| Heart Rate Zone | Heart Rate Percentage | Energy Source | Example |
| Zone One | 65-75% | Muscle Glycogen and fatty acids | Walking or jogging |
| Zone Two | 80-85% | Muscle glycogen and lactic acid | Group exercise classes |
| Zone Three | 86-90% | ATP/CP and muscle glycogen | Sprinting |
To use high-intensity interval training, you first need to determine your max heart rate. One can easily calculate their max heart rate by using the following formula, 220-age. Therefore, if you are 20 years old, your max heart rate would be 200 because 220-20=200. Now, that we have an example, there are multiple heart rate zone training methods you can apply to your exercise program. Each zone is typically categorized by a percentage of your heart rate and uses different energy sources. In my personal experience, using high-intensity interval training while monitoring my heart rate has achieved the best results, especially when I implement these exercises with a heart rate monitor. These heart rate monitors come with a strap you place around the bottom of your chest and a watch. These devices allow you to input your information, determine your desired heart rate, and can also calculate the calories you expend. Some popular brands available at your local Best Buy or Academy Sports + Outdoors include Polar and Garmin. If you are using a heart rate monitor while on the treadmill or elliptical, you would be glad to know the cardio machine will read your heart rate automatically. There will be no need to wrap your sweaty hands around the heart rate sensors to know your heart rate. This is often seen as an inconvenience as it disturbs your cardio session. Using a heart rate monitor is more efficient and mitigates any disruptions during cardio. Now that we have this covered we can explore the three heart rate zones that can be used in your high-intensity interval training program. I have also given examples of how each zone feels just in case purchasing a heart rate monitor is unfeasible.
As you can see from the example, your heart rate increases as you progress through each stage. So, if you are 20 years old with a maximum heart rate of 200 then your Zone One heart rate would be 130-150, Zone Two would be 160-170, and Zone Three would be 172-180. If you know this information, then you can apply low, medium, and high-intensity interval training to your exercise program. Currently, there are various variations of interval training available; I will give you one example you can apply to your training regimen as well as an alternative.
First warm up for 5-10 minutes in Zone One, if you are wearing a heart rate monitor you will see your heart rate pop up on the cardio machine screen. Now, after you feel loose and are ready to go, you can increase your heart rate to Zone Two and keep it there for approximately two minutes. Bear in mind if you are out of shape you will notice your heart rate sky rocket, and if you are in the best shape of your life, you will notice how hard it is to increase your heart rate. Therefore, be self-aware and maneuver the resistance and incline settings to your cardio machine appropriately to meet your desired heart rate. Now, when the two minutes expire you will need to increase your speed or the resistance of the cardio machine to enter Zone Three. You will stay in Zone Three for one minute. At this stage, the level of difficulty is almost at a max; you will be working at an intense level which is not sustainable for the average person. After, this stage your goal should be to decrease your heart rate within one minute to Zone Two. This step will be difficult if you are not in shape. Take two minutes or three if needed. Your last step before you can repeat the whole process again would be to decrease your heart rate to Zone One. If you are having difficulty reaching Zone One after completing this interval, there are other training regimens you can apply to improve your cardiorespiratory fitness.
If you need an alternative running program, keeping the heart rate between Zone One and Two should be prioritized to build your foundation. Bear in mind the following example can be used for elite athletes who need a low to moderate-intensity interval day. Similar to the aforementioned example, a 5-10-minute warm-up under Zone One will start the session. Next, you will need to increase your rate to Zone Two for one minute then gradually decrease your heart rate to Zone One for another 5 minutes before completing the interval again. The number of intervals you will complete will be dependent on your cardiorespiratory fitness, keep in mind you should finish your cardio session at Zone One. On a side note, if you are an elite athlete this alternative running program can easily be applied to your endurance level by just increasing your heart rate to Zone Three at each interval rather than Zone Two.
Overall, using high-intensity interval training is a great way to add variety to your training program. However, it is not for everyone; there are alternative to this method such as the moderate-intensity interval example mentioned above. If you are not an elite athlete using this method should be prioritized before diving into advanced interval training programs. Doing so will improve your running form and mitigate the risk of orthopedic injuries such an ankle, knee, or hip injury. Therefore, be self-aware and prudent when applying these training methods to your cardio sessions.
