IFBB Pro Dallas McCarver and Redcon1 Head Trainer Joe Bennett take us through a grueling workout on this back training video. We really get to see what it takes to be one of the best bodybuilders in the world with this footage. The guys start off with a ridiculously heavy set of Underhand Bent Over Rows. Dallas works his way up to 405lb with perfect form on each rep. Joe follows suit with bent over rows and bangs out an equally clean set of reps using 315lb. After that, they went into Rack Pulls, T-Bar Rows with varying grips, both narrow and wide. From there it was time for Hammer Strength Single Arm Rows. They did drops sets while standing upright instead of sitting on the bench fixed to the machine. To finish the brutal session Dallas hit a few sets of Angle Pull Ups. This training session was not for the faint of heart. If you try and do this one yourself be prepared to be sore for the next week!
Hobson et al conducted a very important bit of literature on beta alanine supplementation and its direct effects on exercise performance in a meta analysis. They stated that “due to the well-defined role of β-alanine as a substrate of carnosine (a major contributor to H+ buffering during high-intensity exercise), β-alanine is fast becoming a popular ergogenic aid to sports performance. There have been several recent qualitative review articles published on the topic, and here we present a preliminary quantitative review of the literature through a meta-analysis. A comprehensive search of the literature was employed to identify all studies suitable for inclusion in the analysis; strict exclusion criteria were also applied. Fifteen published manuscripts were included in the analysis, which reported the results of 57 measures within 23 exercise tests, using 18 supplementation regimes and a total of 360 participants [174, β-alanine supplementation group (BA) and 186, placebo supplementation group (Pla)]. BA improved (P=0.002) the outcome of exercise measures to a greater extent than Pla [median effect size (IQR): BA 0.374 (0.140-0.747), Pla 0.108 (-0.019 to 0.487)]. Some of that effect might be explained by the improvement (P=0.013) in exercise capacity with BA compared to Pla; no improvement was seen for exercise performance (P=0.204). In line with the purported mechanisms for an ergogenic effect of β-alanine supplementation, exercise lasting 60-240 s was improved (P=0.001) in BA compared to Pla, as was exercise of >240 s (P=0.046). In contrast, there was no benefit of β-alanine on exercise lasting <60 s (P=0.312). The median effect of β-alanine supplementation is a 2.85% (-0.37 to 10.49%) improvement in the outcome of an exercise measure, when a median total of 179 g of β-alanine is supplemented” (1.)
Increased power output from muscle carnosine was shown by one of the more popular studies from Baguet et al in rowing performance. Chronic oral β-alanine supplementation is shown to elevate muscle carnosine content and improve anaerobic exercise performance during some laboratory tests, mainly in the untrained. It remains to be determined whether carnosine loading can improve single competition-like events in elite athletes. The aims of the present study were to investigate if performance is related to the muscle carnosine content and if β-alanine supplementation improves performance in highly trained rowers. Eighteen Belgian elite rowers were supplemented for 7 wk with either placebo or β-alanine (5 g/day). Before and following supplementation, muscle carnosine content in soleus and gastrocnemius medialis was measured by proton magnetic resonance spectroscopy ((1)H-MRS) and the performance was evaluated in a 2,000-m ergometer test. At baseline, there was a strong positive correlation between 100-, 500-, 2,000-, and 6,000-m speed and muscle carnosine content. After β-alanine supplementation, the carnosine content increased by 45.3% in soleus and 28.2% in gastrocnemius. Following supplementation, the β-alanine group was 4.3 s faster than the placebo group, whereas before supplementation they were 0.3 s slower (P = 0.07). Muscle carnosine elevation was positively correlated to 2,000-m performance enhancement (P = 0.042 and r = 0.498). It can be concluded that the positive correlation between baseline muscle carnosine levels and rowing performance and the positive correlation between changes in muscle carnosine and performance improvement suggest that muscle carnosine is a new determinant of rowing performance (2.)
