"Just One More Set" (1/2): Metabolic Response to 10,000kg vs. 20,000kg Regimen. EPOC: Do Reps and Loads Both Figure? And What About Elite Athletes Do They Need More?

"Ah come on, just another set!" ... "I don't know man, we've already pumped away 100,000kg today... do you really believe that's going to be productive, I mean, yeah, we are cuttin', but still... I mean I don't dig this epic!", "EPOC man, it's called EPOC!" *shakes his head* "Call it whatever you want, bro, I am out!"

If you want, you can think of today's SuppVersity post as an extension to yesterday's "Bigger, Stronger, Faster" special of the On Short Notice series; to be more precise: As a practically more relevant version of the rodent study on hypertrophy vs. strength training that was part of the aforementioned post. Yep, we are "talking volume" today. How much is too much?  And though this is never-ending debate, it appears that at least as far as research goes, a little more debating certainly would not hurt. Therefore I am happy to have not one, but two studies for you which don't just address this issue, but have also been conducted with human subjects!

In view of the fact that these are no "short notices", I will discuss one today and the other tomorrow - yep, that means that you can already make a mental note to come back tomorrow ;-)

"Just one more set, ..." - how productive can that be?

Today's study comes from the Human Performance Laboratory at the Florida State University and deals with the energetic side of things - specifically the often-cited EPOC (excess post-exercise oxygen consumption), which is often touted as one of the most important aspects why strength training in general and higher volume / intensity strength training, in particularly, would have the edge over cardio training. The reasoning is easy: You don't burn so much energy while you work out, but in the time after, your body will (a) still expend more energy per minute / hour and (b) has the advantage of emptied glycogen stores, which will force it to tap into its body fat stores the source for the required energy.

All of you who have read the complete Athletes' Triad series, will by now already know that at least argument (b) is pretty idiotic, because it wouldn't allow you to replenish your muscle and liver glycogen after workouts and thus pave the way into the dreaded vicious circle of the athlete's triad. The former argument, on the other hand has - on a way more general level - only been confirmed a couple of days ago (see "Scientists resolve the paradox of stable muscle metabolism but greater mitochondrial respiration in muscle of inactive vs. active subjects", read more), the question still remains: How much weight do you have to lift to set the 'afterburner' into full gear? 

10 metric tonne or 20 metric tonnes? What do you say?

I see, you are laughing, but basically the above question is what the George J. Abboud and his colleagues tried to find out, when they recruited 8 healthy men aged19-29 yrs who had 

"at least 12 months of RT experience with no more than 2 wks rest at a time, less than a total of 4 wks off within the last 6 months, or 9 wks off within the last 12 months [and] reported no prior or current use of illegal performance enhancing substances." (Abboud. 2013)

Suggested read "Three is More Than One: Higher Volume Increases Strength Gains in Legs, and Satellite Cell Recruitment and Fiber Size in Legs & Traps."

As usual the subjects had to fill food logs for the three days before the testing and were instructed to replicate the same eating pattern on the second occasion in which they were randomly assigned to perform a standardized resistance training (RT) regimen consisting of 4 exercises performed on a non-counterbalanced smith machine so that the range of motion during

• bench press, 
• squat, 
• bent-over row and 
• Romanian deadlift 

could be controlled for easily. Other than the equipment and the exercises, which were identical on both occasions, the volume of the training sessions varied and if you express this volme in kg or metric tons, it was a competition of 10,000 kg (10 metric tonnes) vs. 20,000 kg (20 metric tonnes) of weight. 

"The loads were divided between the 4 exercises as follows: 35% to squats, 30% to bench press, 20% to bent-over rows and 15% to Romanian deadlift. For each set, subjects lifted approximately 85% of their 1RM for 6-8 repetitions. If 6 repetitions could not be completed at any point, the load was reduced by 10% for the subsequent set." (Abboud. 2013)

Both sessions were supervised by three testers : One monitored the metabolic cart, one made sure the proper range of motion was used and one monitored the proper lifting form. The subjects had to perform the concentric portion of each lift with maximal speed and ensure a controlled eccentric descent. A specific time interval was not dictated. Sets were stopped if "subjects broke form" (Abboud. 2013) and 2 minutes of rest were given between sets. In this fashion the subjects simply kept lifting set after set until the volume prescription for the respective trial was reached.

