74 replies to this topic

[Turnbuckle]

In this protocol, nicotinamide riboside (NR) is used to weaken muscles temporarily to enhance the impact of exercise, while also stimulating mitochondrial quality control.

 

Method: High dosing with NR precursors and exercising about an hour later with weights less than normal—generally substantially less.

 

Dosage: I’ve used up to 2 grams of nicotinamide and 5 grams of ribose. This is equivalent to more than 4 grams of nicotinamide riboside, with the advantage that it doesn’t have to be broken down first and thus the onset doesn’t take hours. This is a large dose and I suggest that one work up to it.

 

Frequency: Once a week to allow NAD levels to drop and for mitochondria to proliferate. I did try this 4 days in a row initially, and regretted it as it took me over a week to recover. 

 

Results: I’ve found that by using weights with only one-half to one-third of what I can lift with C60, I’m getting better results.

 

Rationale: NR efficiently raises the ratio of NAD(+)/NADH, which sets the mitochondrial quality control process running. Mitochondria are divided into minimal size (which is inefficient for ATP production). Exercising forces mitochondria into high (though inefficient) activity, which makes it easier for the cell to identify poor performers and mark them for destruction. So you potentially get muscle credit for lifting substantially less weight, plus you enhance the clearance of defective mtDNA.

 

 

 

References:

 

Nicotinamide-induced mitophagy: event mediated by high NAD+/NADH ratio and SIRT1 protein activation.

 

Here, we present evidence to show that the effect of nicotinamide is mediated through an increase of the [NAD(+)]/[NADH] ratio and the activation of SIRT1, an NAD(+)-dependent deacetylase that plays a role in autophagy flux. The [NAD(+)]/[NADH] ratio was inversely correlated with the mitochondrial content... Together, our results indicate that a metabolic state resulting in an elevated [NAD(+)]/[NADH] ratio can modulate mitochondrial quantity and quality via pathways that may include SIRT1-mediated mitochondrial autophagy . . . Removal of dysfunctional mitochondria requires the activation of autophagy coupled with ongoing mitochondrial fission.

 

https://www.ncbi.nlm...les/PMC3365962/

 

 

Bioenergetic role of mitochondrial fusion and fission

 

Several recent reports underscore the importance of mitochondrial fusion under conditions of high energy demand in mammals. It was shown that some cell stressors, including UV irradiation and several drugs that inhibit cytosolic protein synthesis, can trigger increased mitochondrial fusion in mouse embryonic fibroblasts, a process termed stress-induced mitochondrial hyperfusion. Mitochondria elongate and form a mesh of highly interconnected filaments in an Mfn1 and Opa1-dependent manner. Stress-induced mitochondrial hyperfusion is accompanied by increased mitochondrial ATP production. It is conceivable that fusion is necessary to optimize mitochondrial function in order to allow the cell to cope with increased energy demand during selective forms of stress.

 

http://www.sciencedi...005272812000692

 

 

 

Digestion and Absorption of NAD by the Small Intestine of the Rat

 

Perfused or intact intestine rapidly hydrolyzed NMN to nicotinamide riboside, which accumulated, but was not absorbed. It was slowly cleaved by an enzyme associated with the mucosal cells to nicotinamide, which was the major if not the only labeled compound absorbed.

 

http://nadh.wiki/wp-...-of-the-Rat.pdf

 

 

 

[Kabb]

How does taking supplemental ribose and nicotinamide  increase the level of nicotinamide riboside?  Presumably taking NR's precusors is necessary but not, of itself, sufficient to create NR.  Is the light exercise an important ingredient in activating biochemical processes to combine these precursors?

[Turnbuckle]

How does taking supplemental ribose and nicotinamide  increase the level of nicotinamide riboside?  Presumably taking NR's precusors is necessary but not, of itself, sufficient to create NR.  Is the light exercise an important ingredient in activating biochemical processes to combine these precursors?

