When "No Load Training" Builds Muscle and Classic Biceps Curls Diminish Your Triceps Size, Science Must be Involved

When "No Load Training" Builds Muscle and Classic Biceps Curls Diminish Your Triceps Size, Science Must be Involved

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Do not misunderstand the results of the study at hand. It does not "proof that you don't have to use weights to make size gains" and it does not even suggest that "training without load works as effectively as training with loads for every muscle".

I suspect you will remember that I have previously written about the potential muscle building effects of posing. Now, the isometric contractions you perform when you "pose", are not exactly the same, but at least related to the "maximal contractions through a full range of motion" Counts et al. investigated in their latest study. Accordingly, it doesn't seem to be totally far-fetched to assume that (1) increases in muscle size would be similar with this type of NO LOAD compared to HIGH LOAD training and that (2) HIGH LOAD training would still result in a greater strength increases compared to NO LOAD due to the principle of specificity.

To elucidate whether these hypotheses are accurate, Counts et al. recruited fifteen (6 men, 9 women) participants for a 6-week study (see Figure 1) ... untrained subjects.

It could be a good idea to use NO LOAD training as part of your periodization schemes.

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Untrained? I know what you're thinking, but you got to start somewhere and to measure significant muscle gains in only 6 weeks, your subjects almost have to be untrained; even if this means that it is neither necessarily nor likely possible to transfer your results to trained individuals. It is thus well possible, that the NO LOAD conditions, the authors describe as follows, ...

"[t]he NO LOAD training condition is defined as voluntarily maximally contracting the muscle through the full range of motion without the use of an external load. During each NO LOAD training session, surface electromyography (EMG) electrodes were applied to the biceps to provide feedback to the participant and to help encourage greater activation during each repetition. The participants completed 4 sets of 20 repetitions with 30 seconds of rest between sets. This protocol was based off of pilot work performed in our laboratory which suggested that 4 sets of 20 repetitions should result in increases in both fatigue and muscle activation" (Counts. 2016).

... will have smaller or even no effect at all on the muscle size of already trained individuals - and that would obviously be much in contrast to the tried-and-proven HIGH LOAD training in which the authors completed 4 sets of 8–12 repetitions with 90 s of rest between sets at 70% of their 1RM (weight was increased if more than 12 reps could be done).

Figure 1: Study design outline. 1RM – one repetition maximum (Counts. 2016).

But enough of the "could"s and "might"s. Let's take a look at what we can says for sure: In the study at hand, where both conditions exercised to a metronome at a cadence of 1.5 s for the concentric and eccentric portion of the lift, totaling a 3 s contraction, the subjects were assigned to the NO or HIGH load condition according to a counterbalanced design and the results were quite intriguing:

• Contracting muscle through a full range of motion with no external load increases muscle size similar to high load training.
• High load training produced larger increases in 1RM strength & muscle endurance compared to contracting with no external load.
• Muscle growth can occur independent of the external load provided sufficient tension is produced by the muscle.
• Muscle strength is proportional to the load being used and the modality of exercise being performed (specificity)

More specifically, the study results show that anterior muscle thickness increased similarly from Pre to Post, with no differences between conditions for the 50% [Pre: 2.7 (0.8) vs. Post: 2.9 (0.7)], 60% [Pre: 2.9 (0.7) vs. Post: 3.1 (0.7)] or 70% [Pre: 3.2 (0.7) vs. Post: 3.5 (0.7)] sites, that there is a significant condition × time interaction for one repetition maximum (p = 0.017), with HIGH LOAD (+2.3 kg) increasing it more than the NO LOAD condition (+1 kg) and thus that it is, as Counts et al. write "generally possible to make gains [at least in untrained individuals] across a vast range of external loads and muscle actions" - even independent of external load "provided there are enough muscle fibers undergoing mechanotransduction" (Counts. 2016).

Figure 2: Mean muscle thickness from pre to post training at 50%,60% and 70% sites of the anterior (biceps) & posterior (triceps) upper arm (left) and individual differences in anterior muscle thickness (right | Counts. 2016).

Before you drop the weights altogether, though, you should know that there are a few other limitations of the study (next to the previously hinted at lack of training experience in the subjects) the scientists discuss: They range from the lack of quantitative data on the volume of work completed in the NO LOAD condition (workload is distance times weight - with no weight, you cannot calculate it), of which the scientists say that it "may explain some of the variability in the growth response following NO LOAD training" to the choice of tests which are "more specific to the HIGH LOAD condition and less specific to the NO LOAD condition[. Consequently] it stands to reason that NO LOAD training's effect on strength may be underestimated" (Counts. 2016).