Written by
-Robert E. Salazar, MS, RDN, LDN
]]>Head Trainer at Redcon1, Joe Bennett, better known as The Hypertrophy Coach, is back today to tell us which form of cardio is best: HIIT vs. Steady State. High Intensity Interval Training (HIIT) is much more metabolic on the body, meaning it has a greater impact on your total energy expenditure and calorie burn over the course of the entire day when compared to steady state cardio. If done properly, HIIT is not taxing on the body. Joe gives three options for HIIT exercises: Spin bike, sled push, high incline hills. The biggest factor in determining if you should do HIIT on a given day is how much glycogen have you consumed and currently have stored in your body. If you are on low carbohydrates and depleted, HIIT is not your best option. Start with 3-5 sets of intervals at 15-20 seconds duration for each. Joe recommends picking exercises that you enjoy doing and are more likely to stick to.
]]>The best training style is the one you are probably not doing. The body and muscles constantly need new stimulus to elicit growth and progress. If you are constantly doing the same weights on bench press every Monday for the same amount of reps, for years on end, your body has no reason to adapt. When we weight train the goal is to make your body and muscles uncomfortable and adapt to the increased training stimulus. The body wants to maintain homeostasis, and without adequate stimulation the body will maintain. If you are a high volume trainer, try a low volume higher frequency approach.
2. CHANGING TRAINING TOO MUCH
Changing training styles too frequently is just as bad as not changing at all. It’s difficult to see what works for a specific individual if they are constantly changing things. It’s easy to jump on a website or look at a magazine (do people do that anymore?) and see something along the lines of “Grow Biceps 5 Inches in 30 Days.” While it’s good to change things up, too frequently changing things and you could be stalling progress.
3. OVERUSE OF CARDIO
Cardio is a tremendous tool to help burn extra calories to aid in fat loss. However, if muscle gain is the goal cardio can hinder progress. To gain weight the body needs to be in a caloric surplus, so burning extra calories will only slow down the process of gaining muscle. While cardio is great for cardiovascular health, too much of it will hurt your progress.
4.INSUFFICIENT REST
You don’t actually grow in the gym; you grow out of the gym. After training protein synthesis is upregulated for a period of about 48 hours. During this time is when you grow the most appreciable amount of muscle. When you train you are making micro tears in the muscle tissue; these tears need time to repair. Intense training is also hard on the central nervous system, slowing down progress and putting your immune system in a vulnerable position. Training depletes muscle glycogen stores that take some time to fill back out post workout.
5. IGNORING PROGRESSIVE OVERLOAD
As the saying goes, “If you want something you have never had, you must do something you have never done.” This can be directly applied to training philosophy. Just as we talked about not changing up training style, it’s also important to progress your lifts. Typically a stronger muscle is a bigger muscle. Progressive overload is a gradual increase in volume, intensity, frequency, or time. This means that loading the bar with more weight is not the only way to implement progressive overload. You could still be lifting the same amount for either more reps or more sets. The idea is to constantly progress forward to achieve the greatest stimulus to muscle tissue.
6. NOT PRIORITIZING NUTRITION
Of all the mistakes someone might make to hurt progress, this could be number one. You cannot out-train a bad diet, plain and simple. If muscle growth is the goal, undereating will only cause you to spin your wheels. You must fuel your body with the correct amount of macronutrients to recover correctly and to gain. A caloric surplus over a consistent period of time is the only way to gain weight. As well as proper nutrition, it’s important to fill in the gaps with a solid supplement regiment. Nutritional supplements help to aid with diet, but also to give you things that food alone cannot provide.
7. POOR FORM
Once again, to stimulate muscle growth the muscle must be presented with the correct catalyst. Throwing up weights you cannot control with improper form will do nothing but put your body in a position to get injured. Swinging too much on a biceps curl will take tension away from the biceps and place some of the load on other body parts. Part of progression is mastering the current weight before moving up. Progressive overload that we talked about before could also mean doing the same amount of weight, for the same amount of reps, but with better form. Time under tension and working the muscle instead of the joint will allow for faster muscle gains while also minimizing the risk of injury.
8. RELYING TOO HEAVILY ON MACHINES
The latest fad you see on Instagram these days is filling up the bars on plate loaded chest press machines. Why? Wouldn’t you stimulate the muscle more effectively using heavy compound movements such as a flat barbell press or dumbbell press? Now, machines have their place no doubt. They are safe, especially if training alone. The important thing to remember is that machines cannot completely replace free weights, but are instead supplementary movements to be used in conjunction with compound exercises.