The last and maybe the most important aspect is its potential to increase lipolysis as well as muscular hypertrophy. For this, we must look at two studies: the first from Walter et al titled “Six weeks of high-intensity interval training with and without beta-alanine supplementation for improving cardiovascular fitness in women” and the second from Kern et al titled “Effects of β-alanine supplementation on performance and body composition in collegiate wrestlers and football players.” In the first study we find that 6 grams of beta alanine per day increased lean mass without influencing either fat mass or VO~2~ max (3.) Within the second study, we find that 4 grams of beta alanine per day improved performance as well as overall body composition (4.) Once you dig deeper into both of these studies, we find that the theoretically “fat loss and muscle gaining” effect is most likely due to the athlete’s ability to workout longer and harder utilizing heavier poundages for more overall volume. This is the key point to its use in bodybuilding. We know that it has the ability to increase power output, reduce fatigue, and promote overall endurance, but connecting the dots and finding out that that in and of itself will directly correlate to faster body fat losses as well as faster muscle gain means it is a tremendous aid to any bodybuilder. Research shows standard dosages of anywhere from 2 grams per day to 6 grams per day (divided) but clinically its accepted optimal at 3.2 grams per day to receive its ergogenic benefits. Even further more, carnosine is an antioxidant and potential anti-aging compound, but sadly, the literature on these aspects isn’t as robust as I would like it and therefore, until further studies come on, I cannot comment on that claim. What we do know is beta alanine has its place in not only bodybuilding, but any performance endeavor.
Alex Kikel
MS, PES, CPT, Speed and Explosion Specialist Level II
Owner of www.theprepcoach.com
References
Creatine (a nitrogenous organic acid) is of course the base ingredient in such supplements. Its most important function in the human body is to enable the recycling of adenosine triphosphate (ATP) in muscle and brain tissue. ATP is a muscle cell’s primary source of energy, and is recycled by adenosine diphosphate (ADP) via the accumulation of a phosphate group molecule. Creatine has seen clinical use in treatment of individuals with muscular dystrophy, and has also been commonly utilized by the athletic community for decades. Roughly one half of the human body’s creatine is synthesized in the liver, with animal sources of protein (wild game, fish, lean red meat, etc.) providing the rest. The main benefits associated with a creatine-based preworkout are increased endurance and strength improvements. A dose of 5 grams per day is typically recommended for peak performance.
Another common ingredient is caffeine. Caffeine is a widely-used stimulant in products across the world, and has found a place in many workout supplements as well. 100-200 mg (or about the amount found in 1-2 cups of coffee) should be sufficient. The basis of caffeine’s use is its ability to block the action of the nucleoside adenosine on its receptor. This serves to block or delay the onset of drowsiness, which is typically prompted by adenosine. In practical terms, this means that its value in a preworkout is its propensity to discourage fatigue among athletes who choose to utilize it. Like all stimulants caffeine will somewhat depress the appetite, making it somewhat unhelpful for weightlifters engaging in a bulk phase.
L-arginine is an α-amino acid that, when used in preworkout, converts to nitric oxide upon metabolism. Products that contain this ingredient or are based on it are typically referred to as “vasoactive.” Nitric oxide serves to promote capillary and pulmonary dilation, allowing for faster and more efficient transport of oxygen to muscular tissues being used during training. This increased oxygen flow will result in better muscle contractions and higher production of ATP (created via certain enzymes through a process known as oxidative phosphorylation). Three grams is considered an effective dose. While it also serves other purposes and functions, its use among bodybuilders and similar athletes is by far its best documented.
The presence of a ph buffer such as taurine is also common. During a workout, skeletal muscles function at their best when the blood flowing to them is within a certain alkalytic ph range. A mitochondrial ph gradient exists across the inner membrane of cells, a fact that was demonstrated and proven in the 1960’s and 1970’s. Taurine’s role in the maintenance of this buffer is to stabilize it, keeping it safely within a ph range of 7.5-8.5. If a cell’s buffering capabilities are too low the gradient can potentially shift, ultimately disrupting ATP production in that cell. Simply put, taurine’s role (and that of other ph regulating substances) is to enable cells to produce ATP for energy. Taurine dosing is typically done at around one gram.
The amino acid tyrosine can also be found in many preworkouts. Its most common physiological role is to enable signal transduction in the brain. To this end it serves as a precursor to the organic chemical norepinephrine, which stimulates metabolism. Norepinephrine reserves are depleted as a result of prolonged intense training. 1-2 grams of tyrosine is sufficient to raise norepinephrine levels and enhance brain function.