 

 

See the last link in the OP, which says: Perfused or intact intestine rapidly hydrolyzed NMN to nicotinamide riboside, which accumulated, but was not absorbed. It was slowly cleaved by an enzyme associated with the mucosal cells to nicotinamide, which was the major if not the only labeled compound absorbed.

 

In rats, NR was not absorbed until cleaved and then the resulting free nicotinamide (and ribose as well) could be absorbed. So taking N+R is equivalent to taking a predigested NR. There's no evidence that humans are any different from rats when it comes to the absorption of NR. Thus taking 2g of nicotinamide + 5 grams of ribose (a stoichiometric excess) is equivalent to taking 4g of NR. This is a huge dose, which fissions mitochondria and makes you temporarily weaker, as fissioned mitochondria are not as effective at creating ATP. Thus you won't be able to lift as much weight, but will be able to generate a burn more easily, stimulating muscle growth.

[hamishm00]

 

 

How does taking supplemental ribose and nicotinamide  increase the level of nicotinamide riboside?  Presumably taking NR's precusors is necessary but not, of itself, sufficient to create NR.  Is the light exercise an important ingredient in activating biochemical processes to combine these precursors?

 

 

See the last link in the OP, which says: Perfused or intact intestine rapidly hydrolyzed NMN to nicotinamide riboside, which accumulated, but was not absorbed. It was slowly cleaved by an enzyme associated with the mucosal cells to nicotinamide, which was the major if not the only labeled compound absorbed.

 

In rats, NR was not absorbed until cleaved and then the resulting free nicotinamide (and ribose as well) could be absorbed. So taking N+R is equivalent to taking a predigested NR. There's no evidence that humans are any different from rats when it comes to the absorption of NR. Thus taking 2g of nicotinamide + 5 grams of ribose (a stoichiometric excess) is equivalent to taking 4g of NR. This is a huge dose, which fissions mitochondria and makes you temporarily weaker, as fissioned mitochondria are not as effective at creating ATP. Thus you won't be able to lift as much weight, but will be able to generate a burn more easily, stimulating muscle growth.

 

 

 

I tried this and the weakening effect (combined with burning) in the gym is significant. very interesting.

 

 

Edited by hamishm00, 12 June 2017 - 01:52 PM.

[aconita]

You can try blood flow restriction training (Kaatsu training) since big weights are out of question, it should yield even better results.

[Turnbuckle]

You can try blood flow restriction training (Kaatsu training) since big weights are out of question, it should yield even better results.

 

This is an interesting idea and I will try it. It is said to work by both lowering oxygen levels and boosting lactic acid, so it's possible that supplements like pyruvate would also work with the OP protocol. Most people look to decreasing lactic acid during exercise, but maybe that is backwards.

[aconita]

Lactic acid exposure increases the size of muscle mitochondria thus improving the lactate threshold.

 

Lowering lactic acid is a bad idea, raising the lactate threshold by increasing size of mitochondria is much smarter.

[Ben]

Re. Lactic acid (this is off topic sorry):  I used to workout in below ground floor gym. It was always stuffy in there and I believe with all the people and the poor ventilation, I would get a greater lactic acid build up. I have never felt so "swole" as did when working out at that gym.

[Turnbuckle]

With time I was finding that the burn wasn't as easy to get and the weights were creeping up, so I added pyruvate + ampk activators, and I was back to getting a burn very easily with less weight.

 

N+R (2g + 5g) 

rose hips + gypenosides after 15 mininutes (1g + 75 mg)

pyruvate after another 15 minutes (2g)

weight room after another hour

Edited by Turnbuckle, 01 July 2017 - 11:39 AM.

[Ben]

 

With time I was finding that the burn wasn't as easy to get and the weights were creeping up, so I added pyruvate + ampk activators, and I was back to getting a burn very easily with less weight.

 

N+R (2g + 5g) 

rose hips + gypenosides after 15 mininutes (1g + 75 mg)

pyruvate after another 15 minutes (2g)

weight room after another hour

 

 

Have your strength gains improved from this regimen?