Figure 1: Resting metabolic rate (RMR) per kg body weight, 30min energy expenditure and respiratory exchange ratio (RER; lower values = higher fat, lower glucose  oxidation)  after low and high volume trial (based on Abboud. 2013)

As you can see in figure 1 there were differences as far as the effects of the high (20,000) vs. low (10,000kg) regimen on the resting metabolic rate, 30 min energy expenditure, and the respiratory quotient (lower values = higher fat, lower glucose oxidation), but in view of the fact that the high volume group moved 2x more weight and should thus (at least theoretically) have expended twice the energy (assuming they performed all reps with perfect form and identical speed), those differences are more than disappointing. 

The minuscle effect size is yet not the most "disappointing" (or "surprising" ?) result

In fact, contrary to the low volume workout the 20,000kg workout did not produce any increases in resting metabolic rate and 30min energy expenditure, at all - put simply: There was no EPOC after the high volume training. And this did not change over the whole 48h period (and I know you guys, you won't rest longer anyway ;-).

Now you may say that this was a crazy protocol, but let's do the math, let's assume the guys did squat 100kg, benched and rowed their own body weight of ~80kg and deadlifted 125kg. With 10 reps per set thats 1,000kg + 2x800kg + 1,250kg per set respectively. If they did three sets per exercise they would thus already be up to 9,950kg! If you still think that's crazy, let's hear what the scientists have to say:

"As subjects in the present study were well adapted to RT, the training stimulus needed to elicit increases in EPOC arguably needed to be much higher compared to that used in previous research  Two studies using intensities of 70% 1RM report significant increases in RMR. Melby et al. had subjects perform 6 setsof 10 different exercises for a total of 60 sets. The repetition range for this protocol was 8-12 repetitions per set. This amounts to approximately 600 repetitions performed during the course of the exercise bout. The range of load-volume lifted by these subjects was 15,000-38,000 kg. [...]" (Abboud. 2013)

The list goes on and you just have to go to your gym and I guarantee you, no matter how few people are on the floor you will see a guy who (often without noticing is) will be pounding away much more word within a single workout. Moreover, the the subjects in the present study completed their trials
with a drastically lower number of repetitions -  a mean of 199. Had they performed the crazy rep-volume of the Melby study, they would probably have come close to 50,000 kg. This raises an interesting question is "volume" correctly defined by giving the total amount of weight you lift? Or is the number of reps maybe more important as far as the after-burner EPOC is concerned?

Too much of a good thing? But what if you are a highly trained athlete?

A previous study, by Hackney et al. would support the notion that heavy lifting is an obligatory part of the EPOC equation. In the latter study, EPOC trained individuals who used a lower load-volume than the trainees in the study at hand  had increased resting metabolic rates for up to 72h (Hackney. 2008). Since the Hackney study also put an emphasis on eccentric contractions and will thus probably have lead to even greater muscle damage than the protocol of the study at hand (CK(10,000kg) = 729U/L vs.CK(20,000kg)  = 1,159IU/L), Abboud et al. speculate that ...

"[a]s protein synthesis required for repair is energetically expensive, it is logical that untrained subjects will show greater and longer alterations in EPOC post-RT. Judging by training history, strength levels and CK responses, subjects in the present study had most likely reached a higher level of adaptation than ones in previous studies, and therefore were less sensitive to the metabolic effects of recovery from RT." (Abboud. 2013)

In other words, for you, probably a seasoned strength trainee, the 'more is more' principle is not going to yield better results - even if your goal is to shed body fat. And ...

"Although RT is an important component in any weight loss program to attenuate the loss of fat free mass and therefore better preserve RMR, it is unlikely that the total energetic cost (during and post-exercise) of a typical duration workout will be adequate for significant weight reduction in highly trained recreational lifters without caloric restriction and/or additional aerobic or high intensity interval training." (Abboud. 2013)

And since I rarely encounter a conclusion that's so to the point, I'll leave you with that for today and remind you to come back tomorrow to learn, when and for which body parts doing somewhat more may still be beneficial - read me tomorrow ;-)

References:

• Abboud GJ, Greer BK, Campbell SC, Panton LB. Effects of Load-Volume on EPOC after Acute Bouts of Resistance Training in Resistance Trained Males. J Strength Cond Res. 2013 Oct 18.
• Hackney KJ, Engels HJ, and Gretebeck RJ. Resting energy expenditure and delayed-onset muscle soreness after full-body resistance trainingwith an eccentric concentration. J Strength Cond Res. 2008; 22: 1602-1609.
• Melby C, Scholl C, Edwards G, and Bullough R. Effect of acute resistance exercise on postexercise energy expenditure and resting metabolic rate. J Appl Physiol. 1993; 75: 1847-1853.