At the end of the day it is the consumer’s responsibility to carefully analyze and select supplements that will best serve their personal needs. Many seek to enhance their endurance, strength, focus, and intensity at the gym. For these individuals a preworkout substance may hold great potential benefits. Having such a substance in your supplemental arsenal makes your goals more achievable, and allows your ambitions to rise higher. A good basic understanding of common supplement ingredients will greatly benefit such a person, helping them to select the product best suited for their interests and allowing them to pursue their goals with much more confidence.
Written by Trent Wozniak
]]>On the new video out today from Redcon1, IFBB Pro Dallas McCarver takes us through his day. Before most people are even awake, Dallas headed his chiropractor to get adjusted by Dr. Nick Ruggiero. Dallas has had a little bit of shoulder impingement and is finding that Active Release Therapy (ART) to be helping quite a bit. Then Dallas heads over to the Stretch Zone in Boca Raton, Florida to get further loosened up. Watch as he gets twisted and pulled into submission. Then he heads back home for a Meal #1 and then onto chest training at Busy Body Fitness Center. Watch the 335lb freak jump out at your screen in each scene, you won’t want to miss it.
]]>Vitamin K is an essential vitamin that is one of the four fat-soluble vitamins. Vitamin K comes in different forms (vitamers) that are either phylloquinones (vitamin K1) or menaquinones (vitamin K2 which is abbreviated as MK-x.) The three forms of vitamin K that can be utilized by the body are vitamin K1 and dual forms of K2 (MK-4 and MK-7.) The health benefits of vitamin k seem endless and include regression of preformed arterial calcification, maintenance of bone density, and promotion of a healthy heart and vascular system. As with all of my articles, I do not feel making claims on a product or ingredient is good enough. Instead, we must dig into the research…and luckily for us. vitamin k has well over 400 studies that I have personally read over the years. The first one I wish to look at is from Knapen et al and looked at a three-year low-dose menaquinone-7 supplementation and how it helps decrease bone loss. The results were that MK-7 intake significantly improved vitamin K status and decreased the age-related decline in BMC and BMD at the lumbar spine and femoral neck, but not at the total hip. Bone strength was also favorably affected by MK-7. MK-7 significantly decreased the loss in vertebral height of the lower thoracic region at the mid-site of the vertebrae. This lead to their conclusion that MK-7 supplements may help to prevent bone loss (1.)
But even more importantly that aiding in bone mineral density is its ability to fight atherosclerosis (as this is my main reason for recommending this vitamin to bodybuilders that are using potentially harsh supplements that can cause atherosclerosis over time.) Jennifer Ming has talked extensively on this topic stating that “numerous studies have demonstrated that people with higher intakes of vitamin K2 have a reduced risk for cardiovascular disease. Intrigued by this connection, Polish researchers from the Medical University at Lodz teamed up with researchers from Maastricht University in the Netherlands and Poland’s International Science and Health Foundation to determine if vitamin K2 supplementation could reduce the progression of existing atherosclerosis. The scientists evaluated the progression of atherosclerosis in a group of 42 patients with chronic kidney disease. These patients were ideal for this type of study because they are known to experience a rapid reduction in bone mineral density (a measure of bone strength) as a result of calcium losses from bone. They are also subject to equally excessive deposits of calcium in tissues where it doesn’t belong—particularly in the walls of major arteries. For the study, the subjects were divided into two groups. One group received vitamin K2 (90 mcg per day) plus vitamin D3 (400 IU per day). The second group received only vitamin D3 (400 IU per day). After nine months, it was already evident that the subjects taking the combination of vitamins K2 and D3 experienced a slower progression of the Common Carotid Intima Media Thickness, which is a good indicator of atherosclerosis, as well as a predictor of cardiovascular episodes and death. Specifically, the thickness of the carotid (major neck) arteries increased by 13.73% in the group taking vitamin D3, but in the group taking both vitamins, it only increased by 6.32%. Remember that the group of subjects in this study have a tendency for an increased carotid intima media thickness as a result of calcium losses from bone. In addition, subjects taking the combination of vitamins K2 and D3 showed a reduction in carotid artery calcification score in all patients except those with the highest scores at baseline. This indicates that calcium was staying in the bones, where it belongs, and out of the arteries. These results clearly indicated that vitamin K2 does indeed reduce the progression of atherosclerosis” (2, 3, 4.)