[Turnbuckle]

 

 

With time I was finding that the burn wasn't as easy to get and the weights were creeping up, so I added pyruvate + ampk activators, and I was back to getting a burn very easily with less weight.

 

N+R (2g + 5g) 

rose hips + gypenosides after 15 mininutes (1g + 75 mg)

pyruvate after another 15 minutes (2g)

weight room after another hour

 

 

Have your strength gains improved from this regimen?

 

 

 

Definite strength and muscle gains, but I can't yet say for sure about the pyruvate.

[Advocatus Diaboli]

In conjunction with Turnbuckle protocol, I use the probably-safe supplement  creatine monohydrate post-exercise to increase  power and performance in my high-intensity anaerobic routines. Anyone else use any "performance" supplements while using Turnbuckle protocol?

[Turnbuckle]

In conjunction with Turnbuckle protocol, I use the probably-safe supplement  creatine monohydrate post-exercise to increase  power and performance in my high-intensity anaerobic routines. Anyone else use any "performance" supplements while using Turnbuckle protocol?

 

The point of this protocol is to decrease ATP production during exercise rather than increase it, thus getting more muscle credit for a lighter workout while also getting rid of marginal mitochondria. So creatine will likely work in the opposite direction.

[aconita]

I suppose we can expect a rebound effect too, therefore an increase in ATP once the above protocol is over which might explain part of the gains.

 

The rebound effect is a counter intuitive but indeed interesting one.

 

I remember reading  of a Chinese research about lowering testosterone for a while to have it rebound above previous levels afterwards, for example.

 

It would be interesting to get some numbers about this protocol, like how much time it last, previous max loads (1RM or whatever), afterwards max loads, increase in max loads or in reps (as seen with C60oo, the max load doesn't increase but the number of reps with the same load does).

 

Muscle size measures could be provided too, the best way to do it would be to get a before and after measure of fat percentage estimate by a fat caliper (inexpensive to buy) to make sure increase or decrease of fat isn't involved or at least taken in proper account, muscles size (diameter) like chest, arms, upper legs, 15 cm above the knee legs and calves, which will give a fair estimate of hypertrophy gains.

 

Numbers don't need to be disclosed, just percentages gained or lost. 

 

It would be interesting other people following the protocol reports too, with numbers (please try to follow a standard of measurement as above described in order to make comparison reliable), of course.

 

The more people and data the more reliable it would be, of course.

 

It would be kind of more of a research like thing instead of just anecdotal, I am pushing this way because it seems interesting and it might deserve more attention.

[Monkey_Boy]

 

In conjunction with Turnbuckle protocol, I use the probably-safe supplement  creatine monohydrate post-exercise to increase  power and performance in my high-intensity anaerobic routines. Anyone else use any "performance" supplements while using Turnbuckle protocol?

 

The point of this protocol is to decrease ATP production during exercise rather than increase it, thus getting more muscle credit for a lighter workout while also getting rid of marginal mitochondria. So creatine will likely work in the opposite direction.

 

Exactly!

Creatine supplementation replenishes the supply of ATP during exercise and retards lactic acid generation. You have more endurance but have to exercise longer to get the benefit

from activating AMPK and generating lactic acid.

I stopped creatine after seeing the below research. I substituted SAMe to spare methylation when my body make its own creatine and take magnesium to aid the AMPK cascade.

 

Creatine phosphate has been reported to inhibit AMPK activity (Ponticos M, Lu QL, Morgan JE, Hardie DG, Partridge TA, and Carling D.

Dual regulation of the AMP-activated protein kinase provides a novel mechanism for the control of creatine kinase in skeletal muscle. EMBO J 17: 1688 –1699, 1998. Rafaeloff-Phail R, Ding L, Conner L, Yeh WK, McClure D, Guo H, Emerson K, and Brooks H.

Biochemical regulation of mammalian AMP-activated protein kinase activity by NAD and NADH.
 