Bigger, Stronger, Faster: CoQ10 for Brain & Muscle in Young & Old. The Optimal HIIT Regimen for Fun & Fat Loss - 8s at 100% 60s Idling! Protein Power From Oats? Plus: Rest Times, Clusters, Form & Hypertrophy Training

I decided against calling this the "Get Big, Green and Look Like the Hulk Quickie" (img. Paramount Pictures)

In view of the fact that most of you apparently enjoyed the "Get Lean and Stay Lean Quickies" I posted in the last weeks, I thought you may also be inclined to read a "Get Big, Green and Look Like the Hulk Quickie", but then decided that the name was too long for the headline and "big, green" and maybe even "hulk" in conjunction with "quickie" may have had the SuppVersity turn up on google and other search engines in too close vicinity to websites I do not exactly want this blog to be associated with (just kiddin' ;-)

Be that as it may, enjoy the ride and let me know whether you do prefer this thematically structured approach over the classic news-potpouris ala On Short Notice.

I mean you can obviously argue in favor of both and since this is a place I want you to look forward to visit everyday, I would be inclined to hear whether "innovations" like this make it better or worse.

• CoQ10 supplementations could offer beneficial effects on brain and muscle in elderly individuals and could - at higher doses - work for youngsters, as well (Shetty. 2013) -- In a rodent trial the provision of a relatively high dose of CoQ10 as part of the diet effectively blunted age-induced 'cognitive decline' (whatever that may be in a mouse ;-) and protein breakdown in heart, liver and muscle tissue of the 17.5 months-old mice.
  
  

  

  Figure 1: Carbonyl levels in liver and muscle of young and old mice.

  This result is also interesting, because the mitochondrial protein breakdown in the brain was the one which was least beneficially affected. What's of greater importance, for this news quickie at least, is that the 2.81mg CoQ10 per gram of chow the high dose group received (the human equivalent would be roughly 33mg/kg or 2-3g per day!) elicited beneficial effects on the skeletal muscle carbonyl content, a marker of protein oxidation, in the young animals, as well (see figure 1).
  
  The notion that coQ10 in appropriate doses could be beneficial not just for statin users, but also for perfectly healthy people, even athletes, is also supported by the beneficial effects the administration of coQ10 had in a recent trial where it blunted the oxidative damage due to a high frequency endurance training program in rodents (Okudan. 2013). It does however stand in contrasts with a recent study by Bloomer et al., n which the supplementation of only 300mg (ca. 15% of the HED used in the study at hand) did not yield the desired effects on the exercise performance of 15 perviously individuals (10 men and 5 women; 30-65 years; Bloomer. 2013). Whether this really is just a matter of the correct dosing, or maybe a fundamental difference between mice and men will still have to be elucidated and I would not spent the bucks for anything that's only "maybe" going to work.
• Rats don't do well with hypertrophy training (Scheffer. 2013) -- According to a recently published paper by Scheffer et al., rodents who are afraid of increases in markers of oxidation should refrain from hypertrophy oriented muscle training and stick to lower volume resistance training.
  
  For their study, the Brazilian researchers had analyzed the effects of three different resistance training protocols, namely  muscular resistance training (RT), hypertrophy training (HT), and strength training (ST), which had to be performed twice a week for 12 weeks on muscle lactate and glycogen content, superoxide production, antioxidant enzyme content, and activities, as well as markers of lipid and protein oxidation.
  