Vitamin K clearly has a place on everyone’s health supplement shelf and has more than enough literature and actual application to back that statement up. In terms of practical application, we need to look at a few different minimum effective dosages for the various forms of vitamin k. For phylloquinone (vitamin K1), the minimum effective dosage is 50mcgs. For short chain menaquinones (MK-4), the minimum effective dosage is 1500mcgs. For the longer chain menaquinones (MK-7, MK-8, and MK-9), the minimum effective dose is around 100-250mcgs. So be sure to purchase a vitamin k product that contains the effective forms of vitamin k and in the proper dosages.
Alex Kikel
MS, PES, CPT, Speed and Explosion Specialist Level II
Owner of www.theprepcoach.com
References
Increased power output from muscle carnosine was shown by one of the more popular studies from Baguet et al in rowing performance. Chronic oral β-alanine supplementation is shown to elevate muscle carnosine content and improve anaerobic exercise performance during some laboratory tests, mainly in the untrained. It remains to be determined whether carnosine loading can improve single competition-like events in elite athletes. The aims of the present study were to investigate if performance is related to the muscle carnosine content and if β-alanine supplementation improves performance in highly trained rowers. Eighteen Belgian elite rowers were supplemented for 7 wk with either placebo or β-alanine (5 g/day). Before and following supplementation, muscle carnosine content in soleus and gastrocnemius medialis was measured by proton magnetic resonance spectroscopy ((1)H-MRS) and the performance was evaluated in a 2,000-m ergometer test. At baseline, there was a strong positive correlation between 100-, 500-, 2,000-, and 6,000-m speed and muscle carnosine content. After β-alanine supplementation, the carnosine content increased by 45.3% in soleus and 28.2% in gastrocnemius. Following supplementation, the β-alanine group was 4.3 s faster than the placebo group, whereas before supplementation they were 0.3 s slower (P = 0.07). Muscle carnosine elevation was positively correlated to 2,000-m performance enhancement (P = 0.042 and r = 0.498). It can be concluded that the positive correlation between baseline muscle carnosine levels and rowing performance and the positive correlation between changes in muscle carnosine and performance improvement suggest that muscle carnosine is a new determinant of rowing performance (1.)
Hobson et al conducted a very important bit of literature on beta alanine supplementation and its direct effects on exercise performance in a meta analysis. They stated that “due to the well-defined role of β-alanine as a substrate of carnosine (a major contributor to H+ buffering during high-intensity exercise), β-alanine is fast becoming a popular ergogenic aid to sports performance. There have been several recent qualitative review articles published on the topic, and here we present a preliminary quantitative review of the literature through a meta-analysis. A comprehensive search of the literature was employed to identify all studies suitable for inclusion in the analysis; strict exclusion criteria were also applied. Fifteen published manuscripts were included in the analysis, which reported the results of 57 measures within 23 exercise tests, using 18 supplementation regimes and a total of 360 participants [174, β-alanine supplementation group (BA) and 186, placebo supplementation group (Pla)]. BA improved (P=0.002) the outcome of exercise measures to a greater extent than Pla [median effect size (IQR): BA 0.374 (0.140-0.747), Pla 0.108 (-0.019 to 0.487)]. Some of that effect might be explained by the improvement (P=0.013) in exercise capacity with BA compared to Pla; no improvement was seen for exercise performance (P=0.204). In line with the purported mechanisms for an ergogenic effect of β-alanine supplementation, exercise lasting 60-240 s was improved (P=0.001) in BA compared to Pla, as was exercise of >240 s (P=0.046). In contrast, there was no benefit of β-alanine on exercise lasting <60 s (P=0.312). The median effect of β-alanine supplementation is a 2.85% (-0.37 to 10.49%) improvement in the outcome of an exercise measure, when a median total of 179 g of β-alanine is supplemented” (2.)