Eventually, the results of the study at hand, as intriguing as they may be, must thus be considered preliminary evidence in support of the mechanotransduction theory of muscle building and its implications, namely that no external load is necessary to stimulate the transcription factors that will eventually initiate the adaptive response to "no-weight lifting" (see Figure below)

Overview of the main events during signal transduction and gene regulation leading to muscle hypertrophy (my orange emphasis in a figure from Rennie, et al. 2004)

So, yes further research is war-ranted to evaluate whether training w/out load could make sense for trained individuals as well.  I have to admit, though, that the existing evidence on the underlying mechanisms of muscle growth supports the notion that training for size does not necessarily involve high weights or muscle damage. After all, the hypertrophy driving trans-criptional factors (see Figure on the right) can be induced by Ca2+ increa-ses, stretch and hypoxia, which can all be achieved in the absence of high loads or sign. muscle damage (Rennie. 2004)... and still, I have my doubts about the effects on trained individuals.

What? Oh, yes... the hint at the reduced posterior muscle (=tripecs) size from the headline. I almost forgot that. Well, the scientists were probably not less surprised than you were when you looked at Figure 2 and realized that the tried and proven "HIGH LOAD condition decreased posterior upper arm muscle thickness following 6 weeks of bicep curl training" (Counts. 2016). Just like me Counts et al. are "not aware of any studies that investigated HIGH LOAD resistance training that targeted only the biceps and measured muscle size of both the biceps and triceps"; and in contrast to what I previously suggested, this cannot be a methodological artifice, because the ultrasound measures the scientists used could distinguish between muscle and fat. What exactly the reason for the ostensible 'atrophy' of the triceps muscle is, may thus still be called a 'mystery' - one that needs to be addressed in future studies, though... (thx Jeremy for spotting this mistake) | What do you think, any ideas on the mechanism? Comment on Facebook!

References:

• Counts, Brittany R., et al. "The acute and chronic effects of “NO LOAD” resistance training." Physiology & Behavior (2016).
• Rennie, Michael J., et al. "Control of the size of the human muscle mass." Annu. Rev. Physiol. 66 (2004): 799-828.

Your Post-Workout Testosterone Levels Can Predict Your Gains - Study Takes Novel Approach to the T ↔ Muscle Link

Your Post-Workout Testosterone Levels Can Predict Your Gains - Study Takes Novel Approach to the T ↔ Muscle Link

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GainZ - Are they all about T and we just didn't do the right statistical tests in previous studies to realize that?

Only recently one of the longstanding "truths" of protein anabolism has been busted (learn why the acute muscle protein synthesis response matters more than prev. thought). And now, a new paper in the Journal of Strength and Conditioning Research (Mangine. 2016), appears to suggest that the lack of effect of exercise induced hormone elevations may have been misunderstood, too.

In the conclusion of their study, Mangine et al. point out that the previously used "[t]raditional statistical measures do not adequately assess the relationships between multiple variables that exist across time" (Mangine. 2016).

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In order to overcome this problem, their study used what the scientists call a "unique method for analyzing these types of relationships without the need for transforming data"; and - first things first - their the PLS-SEM analysis (details below) shows: "baseline muscle size and the hormonal response to resistance exercise are related to muscle hypertrophy following 8 wks of training  (Mangine. 2016).

Figure 1: The scientists ,odel for the relationship between changes in muscle size and the endocrine response to resistance exercise predicts influence of all hormones on muscle size and vice versa(!); RF_CSA = Rectus femoris cross-sectional area; RF_MT = Rectus femoris muscle thickness; VL_CSA = Vastus lateralis cross-sectional area; VL_MT = Vastus lateralis muscle thickness; WK1 = Week 1; WK8 = Week 8 (Mangine. 2016).

Moreover, the data from the Kennesaw State University, the University of Central Florida and the College of New Years appears to suggest that the often derided exercise-induced post-workout (PWO) increases in testosterone concentrations may be the most important agent in the hormone quintet of testosterone, cortisol, growth hormone, IGF-1, and insulin that is going to react to every intense resistance training study.

Figure 2: Sign. associations between PWO hormone levels and lean mass, as well as fiber size increases (West. 2012).