  

  While you certainly don't want a fire inferno, doing too little is not going to yield the results you are looking for either (suggested read "The emerging role of an auto-/endocrine-immune axes")

  "Results showed increased superoxide production (UT = 5.348; RT = 5.117; HT = 8.412 ; ST = 6.354), SOD (UT = 0.078 ; RT = 0.101 ± 0.013; HT = 0.533 ± 0.109; ST = 0.388), GPx (UT = 0.290; RT = 0.348; HT = 0.529; ST = 0.384) activities, and content of GPx (HT = 3.8 times; ST = 3.0 times) compared with the UT group. CAT activity was lower (UT = 3.966; RT = 3.47; HT = 2.276 ; ST = 2.028) in HT and ST groups. Oxidative damage was observed in the HT group (TBARS = 0.082; carbonyl = 0.73; thiol = 12.78) compared with the UT group.

  The way in which the authors' conclusion that these "findings indicate that HT causes an imbalance in oxidative parameters in favor of pro-oxidants, causing oxidative stress in skeletal muscle" does implicitly suggest that this is a bad thing that has to be avoided at all cost, which is obviously totally beside the point - if you don't challenge your body he has nothing to adapt to and neither your conditioning, nor your strength or muscle mass are going to improve. The absence of statistically significant increases in oxidative damage in the low volume strength training routines, on the other hand supports the notion that you can use phases of very low volume training with heavy weights in between intense phases of overreaching to monetize on the muscular gains (which will probably keep coming in these 2-4 weeks) by taking all your lifts to another level and thus lying the foundation for future growth.
• Optimized HIIT regimen for overweight kids: 4s max sprinting + 60s active recovery do the trick - could work four you, as well! (Crisp. 2013) -- Either from the SuppVersity news or from listening to Super Human Radio you may remember that a recent study by Deighton et al. has found that sprinting will increase your appetite more and burn less calories than workload matched steady state cardio training. A novel study from Australia does now suggest that this may well be the case, but probably only as a result of doing it wrong - the sprinting, I mean.
  
  
  In their study Nicole A. Crisp and her colleagues from the School of Sport Science at the The University of Western Australia, describe how the combination of 8s all-out sprints on a cycle-ergometer with 60s of active rest easily outperforms its 30min steady state counterpart (30min moderate pace) and its "little brother" and "big" bother the 8s sprint, 120s active rest and the 8s sprint, 30s active rest protocol, respectively.
  
  

  

  This is not the first study to show the superiority of HIIT training in obese boys. In February 2013, I have already covered a very similar study where a brief HIIT session that burns "only" 360kcal was a major motor to teenage weight loos.

  In that, it's important to note that despite a linear increase in energy expenditure from the 60s to the 30s rest group, the latter failed to reach statistical significance (p = 0.076), ...
  

  "[...] likely as a result of decreased sprint quality as indicated by a significant decline in peak power output from SI₆₀ to SI₃₀ (p = 0.034)" (Crisp. 2013)

  In conjunction with the absence of the overcompensation effect at the following breakfast buffet (which was present in the 8/30s and to a lesser degree even the 30min steady state trial), this makes the 8/60s protocol the superior choice for everyone doing HIIT mainly to get or stay lean.
  
  And aside from its practical value, the 8/60s regimen was also the one the boys enjoyed the most.
  
  "And what about me?" I don't see why doing this very short sprints with large bouts of active recovery in between would not be right for you, as well. At least if the activation of your metabolism and / or fat loss during a diet is your primary goal and not an improvement in VO2 max., you would thus probably get many of the benefits at a smaller risk of overtraining. Just make sure you are actually sprinting all-out for the whole 8s and don't stop, when you are just about to get up to speed ;-)
• Long rest times necessary for high jumpers - with 8-12 min pause your performance on the next jump will increase not decrease (Gouvêa . 2013) -- In a recent meta-analysis that's soon going to be published in the Journal of Sports Sciences André Luiz Gouvêa and his co-workers report that the manipulation of rest intervals seems to affect post-activation potentiation magnitude and jump height.
  
  After analyzing fourteen studies, which met the criteria of having a crossover design, being randomised, or non-randomised and counterbalanced and observed the voluntary muscle action-induced post-activation potentiation on jumping performance, the scientists state that the...
  