[Advocatus Diaboli]

Regarding posts #13 and #15

 

To my knowledge, the ramp-up-to-maximum-plasma-concentrations for both nicotinamide/D-ribose (N+R) ingestion and creatine monohydrate (CR) ingestion aren't represented by variants of Dirac delta functions --i.e. there isn't an instantaneous ramp-up to maximal plasma levels. There probably are some smooth increases up to maximum concentrations for N+R and for CR. I don't know how quickly the start of detectable plasma concentration would be, but this article might provide some clues for N+R.

Turnbuckle protocol suggests a 1-1.5 hour delay between taking N+R and the start of exercise (posts #1 and #9)--which might imply that, at the 1-1.5 hour mark after N+R ingestion, there is adequate plasma concentration of N+R (and/or along with, perhaps, additional considerations) to justify the start of exercise as per the goal of the protocol. Duration of exercise is unknown from this thread.

Endogenous creatine production is about 1gm/day. In addition, exogenous creatine ingestion is typically 1g/day for an omnivorous diet (same citation as above) for a total exogenous plus endogenous average of 2 grams per day (the exogenous creatine probably is accumulated in peaks following meals that include meat, for example). From the positive anecdotal reports from some in the "Manipulating mitochondrial dynamics" thread, who are following the protocol, it would appear that this 2gm/day "background" creatine availability might not have a significant impact on protocol goals.

 

I specifically mentioned in my comments in post #12 that the CR I take was post-exercise, not pre-exercise (pre-exercise ingestion of CR might suggest detectable plasma concentration of CR "during exercise", probably depending upon timing). Pre-exercise CR ingestion  possibly might allow for sufficient CR plasma concentration during exercise (timing caveat) to interfere with the protocol goal via some antithetical action of the CR, as Monkey_Boy and Turnbuckle have both implied. However, knowledge of the plasma concentrations of CR and N+R over time would be needed to assess the extent, if any, to which CR, post-exercise (as I use per my post #12), might interfere with protocol goals.

My creatine monohydrate ingestion immediately post-protocol is no more than 5 grams or about 2-1/2 times the per-day "background" level, albeit as a liquid-suspension bolus administration.

@Monkey_Boy, You state in post #15 "Creatine phosphate has been reported to inhibit AMPK activity". Creatine phosphate isn't creatine monohydrate (hydrated creatine)

 

From your citation:

"In contrast, Cr (creatine) had no direct  effect on AMPK activity (Figure  2B),  even  at 20 mM Cr, a concentration well above the physiologic range (5–10 mM) (M.J.Sullivan et al., 1994; Wallimann, 1994; Steeghs et al., 1997). In the presence of 10 mM Cr,
however, inhibition of AMPK by 20 mM PCr (phosphocreatine)  was totally abolished (Figure 2B). This antagonistic effect is dependent not only on Cr concentration but also on the concentration of PCr ( (Figure 2C). This shows that the inhibition of AMPK  is  dependent  on  the  ratio  of  PCr:Cr,  rather  than on  the  concentration  of  PCr  alone.  Although  we  used AMPK purified from rat liver for these studies, the effect of  PCr  and  Cr  was  identical  if  kinase  isolated  from  rat skeletal muscle was used (data not shown). A fall in the PCr:Cr ratio within the cell would be expected, therefore, to cause activation of AMPK as a result of the release of inhibition exerted by PCr. This effect mirrors the situation in hepatocytes, where a fall in the ATP:AMP ratio leads to stimulation of AMPK activity (Corton et al., 1994). In this  case,  however,  activation  is  brought  about  by  an increase  in  the  allosteric  activator,  AMP.  The  effect  of PCr/Cr on AMPK activity in vitro occurs in the absence or  presence  of  AMP  (data  not  shown).  These  results suggest that the regulation of AMPK by the PCr:Cr ratio and  the  ATP:AMP  ratio  may  act  in  parallel  within  the cell. Since a synthetic peptide (SAMS) was used to assay for  AMPK  activity,  it  seems  likely  that  inhibition  is  a direct effect of PCr on AMPK, rather than being substrate mediated."