Finally, we’ll conclude on its ability to reduce fatigue from the works of Hoffman et al. The purpose of this study was to examine the effect of 30 days of beta-alanine supplementation in collegiate football players on anaerobic performance measures. Subjects were randomly divided into a supplement (beta-alanine group [BA], 4.5 g x d(-1) of beta-alanine) or placebo (placebo group [P], 4.5 g x d(-1) of maltodextrin) group. Supplementation began 3 weeks before preseason football training camp and continued for an additional 9 days during camp. Performance measures included a 60-second Wingate anaerobic power test and 3 line drills (200-yd shuttle runs with a 2-minute rest between sprints) assessed on day 1 of training camp. Training logs recorded resistance training volumes, and subjects completed questionnaires on subjective feelings of soreness, fatigue, and practice intensity. No difference was seen in fatigue rate in the line drill, but a trend (P = .07) was observed for a lower fatigue rate for BA compared with P during the Wingate anaerobic power test. A significantly higher training volume was seen for BA in the bench press exercise, and a trend (P = .09) for a greater training volume was seen for all resistance exercise sessions. In addition, subjective feelings of fatigue were significantly lower for BA than P. In conclusion, despite a trend toward lower fatigue rates during 60 seconds of maximal exercise, 3 weeks of beta-alanine supplementation did not result in significant improvements in fatigue rates during high-intensity anaerobic exercise. However, higher training volumes and lower subjective feelings of fatigue in BA indicated that as duration of supplementation continued, the efficacy of beta-alanine supplementation in highly trained athletes became apparent (3.)
It is clear that beta alanine is a supplement that is beyond beneficial for any athletic endeavor! In these studies, we see a wide array of dosages from 2 grams all the way up to 5 grams. It has been concluded that 3.2 grams of beta alanine is the accepted clinical dosage. If your taking a pre workout that has LESS than that clinical amount then you’re pretty much wasting your money as you will not reap the full benefits. Luckily, supplements like Total War from RedCon1 provide the full 3.2 gram clinical dosage of beta alanine along with other great ergogenic aids like citrulline malate, agmatine sulfate, and a number of others ALL having the correct clinical dosage.
Alex Kikel
MS, PES, CPT, Speed and Explosion Specialist Level II
Owner of www.theprepcoach.com
References
In this instructional video, Redcon1 Head Trainer Joe Bennett teaches us the differences in using overhand vs. underhand grip on a barbell row. Both variations are useful, but as Joe explains they really need to be treated as two separate exercises. Overhand barbell rows tend to naturally bow a persons elbows out and make for more muscle activation in the upper back, rhomboids, and traps. Underhand rows work more of the lats. The goal for every person is to have the elbows tucked near the body and pulled back. You do not want the elbows to flare out if possible. With a barbell laying on a fixed plane of 180 degrees it makes wrist flexibility an important aspect when choosing which grip variation to use. If you lack wrist flexibility it will lead to the elbows flaring, which can then lead to a greater risk of injury in the elbow and shoulder. Regardless of the grip you use, it is important to lock the hips in place to keep the attention off of the spinal erectors.
]]>Now, the moment you’ve been waiting for, MYOSTATIN INHIBITION! I’m sure many of you have skipped ahead to this part so I wont waste anymore time digging into the literature! Sulforaphane seems to repress myostatin transcription and suppression within skeletal muscle satellite cells. Fan et al discusses this relationship in great detail. Satellite cells function as skeletal muscle stem cells to support postnatal muscle growth and regeneration following injury or disease. There is great promise for the improvement of muscle performance in livestock and for the therapy of muscle pathologies in humans by the targeting of myostatin (MSTN) in this cell population. Human diet contains many histone deacetylase (HDAC) inhibitors, such as the bioactive component sulforaphane (SFN), whose epigenetic effects on MSTN gene in satellite cells are unknown. Therefore, we aimed to investigate the epigenetic influences of SFN on the MSTN gene in satellite cells. The present work provides the first evidence, which is distinct from the effects of trichostatin A (TSA), that SFN supplementation in vitro not only acts as a HDAC inhibitor but also as a DNA methyltransferase (DNMT) inhibitor in porcine satellite cells. Compared with TSA and 5-aza-2′-deoxycytidine (5-aza-dC), SFN treatment significantly represses MSTN expression, accompanied by strongly attenuated expression of negative feedback inhibitors of the MSTN signaling pathway. miRNAs targeting MSTN are not implicated in posttranscriptional regulation of MSTN. Nevertheless, a