That's surprising in two ways: (A) the majority of previous studies refuted the existence of a practically relevant link between the amount of muscle you will gain and the change in hormone levels, altogether. And (B) you will remember that my hitherto favorite study on the "[a]sociations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training" by West and Phillips (2012) showed in a large cohort that - if there is any link between the PWO hormone response to resistance training and the changes in muscle size it would be a link to growth hormone (GH) and cortisol (see Figure 2).

Free testosterone (upper line) and cortisol (lower line) levels before and after exhaustive endurance exercise in trained young men (Anderson. 2016).

Excess cardio cannot, it will ruin your testosterone levels and (surprise) 24h post also your cortisol levels: The data in the figure on the left hand side was recorded in a recent study by Anderson et al. (2016) who observed that the full recovery of free testosterone and cortisol after an exhaustive endurance exercise session (prolonged exercise run on the treadmill until volitional fatigue, running at 100 % of ventilatory threshold (VT), within 3 % - 75 minutes) will take 48h - even in endurance trained fit, young men such as the 12 subjects (VO2max 66.3±4.8 ml/kg/min, age 22.8 ± 3.1 years, body fat 11.0 ± 1.4 %, training 7.1y) Anderson et al recruited.

That's obviously significantly different from what we see in the Magine study, at hand, where the likewise previously trained subjects completed at least 28 resistance training sessions (~90%) of an 8-wk resistance-training program (4 sessions/wk) that included six upper- and lower-body exercises during each session, under supervision of certified strength & conditioning specialists.

With the inclusion of potential influence of the initial muscle mass on the hormonal response to exercise Magine's study does now suggest what many trainees still believed, anyways: "When it comes to making gainz, the testosterone response to workouts counts." Furthermore, the scientists argue that the reason studies like McCall et al. (1999), Ahtianinen et al. (2003), and Walker et al. (2015), which used Pearson’s product moment correlation coefficients or Spearman’s rank correlation coefficients (Walker. 2014) were conflicting and not really reliable, because...

"significant amount of information [that] is lost when using either of these statistical procedures for assessing the relationships between concepts that exist across time (i.e. hypertrophy, multiple endocrine responses) because the statistics can only assess the relationship between two sets of values" (Mangine. 2016). 

With their approach, on the other hand, Mangine et al. (2016) transformed the correlation between hypertrophy and the endocrine response from baseline and post-testing into a single value (i.e. change score, average score). The method to do this is called "partial least squares structural equation modeling" (PLS-SEM) and it allows estimating complex cause-effect relationship models with latent variables. Since it is a component-based estimation approach, it differs from the covariance-based structural equation modeling you'd usually expect to be used and constitutes, as the scientists summarize

"[...] a variance based procedure that utilizes bootstrapping to statistically assess the relationships between multiple latent variables that are developed from several collected indicator variables [which has] been used to assess relationships within the biomedical sciences [already... even though] it has not yet been used to assess the relationships between the post-exercise endocrine response and muscle hypertrophy" (Mangine. 2016).

For it to work, the authors obviously have to assume that "the related variables were collected without systematic or random error" in their experiment that included pre-tests (PRE) of measures of muscle size (thickness and cross-sectional area) of the vastus lateralis and rectus femoris in 26 resistance-trained men who were randomly selected to complete a high-volume (VOL, n=13, 10–12RM, 1-min rest) or high-intensity (INT, n = 13, 3–5RM, 3-min rest) resistance training program while following a food-log controlled diet that was supplemented with a standardized supplement containing ~235 mL of chocolate milk (170 calories; 2.5g Fat; 29g Carbohydrate; 9g protein) or Lactaid® (150 calories; 2.5g Fat; 24g Carbohydrate; 8g protein) to each participant immediately following each workout.

A pre- vs post-workout salivary testosterone test could hold the clue to the perfect workout | more

Another argument that "testosterone may count" comes from a previously discussed, but in my humble opinion largely overlooked study by Beaven et al. (2008) whose study into the correlation between the individual testosterone response to a certain workout style and the subsequent gains subjects in a randomized cross-over design study made also suggests that "testosterone counts". Sounds intruiging? I know, but the corresponding SuppVersityarticle from 2013 went almost as unrecognized as the original paper that was published 5 years before in the Journal of Strength and Conditioning Research - the same journal in which Mangine et al. have now published the results of their study.

Blood samples were collected at baseline, immediately post-exercise, 30-min, and 60-min post-exercise during weeks 1 (WK1) and 8 (WK8) of training and testosterone, growth hormone [22 kD], insulin-like growth factor-1, cortisol, and insulin levels were evaluated using area-under-the-curve (AUC) analyses of the blood values, based on which the scientists were able to identify the relationships between muscle size (PRE), AUC values (WK1 + WK8) for each hormone, and muscle size (POST) "using a consistent PLS-SEM algorithm and tested for statistical significance (p<0.05) using a 1000 samples consistent bootstrapping analysis" (Mangine. 2016).