 

I have added parenthetical notes in the above for clarity, such as Cr (creatine) as above.
 

[Monkey_Boy]

 

 

In conjunction with Turnbuckle protocol, I use the probably-safe supplement  creatine monohydrate post-exercise to increase  power and performance in my high-intensity anaerobic routines. Anyone else use any "performance" supplements while using Turnbuckle protocol?

 

The point of this protocol is to decrease ATP production during exercise rather than increase it, thus getting more muscle credit for a lighter workout while also getting rid of marginal mitochondria. So creatine will likely work in the opposite direction.

 

Exactly!

Creatine supplementation replenishes the supply of ATP during exercise and retards lactic acid generation. You have more endurance but have to exercise longer to get the benefit

from activating AMPK and generating lactic acid.

I stopped creatine after seeing the below research. I substituted SAMe to spare methylation when my body make its own creatine and take magnesium to aid the AMPK cascade.

 

EDIT: I've gone back over the methionine cycle. If I focus on  homocysteine instead of creatine, SAMe is be more problem than solution. I've stopped the SAMe and will find a better alternative.

 

Creatine phosphate has been reported to inhibit AMPK activity (Ponticos M, Lu QL, Morgan JE, Hardie DG, Partridge TA, and Carling D.

Dual regulation of the AMP-activated protein kinase provides a novel mechanism for the control of creatine kinase in skeletal muscle. EMBO J 17: 1688 –1699, 1998. Rafaeloff-Phail R, Ding L, Conner L, Yeh WK, McClure D, Guo H, Emerson K, and Brooks H.

Biochemical regulation of mammalian AMP-activated protein kinase activity by NAD and NADH.
 

 

[Monkey_Boy]

Regarding posts #13 and #15

 

To my knowledge, the ramp-up-to-maximum-plasma-concentrations for both nicotinamide/D-ribose (N+R) ingestion and creatine monohydrate (CR) ingestion aren't represented by variants of Dirac delta functions --i.e. there isn't an instantaneous ramp-up to maximal plasma levels. There probably are some smooth increases up to maximum concentrations for N+R and for CR. I don't know how quickly the start of detectable plasma concentration would be, but this article might provide some clues for N+R.

Turnbuckle protocol suggests a 1-1.5 hour delay between taking N+R and the start of exercise (posts #1 and #9)--which might imply that, at the 1-1.5 hour mark after N+R ingestion, there is adequate plasma concentration of N+R (and/or along with, perhaps, additional considerations) to justify the start of exercise as per the goal of the protocol. Duration of exercise is unknown from this thread.

Endogenous creatine production is about 1gm/day. In addition, exogenous creatine ingestion is typically 1g/day for an omnivorous diet (same citation as above) for a total exogenous plus endogenous average of 2 grams per day (the exogenous creatine probably is accumulated in peaks following meals that include meat, for example). From the positive anecdotal reports from some in the "Manipulating mitochondrial dynamics" thread, who are following the protocol, it would appear that this 2gm/day "background" creatine availability might not have a significant impact on protocol goals.

 

I specifically mentioned in my comments in post #12 that the CR I take was post-exercise, not pre-exercise (pre-exercise ingestion of CR might suggest detectable plasma concentration of CR "during exercise", probably depending upon timing). Pre-exercise CR ingestion  possibly might allow for sufficient CR plasma concentration during exercise (timing caveat) to interfere with the protocol goal via some antithetical action of the CR, as Monkey_Boy and Turnbuckle have both implied. However, knowledge of the plasma concentrations of CR and N+R over time would be needed to assess the extent, if any, to which CR, post-exercise (as I use per my post #12), might interfere with protocol goals.

My creatine monohydrate ingestion immediately post-protocol is no more than 5 grams or about 2-1/2 times the per-day "background" level, albeit as a liquid-suspension bolus administration.

