caffeine supplementation in low-intensity exercised rats significantly increased muscle mass, satellite cell activity, and phosphorylation of mTOR and P70SK (Oishi, et al., 2015) relative to the same exercise protocol without supplementation. Though more research is clearly needed, these results indicate that lactate may be involved in the direct activation of anabolic signaling pathways, including mTOR."

If any body is curious about any of the references I can find them a list upon request. Not enough time to hunt them each down if nobody cares. :)
 
The concept of metabolic stress being important for muscle hypertrophy was one of the main ideas in my dissertation. I questioned the consensus idea that blood flow restriction exercise makes muscle grow because you get more recruitment as the muscle begins to suffer from metabolic congestion. I made the argument that it made more sense that it was the metabolic stress itself that was the cause of the muscle growth, and that this metabolic stress was basically a redundant signaling pathway to mechanical stress, both being able to generate muscle hypertrophy but with little additive effects when load is optimized. Here's a spinet:

"While mechanical load alone (e.g. passive stretch, eccentric contractions) is able to stimulate compensatory hypertrophy, in real world conditions mechanical loading is seldom if ever not also accompanied by the production of metabolic by products of muscle contraction (Bangsbo, Johansen, Graham, & Saltin, 1993; Bangsbo, Krustrup, González-Alonso, & Saltin, 2001; Li, King, & Sinoway, 2003; Mohr, et al., 2007). Anaerobic metabolism in working muscle leads to the accumulation of metabolic byproducts such as lactate, H+, inorganic phosphate (Pi), adenosine diphosphate (ADP), H2PO4-, and generates reactive oxygen and nitrogen species. This metabolic disturbance of the internal milieu of working muscle may serve as a coactivator of anabolic signaling. It has been proposed that increased levels of metabolic stress can affect several downstream mechanisms to facilitate muscular hypertrophy (Toigo & Boutellier, 2006; Takada, et al., 2012; Wadley, 2013; Ito, Ruegg, Kudo, Miyagoe-Suzuki, & Takeda, 2013; Schoenfeld, 2013; Scott, Slattery, Sculley, & Dascombe, 2014; Feriche, García-Ramos, Morales-Artacho, & Padial, 2017; de Freitas, Gerosa-Neto, Zanchi, Lira, & Rossi, 2017; Popov, et al., 2015).

lactate.

Most research to date has focused on lactate’s metabolic role during exercise. More recently, lactate has been recognized as playing a role in anabolic signaling as well (Oishi, et al., 2015; Nalbandian & Takeda, 2016). In support of an anabolic role for lactate, a recent study reported that lactate promotes differentiation in satellite cells (Oishi, et al., 2015). Lactate also significantly increased myogenin protein content and P70S6K phosphorylation. While not reaching significance, lactate also showed a trend for increasing Pax7, MyoD, and mTOR phosphorylation. Interestingly, lactate also significantly increased follistatin levels and decreased levels of myostatin in C2C12 cells, both factors associated with the conditions necessary for myofiber hypertrophy. In vivo, oral lactate with caffeine supplementation in low-intensity exercised rats significantly increased muscle mass, satellite cell activity, and phosphorylation of mTOR and P70SK (Oishi, et al., 2015) relative to the same exercise protocol without supplementation. Though more research is clearly needed, these results indicate that lactate may be involved in the direct activation of anabolic signaling pathways, including mTOR."

If any body is curious about any of the references I can find them a list upon request. Not enough time to hunt them each down if nobody cares. :)

Really cool info Bryan, thanks for sharing that info, very interesting!

hey have you seen this? We know fiber activation is via intracellular calcium, and apparently, calcium also signals the mechano signals It almost seems like high calcium means high activation which 'should' mean high tension even if actual tension isn't maximal. (does that make sense?)

https://www.karger.com/Article/Fulltext/356667
 
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