Figure 3: Actually significant was only the link between the effect of the muscle mass before the study and the testosterone response and the testosterone response on the muscle mass after the 8-wk study (Mangine. 2016).

The model the scientists developed was capable of explaining 73.4% (p<0.001) of variance in muscle size at POST and revealed "[s]ignificant pathways between testosterone and muscle size PRE (p=0.043) and muscle size at POST (p=0.032) were observed.

Table 1: In contrast to what you may have expected, there was no sign difference in the way the hormones effected the outcomes of the 8-wk resistance training study between the high intensity and volume arm (Magine. 2016).

And while the ability to explain muscle size at POST improved when the model was analyzed by group (INT: VOL: p<0.001), the data in Table 1 goes to show you that the researchers found no group differences between the intense low volume and the moderate intensity high volume training. This in turn suggests that the link between muscle size and post-exercise increases in hormone levels - especially the effects on testosterone - are universal and do not dependent on the training type (volume vs. high intensity), as previous studies that argued in favor of volume training based on its more pronounced effects on the hormone response to exercise suggested.

In view of the conflicting evidence and hitherto relatively conclusive evidence that endogenous T & co elevations do not matter, I would not begin to train "for testosterone elevations", now... you may after all still be barking up the wrong tree. Correlations and links are after all no causations | learn more

Bottom line: I would like to point out that the study at hand does not provide sufficiently reliable evidence to say that Mangine, et al. had 'proven that the post-workout testosterone increase had a mechanistic effect on your muscle gains'. What it does show, however, is, just as the scientists say, that "[e]xercise-induced testosterone elevations, independent of the training programs used in this study, appear to be related to muscle growth" (Magine. 2016, my emphasis in the quote).

This is in contrast to previous studies, where the pre-tfiraining correlation between muscle mass and thus testosterone levels had not been accounted for. The scientists' partial least squares regression structural equation modeling (PLS-SEM), however, is eventually just "statistical shenanigan". Therefore, its impressive explanatory power of 73.4% of the variance in muscle size following 8 wks of resistance training is a neat figure, but no proof of a mechanistic link.

Furthermore, one has to be careful to falsely single out testosterone among the five hormones that were assessed. After all, restricting the model to T, which was the only significant hormonal correlate of muscle gains, reduced the explanatory power of the model by only 30.8%. This leaves the rest of the hormones with an explanatory power of 42.6% (all statistics, obviously ;-). To say that GH, IGF-1, insulin and cortisol had 'no say' in skeletal muscle hypertrophy is thus just as unwarranted as the previously hinted at (false) conclusion that the study at hand would provide the long-sought definitive evidence of the muscle building effects of exercise-induced, natural testosterone surges, i.e. the temporary elevation of T-levels after a workout | Comment!

References:

• Ahtiainen, Juha P., et al. "Muscle hypertrophy, hormonal adaptations and strength development during strength training in strength-trained and untrained men." European journal of applied physiology 89.6 (2003): 555-563.
• Beaven CM, Cook CJ, Gill ND. Significant strength gains observed in rugby players after specific resistance exercise protocols based on individual salivary testosterone responses. J Strength Cond Res. 2008 Mar;22(2):419-25.
• Mangine, Gerald T., et al. "Exercise-Induced Hormone Elevations Are Related To Muscle Growth." The Journal of Strength & Conditioning Research (2016).
• McCall, Gary E., et al. "Acute and chronic hormonal responses to resistance training designed to promote muscle hypertrophy." Canadian Journal of Applied Physiology 24.1 (1999): 96-107.
• Walker, Simon, et al. "Effects of prolonged hypertrophic resistance training on acute endocrine responses in young and older men." Journal of Aging & Physical Activity 23.2 (2015).
• West, Daniel WD, and Stuart M. Phillips. "Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training." European journal of applied physiology 112.7 (2012): 2693-2702.

High Dose NSAID Boosts Muscle Gains in Elderly Men - 11% Increase in Type II Fiber Size, Type I Grew Only 'on' Tylenol

High Dose NSAID Boosts Muscle Gains in Elderly Men - 11% Increase in Type II Fiber Size, Type I Grew Only 'on' Tylenol

aspirin build muscle COX COX II elderly fiber type gains gainz lean gains muscle fiber type muscle gains NSAID NSAIDs older people tylenol type I fiber type II fiber

Are NSAIDs over-the-counter anabolics from the pharmacy next door?