@Monkey_Boy, You state in post #15 "Creatine phosphate has been reported to inhibit AMPK activity". Creatine phosphate isn't creatine monohydrate (hydrated creatine)

 

From your citation:

"In contrast, Cr (creatine) had no direct  effect on AMPK activity (Figure  2B),  even  at 20 mM Cr, a concentration well above the physiologic range (5–10 mM) (M.J.Sullivan et al., 1994; Wallimann, 1994; Steeghs et al., 1997). In the presence of 10 mM Cr,
however, inhibition of AMPK by 20 mM PCr (phosphocreatine)  was totally abolished (Figure 2B). This antagonistic effect is dependent not only on Cr concentration but also on the concentration of PCr ( (Figure 2C). This shows that the inhibition of AMPK  is  dependent  on  the  ratio  of  PCr:Cr,  rather  than on  the  concentration  of  PCr  alone.  Although  we  used AMPK purified from rat liver for these studies, the effect of  PCr  and  Cr  was  identical  if  kinase  isolated  from  rat skeletal muscle was used (data not shown). A fall in the PCr:Cr ratio within the cell would be expected, therefore, to cause activation of AMPK as a result of the release of inhibition exerted by PCr. This effect mirrors the situation in hepatocytes, where a fall in the ATP:AMP ratio leads to stimulation of AMPK activity (Corton et al., 1994). In this  case,  however,  activation  is  brought  about  by  an increase  in  the  allosteric  activator,  AMP.  The  effect  of PCr/Cr on AMPK activity in vitro occurs in the absence or  presence  of  AMP  (data  not  shown).  These  results suggest that the regulation of AMPK by the PCr:Cr ratio and  the  ATP:AMP  ratio  may  act  in  parallel  within  the cell. Since a synthetic peptide (SAMS) was used to assay for  AMPK  activity,  it  seems  likely  that  inhibition  is  a direct effect of PCr on AMPK, rather than being substrate mediated."

 

I have added parenthetical notes in the above for clarity, such as Cr (creatine) as above.
 

 

Parallel increases in phosphocreatine and total creatine in human vastus lateralis muscle during creatine supplementation
Jeffrey J. Brault, Theodore F. Towse, Jill M. Slade, Ronald A. Meyer

International Journal of Sport Nutrition and Exercise Metabolism - Dec 2007

 

The PCr:Cr ratio does not change, instead you maintain your muscle storage at saturation levels.

You can still activate AMPK starting at saturation. It just takes longer.

 

 

 

[Advocatus Diaboli]

@Monkey_Boy, in your post #18 you have quoted the entirety of my post #16. What is it specifically that your post #18 is addressing regarding the fact that I use creatine monohydrate post-exercise--the main thrust of the clarification intent of my post #16?

 

Note that you, in your post #15, mention "during exercise". It was my intent in to disabuse any malentendu that suggested (as a reading of your post #15 might be implying) that I might have ingested creatine monohydrate at a time, possibly pre-exercise, such that the ingested creatine monohydrate might interfere with the goals of the Turnbuckle protocol "during exercise". 

 

Here is a link to the full text of the study you mention in post #18. There are some obvious problems with the study that you will recognize if you care to read through the text.

[Nate-2004]

How would say, Muscle Feast 100% whey protein prior to a workout, work in terms of fission? What about beta alanine? Something I usually add to the protein shake.

Edited by Nate-2004, 10 September 2017 - 03:37 PM.

[Turnbuckle]

How would say, Muscle Feast 100% whey protein prior to a workout, work in terms of fission? What about beta alanine? Something I usually add to the protein shake.

 

 

The purpose of fission in this protocol is dual--to lower ATP production to get more credit for a given amount of exercise, and to target defective mitochondria for mitophagy. Calorie restriction tends to increase mitophagy--

 

 

As reported earlier, caloric restriction diet leads to increased mitophagy and decrease in both mitochondrial damage and markers of senescence in rats

https://www.ncbi.nlm...les/PMC4935730/

 

 

 

I generally do this protocol first thing in the morning--sometimes with a single raw egg--and then hold off for an hour after the gym before having a protein shake. Of course you can exercise at other times as well, and then you can do whatever you find works for you. But for mitophagy and decreasing ATP, I would avoid all those extras.