  "[...]results demonstrated medium effect sizes for rest intervals 0–3 and 8–12 min (-0.25 for 0–3 min; 0.24 for 8–12 min) and a small effect for other ranges (0.15, CI: -0.08 to 0.38 for 4–7 min; for ≥16 min)." (Gouvêa . 2013)

  Since there was little to no evidence for heterogeneity among the sub-groups and no indication of publication bias, these results clearly suggest that rest intervals of 0–3 min have detrimental, rest intervals between 4-8 min neutral and rest intervals of 8-12 min beneficial impact on jump height. In that, the improvements are likely to be mediated by post-activation potentiation.
• The science of cluster training - Conventional wisdom prevails, 10 deep breaths would yield optimal rest time between reps (Hardee. 2013) -- At lest with respect to proper form, which may also have consequences for optimal muscle recruitment and hypertrophy, the optimal rest time between two reps in a cluster appears to be 20s, which is actually what the good old "10 deep breaths rule" would state, as well.
  
  
  What is a cluster? When you are "clustering" your sets you are doing one (sometimes also 2-3) rep(s), rack the weight, rest, do another rep etc. This is a very good technique to increase your strength and break through plateaus that's useful for powerlifters and bodybuilders alike.
  In order to examine the effects of three different cluster set configurations on power clean technique, the scientists recruited 10 male, recreational weightlifters who had to perform clustered or non-clustered power-cleasn: 3 sets of 6 repetitions at 80% of their individual repetition max with 0 (P0), 20 (P20) or 40 seconds (P40) inter-repetition rest.
  
  In the P0 (no cluster) condition, the scientists observed how the form suffered and got worse and worse from the first to the last rep (the catch and first pull were in a more forward position during repetition 6 as compared to repetition 1). With the long rest times in the P40 condition, on the other hand,  "differences in horizontal displacement were found between repetitions 1 and 6 for the second pull and the loop" (Hardee. 2013).
  
  In the P20 condition the researchers did not observe any differences in horizontal displacement between repetitions 1 and 6 during P20. Reason enough for the scientists to conclude that their results would demonstrate that cluster sets with greater tha 20s of inter-repetition rest would be useful to maintain appropriate form without significantly dropping the density of your workout - whether this did actually facilitate strength or size gains was yet not evaluated in the study.
  
  The evidence for the efficacy of this training regimen (aside from simply providing a novel stimulus, which is obviously always a good thing) does come from a 2011 study by  Hansen et al who compared the response of highly trained rugby players to on traditional vs. clustered leg training program and found the latter to be slightly superior with respect to the increase in peak velocity and strength , while the classic continouus set training had an edge as far as total power increases in the lower limbs were concerned (Hansen. 2011).
• Oats healthy car source with performance protein? (Xu. 2013) Who would have thought that, oats are not just an excellent source of slow digesting carbs and potentially fat-burning beta glucan (listen to the SuppVersity Science Round-Up from two weeks ago), they also contain a non-negligible amount of protein of which researchers from the College of Food Science and Engineering at the Northwest A&F University in Yangling, China, have now shown that it ameliorates the increase in lipid oxidation (MDA) and decrease in antioxidant activity (SOD) during an exaustive bout of swimming in 30 male mice.
  
  After the oat protein had been purified from oat meal thirty male Kun-ming mice were divided kept on either a normal control diet, a diet that was enriched with oatmeal and a diet that contained only the protein fraction of the oats. After 20 days, the rodents were subjected to swim to exhaustion. Their swimming endurance and the major metabolic substrates were measured from serum, liver and muscle.
  

  

  Figure 2: Antioxidant enzymes up, lipid oxidation down. That's the result of a comparison of the detrimental effects of an exhaustive swimming test in mice fed regular, oat enriched or oat protein pimped diets for 30 days (Xu. 2013). What the study cannot answer is however whether identical effects would have been seen w/ any other high quality protein as.

  "The results showed that no significant differences were observed in swimming endurance test between the normal control group and the oat protein group (P > 0.05). Mice in the oat meal group had significantly longer swimming endurance compared to the normal control group (P < 0.05). Furthermore, dietary oat protein increased the levels of liver glycogen, enhanced the activities of lactic dehydrogenase and superoxide dismutase, and decreased the levels of blood urea nitrogen and malondialdehyde in serum." (Xu. 2013)

  Now the good news certainly is that id did work. The "bad" or at least not so good news, on the other hand is that there is no adequate control group, since the addition of both the oats and the oat protein will have increased the amount of essential amino acids in the rodent chow significantly.