Even though this is not the first SuppVersity article about the effects of NSAIDs or COX-inhibitors like Aspirin, Tylenol, Pain-Eze and co., I would like to highlight one again that the existing evidence suggests differential effects in young(er) vs. old(er) individuals, with the former seeing no or detrimental and the latter no or beneficial effects when using NSAIDs during resistance training regimen.

It is thus neither guaranteed, nor likely that a young man or woman would see the same 28% extra-increase in type I fiber and 11% extra-increase in type II fiber diameter, Trappe et al. describe in their soon-to-be-published paper in the journal of the Gerontological Society of America (Trappe. 2016).

The link to hormesis research is far from being straight-forward

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I do understand, though that the numbers still got your attention. Well, let's take a close look at how the researchers got to these impressive results. It all started with previous research that suggested that common cyclooxygenase (COX)-inhibiting drugs enhance resistance exercise induced muscle mass and strength gains in older individuals.

Unfortunately, the results of the few studies we have, are conflicting (Schoenfeld. 2012; see Table 1) - with one showing benefits and two showing no effect at all. The purpose of Trappe's latest study was thus to (a) simply gather more evidence and (b) investigate the mechanism behind the changes that were observed in previous studies. Or, as the scientists put it "whether the underlying mechanism regulating this effect was specific to Type I or Type II muscle fibers" (Trappe. 2016).

Table 1: Summary of human studies investigating the effect of nonsteroidal anti-inflammatory
drug consumption on muscle hypertrophy (Schoenfeld. 2012).

To this ends, the scientists obtained muscle biopsies from the vastus lateralis of healthy older men who consumed either a placebo (n = 8; 64±2 years) or COX inhibitor (acetaminophen, 4 gram/day; n = 7; 64±1 years | compliance was monitored by researchers, when tablets were taken at the lab or camera when taken at home) during a standardized 12 weeks resistance training program (only the knee-extensor was trained - albeit on 3 days/week) the scientists describe as follows:

"All participants completed a progressive resistance exercise training program of bilateral knee extension that was designed to hypertrophy and strengthen the m. quadriceps femoris, using a protocol employed for several previous investigations in our laboratory. Each participant was scheduled for resistance training three times per week over the 12 weeks for a total of 36 sessions on an isotonic knee extension device (Cybex Eagle, Medway, MA). All sessions were supervised by a member of the research team. Each session was separated by at least 1 day and consisted of 5 minutes of light cycling(828E, Monark Exercise AB, Vansbro, Sweden), two sets of five knee extensions at a light weight, followed by three sets of 10 repetitions with 2 minutes of rest between sets. Training intensity was based on each individual’s one repetition maximum (1RM) and adjusted during the training based on each individual’s training session per formance and biweekly 1RM" (Trappe. 2016).

The compliance of the subjects of this double-blinded study is described as excellent. Therefore, we can assume that the significance of the results of the scientists' analysis of muscle samples that were examined for Type I and II fiber cross-sectional area, capillarization, and metabolic enzyme activities (glycogen phosphorylase, citrate synthase, β-hydroxyacyl-CoA-dehydrogenase) is high.

Figure 1: Pre-/post comparison on fiber (according to fiber type) and muscle size (Trappe. 2016).

Obviously, the most important results of these analysis have been mentioned before: While the type I fiber size did not change with training in the placebo group (304±590 μm²), it increased by a statistically significant and practically relevant 28% in the COX inhibitor group (1,388±760 μm²).

Schematic of the prostaglandin (PG) producing cyclooxygenase (COX) pathway and specific receptors that influence growth and atrophy in skeletal muscle (Trappe. 2013b).

How do COX inhibitors promote hypertrophy? As Trappe et al. point out "[e]vidence from the larger cohort suggests that the augmented muscle growth was primarily mediated by a reduction in intramuscular PGE2 and resultant PGE2 receptor downstream signaling effects (Standley. 2013; Trappe. 2013a,b). Specifically, the COX inhibitor appeared to reduce the negative effects of PGE2 on protein synthesis and degradation, working through established myokines and other cellular regulators of protein turnover. The myocellular findings from the current study suggest that these effects were more pronounced in the Type I fibers, possibly due to a more active PGE2/COX pathway in this fiber type" (Trappe. 2016).