9. FAILURE (OR LACK THEREOF)
Failure is necessary when it comes to making optimal progress in the gym. You need to reach muscular failure occasionally to elicit the greatest amount of muscle damage and then in turn muscular growth. Dorian Yates said “I’m not really good at knowing where 85 or 90 percent is. I only know where 0 and 100 percent is.” You must reach that 100 percent of training to see your body reach its full 100 percent potential.
10. MARATHON WORKOUTS
If you are training as hard and as intense as you can, there is no reason why it should take you three hours to train. Your training is severely lacking something if you can complete marathon type workouts. Someone once said “If you can text in between sets you are not training intensely enough.” This also goes back to rest and your body’s ability to recover. If you are training with the right type of intensity then it should not take you more than 90 minutes to complete a session.
-Daniel Henigsmith
]]>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
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.
]]>First off, lets look into GABA! GABA is known as the ‘downer’ neurotransmitter that counters glutamate and has a tough time crossing the blood brain barrier. GABA is the main inhibitory neurotransmitter of the CNS. It is well established that activation of GABA(A) receptors favors sleep. Three generations of hypnotics are based on these GABA(A) receptor-mediated inhibitory processes. The first and second generation of hypnotics (barbiturates and benzodiazepines respectively) decrease waking, increase slow-wave sleep and enhance the intermediate stage situated between slow-wave sleep and paradoxical sleep, at the expense of this last sleep stage. The third generation of hypnotics (imidazopyridines and cyclopyrrolones) act similarly on waking and slow-wave sleep but the slight decrease of paradoxical sleep during the first hours does not result from an increase of the intermediate stage. It has been shown that GABA(B) receptor antagonists increase brain-activated behavioral states (waking and paradoxical sleep: dreaming stage). Recently, a specific GABA(C) receptor antagonist was synthesized and found by i.c.v. infusion to increase waking at the expense of slow-wave sleep and paradoxical sleep. Since the sensitivity of GABA(C) receptors for GABA is higher than that of GABA(A) and GABA(B) receptors, GABA(C) receptor agonists and antagonists, when available for clinical practice, could open up a new era for therapy of troubles such as insomnia, epilepsy and narcolepsy. They could possibly act at lower doses, with fewer side effects than currently used drugs (1.)
Second, we look into taurine. Taurine is an organic acid which acts as a lipid/membrane stablilizer in the body and is one of the major inhibitory amino acid neurotransmitters in the brain along with the previously mentioned GABA. When Taurine reaches the brain, it interacts with GABA receptors in the thalamus which is involved in controlling how much sensory information is forwarded to the processing cortex of the brain. Its in this way that taurine is more like a depressant than a stimulant and results in a suppression of excitatory activity. Lin et al stated in a paper entitled the “Effect of taurine and caffeine on sleep–wake activity in Drosophila melanogaster” that “Taurine is a GABA receptor agonist, which is inhibitory to neuronal firing. We show here that flies receiving a low dose of caffeine (0.01%) increase locomotor activity by 25%, and decrease total sleep by 15%. Treatment with taurine at 0.1% to 1.5% reduces locomotor activity by 28% to 86%, and shifts it from diurnal to nocturnal. At 0.75%, taurine also increases total sleep by 50%. Our results show that taurine increases sleep, while caffeine, as previously reported, attenuates sleep. Flies treated with both caffeine and taurine exhibit two differential effects which depend upon the ratio of taurine to caffeine. A high taurine:caffeine ratio promotes sleep, while a low ratio of taurine:caffeine inhibits sleep to a greater extent than the equivalent amount of caffeine alone” (2.)
Last, we look into Mucuna Puriens. Mucuna Pruriens are beans that are a good source of L-DOPA. One of the main reasons I’m a big fan of mucuna pruriens is because of their ability to induce a feeling of well being which aids in cortisol reductions and clearly is a good choice when looking at improving your quality of sleep. Shukla et al stated “This study included 60 subjects who were undergoing infertility screening and were found to be suffering from psychological stress, assessed on the basis of a questionnaire and elevated serum cortisol levels. Age-matched 60 healthy men having normal semen parameters and who had previously initiated at least one pregnancy were included as controls. Infertile subjects were administered with M. pruriens seed powder (5 g day(-1)) orally. For carrying out morphological and biochemical analysis, semen samples were collected twice, first before starting treatment and second after 3 months of treatment. The results demonstrated decreased sperm count and motility in subjects who were under psychological stress. Moreover, serum cortisol and seminal plasma lipid peroxide levels were also found elevated along with decreased seminal plasma glutathione (GSH) and ascorbic acid contents and reduced superoxide dismutase (SOD) and catalase activity. Treatment with M. pruriens significantly ameliorated psychological stress and seminal plasma lipid peroxide levels along with improved sperm count and motility. Treatment also restored the levels of SOD, catalase, GSH and ascorbic acid in seminal plasma of infertile men. On the basis of results of the present study, it may be concluded that M. pruriens not only reactivates the anti-oxidant defense system of infertile men but it also helps in the management of stress and improves semen quality” (3.)