 

How long does mitophagy actually take? 

 

 

Kinetic studies of mitophagic clearance of entire mitochondria by PINK1 and parkin have demonstrated that this process occurs on the scale of several hours to days...

https://www.ncbi.nlm...les/PMC3989637/

 

 

 

 

Of course, once the mitochondrion is engulfed in a lysosome, its destiny is determined and it's going to be digested. Still, this argues for only doing this protocol every few days. Another argument is that biogenesis also takes time. I cycle this about once every five days.

[Nate-2004]

What about the fact that you're only exercising about 2x a week this way max? Also, I've been having a tbsp of olive oil every day for months now, should I avoid that on fission days? I will probably try this routine out for about 10 weeks to see what happens.

 

Also, wondering if propranolol, which I take as needed for ET (which is why I wanna try this), would affect any of this.

Edited by Nate-2004, 10 September 2017 - 08:24 PM.

[Turnbuckle]

What about the fact that you're only exercising about 2x a week this way max? 

 

 

Exercise all you want, as I said.

[Nate-2004]

 

What about the fact that you're only exercising about 2x a week this way max? 

 

 

Exercise all you want, as I said.

 

 

Oops I missed that bit. 

[able]

Nate,

 

I've seen a couple other threads where you mention you need to exercise at least 4 times a week, all hiit.

 

While I agree some exercise 5 or 6 days a week is best, I'm quite convinced 2-3 HIIT sessions a week are best, especially for older folks. 

 

I'm 58, and can't HIIT hard 3 times a week without getting burned out.

 

I can find references that support 2-3 times a week max HIIT if you care.

 

You may already have  read similar, but I just wanted to throw this suggestion out there.

 

 

[Turnbuckle]

An update: After half a year of doing fission/fusion with NAD+ precursors (N+R), I've noticed that the fission weakening is substantially less than when I started, which suggests a reduction in defective mitochondria. Nevertheless, I still get the same pumped up appearance afterward with a rather minimal workout of 20 minutes--which I don't get without the NAD+ precursors. The temporary nature of a post-workout pump has been discussed on various muscle building forums, but I haven't found any that know how to make it permanent, or even make it last for more than a few hours. (If such a thing could be done with a supplement, it could be worth millions.)

Edited by Turnbuckle, 10 October 2017 - 04:44 PM.

[Nate-2004]

I thought that "pump" or "burn" feeling was lactic acid?

[Turnbuckle]

I thought that "pump" or "burn" feeling was lactic acid?

 

 

Those are different things. The pumping up is an actual increase in the size of a muscle due to vasodialation, and this lasts much longer than the lactic acid increase. The technical word is hyperemia, and according to the findings of the paper below, it appears to be a response to ATP levels—

 

 

Summary

In humans, prolonged infusions of exogenous ATP can evoke consistently high and prolonged levels of forearm blood flow and vascular conductance, similar to those seen during moderate intensity exercise. The additional dilation observed when exercise was performed during the ATP infusion suggests that additional vasodilating mechanisms are available and remain intact in spite of a level of blood flow far in excess of metabolic demand. The latter observation demonstrates that under some circumstances, it is possible to disconnect the usual matching of blood flow and oxygen delivery during exercise, challenging the metabolic theory of exercise hyperemia.

 

https://www.ncbi.nlm...exercise[Title]

 

 

 

[Nate-2004]

Wait now I'm more confused, if it's due to more ATP then for fission isn't the goal to try and deplete the ATP?

[Turnbuckle]

Wait now I'm more confused, if it's due to more ATP then for fission isn't the goal to try and deplete the ATP?

 

 

Right. And frankly I can't remember any pumped up feeling when I first started. I know I said I was still getting that pumped up effect, but that is only in the past few weeks. Previously I noted a lot of muscle tone and was getting a burn with less weight, but this pumped-up effect seems to have crept up on me over time, along with the weights creeping up. I wasn't looking for it as I'd never experienced it before.