In addition, the authors point out that previous evidence suggests an "additional mechanism for the COX inhibitor–induced supplemental growth, working through PGF2α receptor and protein synthesis upregulation" (Trappe. 2016; referring to Trappe. 2013a,b).

For the type II fibers, both groups recorded significant increases in fiber size. With "only" 26%, the gains of the subjects in the the placebo group (1,432±499 μm2, p < .05) were yet measurably lower than those in the COX inhibitor group whose vastus lateralis type II muscle fiber size increased by 37% (1,825±400 μm², p < .05). In view of the overall benefits the COX group saw, it is thus hardly surprising that the subjects consuming the COX inhibitor recorded significantly greater total muscle CSA gains (see Figure 1, right | note: only the total mass gain was sign. different between groups).

Figure 2: Change in fiber type–independent (A) and fiber type–specific (B) muscle capillarization from the beginning to the end of the 12-week resistance exercise training and drug interventions. CCEF = capillaries in contact with each fiber; CSA = cross-sectional area. *p < .05 vs pre. **p < .1 vs pre.

While enzyme activity (not shown in Figure 2) and capillarization were generally maintained in the placebo group, the capillary to fiber ratio of the subjects in the COX inhibitor group increased by an albeit only borderline significant 24% (p < .1). The citrate synthase activity, on the other hand, increased statistically significantly, but by "only" 18% (p < .05). These differential changes in citrate synthase (important for fat oxidation and endurance) and muscle capillarization further underline the beneficial effects of NSAIDs on the adapatational response to exercise in the elderly.

Figure 2: Two out of three studies find that NSAIDs blunt the satellite cell response to resistance training young people | A: Number of Pax7 cells expressed per number of myonuclei (in %) in muscle biopsies (vastus lateralis muscles) obtained before (pre) and 8 days after maximal eccentric exercise (no block and NSAID); B: Immunohistochemical staining with the use of Pax7 antibody to identify satellite cells on a muscle cross-section (7 m) taken 8 days after exercise (from Mikkelsen. 2009).

Bottom line: There's no reason to doubt the scientists' conclusion that "COX inhibitor consumption during resistance exercise in older individuals enhances myocellular growth, and this effect is more pronounced in Type I muscle fibers" (Trappe. 2016). It is important however, that their results apply only to healthy elderly individuals.

Why only in the elderly? Well based on previous research, there's in fact good reason to doubt that similar benefits would have been observed in younger individuals. The hitherto published results in young people are mixed. A possible explanation for that would be the previously observed "impairment of satellite cell activity" (Schoenfeld. 2012) in response to chronic NSAID consumption - a side effect that may turn out to be detrimental in the long(er)-term, because unlike older individuals, in whom the satellite cell function is compromised, already (Thornell. 2011), young people's long-term gains appear to rely on the myostatin lowering recruitement of additional myonuclei.

Overall, the potential negative effects on satellite cell activity and thus long-term muscle growth, the lack of convincing evidence of benefits in younger individuals and, for young and old alike, the negative side effects of chronic NSAID use on your tendons, gut, kidney and other organs are three good reasons I certainly don't advise to seriously consider "supplementing" NSAIDs daily to augment your muscle gains | Comment on Facebook!

References:

• Mikkelsen, U. R., et al. "Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise." Journal of applied physiology 107.5 (2009): 1600-1611.
• Schoenfeld, Brad J. "The Use of Nonsteroidal anti-inflammatory drugs for exercise-induced muscle damage." Sports medicine 42.12 (2012): 1017-1028.
• Standley, R. A., et al. "Prostaglandin E 2 induces transcription of skeletal muscle mass regulators interleukin-6 and muscle RING finger-1 in humans." Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) 88.5 (2013): 361-364.
• Trappe, Todd A., and Sophia Z. Liu. "Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise." Journal of Applied Physiology 115.6 (2013a): 909-919.
• Trappe, Todd A., et al. "Prostaglandin and myokine involvement in the cyclooxygenase-inhibiting drug enhancement of skeletal muscle adaptations to resistance exercise in older adults." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304.3 (2013b): R198-R205.
• Trappe, Todd A., et al. "COX Inhibitor Influence on Skeletal Muscle Fiber Size and Metabolic Adaptations to Resistance Exercise in Older Adults." J Gerontol A Biol Sci Med Sci (2016): Advance Access publication January 27, 2016.
• Thornell, Lars-Eric. "Sarcopenic obesity: satellite cells in the aging muscle." Current Opinion in Clinical Nutrition & Metabolic Care 14.1 (2011): 22-27.