There are obviously more tremendous sleep aids when it comes to supplementation but GABA, Taurine, and Mucuna Puriens are three that are easily in my top ten favorite sleep ingredients along with melatonin, l-theanine, and a few others. Luckily, GABA, Mucuna Puriens, melatonin, and l-theanine are all in RedCon1’s sleep product Fade Out which also contains other ingredients to aid in growth hormone support, getting you into a deeper REM sleep, as well as to improve muscle recovery!
Alex Kikel
MS, PES, CPT, Speed and Explosion Specialist Level II
Owner of www.theprepcoach.com
References
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
The best place to start is its anti-aging properties that seem to be based around its ability to reduce cellular build up of modified proteins, and the research comes to us from three different authors: Stadtman et al, Gan et al, and Kwak et al. Stadtman stated that a number of systems that generate oxygen free radicals catalyze the oxidative modification of proteins. Such modifications mark enzymes for degradation by cytosolic neutral alkaline proteases. Protein oxidation contributes to the pool of damaged enzymes, which increases in size during aging and in various pathological states. The age-related increase in amounts of oxidized protein may reflect the age-dependent accumulation of unrepaired DNA damage that, in a random manner, affects the concentrations or activities of numerous factors that govern the rates of protein oxidation and the degradation of oxidized protein (1.) It is conceivable that stimulating proteasome activity for rapid removal of misfolded and oxidized proteins is a promising strategy to prevent and alleviate aging-related diseases. Sulforaphane (SFN), an effective cancer preventive agent derived from cruciferous vegetables, has been shown to enhance proteasome activities in mammalian cells and to reduce the level of oxidized proteins and amyloid β-induced cytotoxicity. Here, we report that SFN activates heat shock transcription factor 1-mediated heat shock response. Specifically, SFN-induced expression of heat shock protein 27 (Hsp27) underlies SFN-stimulated proteasome activity. SFN-induced proteasome activity was significantly enhanced in Hsp27-overexpressing cells but absent in Hsp27-silenced cells. The role of Hsp27 in regulating proteasome activity was further confirmed in isogenic REG cells, in which SFN-induced proteasome activation was only observed in cells stably overexpressing Hsp27, but not in the Hsp27-free parental cells. Finally, we demonstrated that phosphorylation of Hsp27 is irrelevant to SFN-induced proteasome activation. This study provides a novel mechanism underlying SFN-induced proteasome activity. This is the first report to show that heat shock response by SFN, in addition to the antioxidant response mediated by the Keap1-Nrf2 pathway, may contribute to cytoprotection (2.) The 26S proteasome is responsible for degradation of abnormal proteins and may play a role in cell survival upon oxidative stress. The indirect antioxidant sulforaphane (SFN) protects animal tissues from chemical toxicants by increasing the expression of several families of Nrf2-regulated genes. The role of induction of the 26S proteasome in cytoprotection by SFN was investigated in murine neuroblastoma Neuro2A cells. SFN enhanced the expression of the catalytic subunits of the proteasome, as well as proteasomal peptidase activities in these cells. Such treatment with SFN protected cells from hydrogen peroxide-mediated cytotoxicity in a manner dependent on proteasomal function. Inhibition of proteasome activities using pharmacological interventions significantly attenuated the protective effects of SFN against hydrogen peroxide cytotoxicity, as well as protein oxidation. Moreover, overexpression of the catalytic subunit PSMB5 enhanced proteasome function and led to elevated resistance against hydrogen peroxide toxicity and extent of protein oxidation compared to blank-plasmid-transfected cells. Pretreatment of PSMB5-overexpressing cells with SFN did not further enhance this resistance. Collectively, these results suggest that the cytoprotective effects of SFN against oxidative stress are in part due to up-regulation of the proteasome system. Therefore, inducers of proteasome expression may ameliorate the accumulation of damaged proteins associated with neurodegeneration and other diseases in whose etiologies protein oxidation plays a role (3.)
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