weakly enriched myoblast determination (MyoD) protein associated with diminished histone acetylation in the MyoD binding site located in the MSTN promoter region may contribute to the transcriptional repression of MSTN by SFN. These findings reveal a new mode of epigenetic repression of MSTN by the bioactive compound SFN. This novel pharmacological, biological activity of SFN in satellite cells may thus allow for the development of novel approaches to weaken the MSTN signaling pathway, both for therapies of human skeletal muscle disorders and for livestock production improvement (7.) Even furthermore CJ et al states “Sulforaphane (SFN) is a dietary isothiocyanate that exerts chemopreventive effects via NF-E2-related factor 2 (Nrf2)-mediated induction of antioxidant/phase II enzymes, such as heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). This work was undertaken to evaluate the effects of SFN on hepatic fibrosis and profibrotic transforming growth factor (TGF)-β/Smad signaling, which are closely associated with oxidative stress. SFN suppressed TGF-β-enhanced expression of α-smooth muscle actin (α-SMA), a marker of hepatic stellate cell (HSC) activation, and profibrogenic genes such as type I collagen, fibronectin, tissue inhibitor of matrix metalloproteinase (TIMP)-1, and plasminogen activator inhibitor (PAI)-1 in hTERT, an immortalized human HSC line. SFN inhibited TGF-β-stimulated activity of a PAI-1 promoter construct and (CAGA)(9) MLP-Luc, an artificial Smad3/4-specific reporter, in addition to reducing phosphorylation and nuclear translocation of Smad3. Nrf2 overexpression was sufficient to inhibit the TGF-β/Smad signaling and PAI-1 expression. Conversely, knockdown of Nrf2, but not inhibition of HO-1 or NQO1 activity, significantly abolished the inhibitory effect of SFN on (CAGA)(9) MLP-Luc activity. However, inhibition of NQO1 activity reversed repression of TGF-β-stimulated expression of type I collagen by SFN, suggesting the involvement of antioxidant activity of SFN in the suppression of Smad-independent fibrogenic gene expression. Finally, SFN treatment attenuated the development and progression of early stage hepatic fibrosis induced by bile duct ligation in mice, accompanied by reduced expression of type I collagen and α-SMA. Collectively, these results show that SFN elicits an antifibrotic effect on hepatic fibrosis through Nrf2-mediated inhibition of the TGF-β/Smad signaling and subsequent suppression of HSC activation and fibrogenic gene expression” (8.)
References
So far, we see sleep deprivation interrupting normal circadian rhythms that interrupt and cause a cascading effect with normal hormone functioning. Now onto one final hormone thats released during sleep that everyone is highly concerned with…growth hormone. Growth hormone has its biggest spike with is roughly half of our daily growth hormone amount. If this process is interuppted, could this be another big reason why you’re not growing? Plasma growth hormone (GH), insulin, cortisol, and glucose were measured during sleep on 38 nights in eight young adults in a study from Takahashi et al (6.) Blood was drawn from an indwelling catheter at 30-min intervals; EEG and electrooculogram were recorded throughout the night. In seven subjects, a plasma GH peak (13-72 mmug/ml) lasting 1.5-3.5 hr appeared with the onset of deep sleep. Smaller GH peaks (6-14 mmug/ml) occasionally appeared during subsequent deep sleep phases. Peak GH secretion was delayed if the onset of sleep was delayed. Subjects who were awakened for 2-3 hr and allowed to return to sleep exhibited another peak of GH secretion (14-46 mmug/ml). Peak GH secretion was not correlated with changes in plasma glucose, insulin, and cortisol. The effects of 6-CNS-active drugs on sleep-related GH secretion were investigated. Imipramine (50 mg) completely abolished GH peaks in two of four subjects, whereas chlorpromazine (30 mg), phenobarbital (97 mg), diphenylhydantoin (90 mg), chlordiazepoxide (20 mg), and isocarboxazid (30 mg) did not inhibit GH peaks. Altered hypothalamic activity associated with initiation of sleep results in a major peak of growth hormone secretion unrelated to hypoglycemia or changes in cortisol and insulin secretion. Now, although that is disrupted, we know that our bodies are very good at compensating, and it seems overall 24 hour growth hormone levels are compensated for (7.) But the issue is, is this disruption causing a bigger issue? Could this change if it is chronic sleep deprivation? Would our bodies still compensate? I cannot answer that with certainty.
Sleep deprivation is also correlated to possible decline in thyroid hormone output, insulin sensitivity, and overall cognitive output (8, 9, 10.) The literature in this article makes it very clear that sleep deprivation very well COULD be why you’re not growing. So next time you hit a sticking point, remember to assess EVERY variable (looking at sleep first.) Once proper sleep patterns are assessed and corrected, you can move on to the next variable which could be holding back your progress.
References