That's it! At least as far as news on getting bigger, stronger and faster is concerned. In case yo are also interested in something else, for example...

• how scientists have successfully transformed former breast cancer cells back to benign mammary epithelial cells by placing them in a non-carcinogenic environment like a healthy non-inflamed mouse
• that continously taking 25,000IU of supplemental vitamin A is at least not particularly healthy for young lean and obese women
• why Munuka honey, when Greek or Cypriot Honeys are the more potent antimicrobials?

and whatever else I will still be posting before tomorrow's SuppVersity news, you are alway welcome to visit the SuppVersity Facebook Wall.

References:

• Bloomer RJ, Canale RE, McCarthy CG, Farney TM. Impact of oral ubiquinol on blood oxidative stress and exercise performance. Oxid Med Cell Longev. 2013;2013:465020. doi: 10.1155/2013/465020. Epub 2013 Aug 23. 
• Crisp NA, Fournier PA, Licari MK, Braham R, Guelfi KJ. Optimising sprint interval exercise to maximise energy expenditure and enjoyment in overweight boys. Applied Physiology, Nutrition, and Metabolism, 10.1139/h2013-111. 
• Gouvêa AL, Fernandes IA, César EP, Silva WA, Gomes PS. The effects of rest intervals on jumping performance: A meta-analysis on post-activation potentiation studies. J Sports Sci. 2013 Nov 9.
• Hansen KT, Cronin JB, Pickering SL, Newton MJ. Does cluster loading enhance lower body power development in preseason preparation of elite rugby union players? J Strength Cond Res. 2011 Aug;25(8):2118-26.
• Hardee JP, Lawrence MM, Zwetsloot KA, Triplett NT, Utter AC, McBride JM. Effect of cluster set configurations on power clean technique. J Sports Sci. 2013 Nov 5.
• Okudan N, Revan S, Balci SS, Belviranli M, Pepe H, Gökbel H. Effects of CoQ10 supplementation and swimming training on exhaustive exercise-induced oxidative stress in rat heart. Bratisl Lek Listy. 2013;113(7):393-9. 
• Scheffer DL, Silva LA, Tromm CB, da Rosa GL, Silveira PCL, de Souza CT, Latini A, Pinho RA. Impact of different resistance training protocols on muscular oxidative stress parameters. Applied Physiology, Nutrition, and Metabolism, 10.1139/h2013-115
• Shetty RA, Forster MJ, Sumien N. Coenzyme Q(10) supplementation reverses age-related impairments in spatial learning and lowers protein oxidation. Age (Dordr). 2013 Nov 10. 
• Xu C, Lv J, You S, Zhao Q, Chen X, Hu X. Supplementation with oat protein ameliorates exercise-induced fatigue in mice. Food Funct. 2013 Nov 12.

Sulforaphane from Cruciferous Vegetables Inhibits Myostatin and Increases Cell Viability in Skeletal Muscle Satellite Cells

Chicken Egg Rolls with Red Cabbage, Mango & Lime (CleanEatingMag); small inset shows sulforaphane content (µg/ml) of a juice made cauliflower, broccoli, red and white cabbage and brussel sprouts (based on Totušek. 2011).

When I am looking at the currently top-rated posts (see box "Most Popular (last 30 days)" on in the right navigation bar), it appears as if someone must have found my older article on the myostatin boosting effects of clenbuterol and told all his facebook friends about it.

Don't forget to check out and tell your friends about the latest SuppVersity Facebook News, as well!

In case this hypothesis is right, he (or she?) and all the friends will probably be happy to hear that there is a virtually side-effect free over-the-counter alternative that can suppress myostatin and thus make your muscles grow faster: Broccoli, cauliflower, cabbage and co (see image on the right and realize Red Cabbare, not broccoli is the King!) - the sulforaphane in these cruciferous vegetables appears to make that possible.

Muscle building veggies... yamyol!

Back in the day Popeye was invented to convince children that it would be worth eating their spinach (unfortunately this advise was based on the false assumption that it was a good source of iron and would thus help build the kids' stamina). I guess when the inventors of Popeye get wind of the soon to be published paper we are going to look at, today, we are soon going to see a digital avatar of Mr. O. munching broccoli in a 3D animated cartoon.

Sulforophane protects muscle against exercise induced damage: Although pertinent studies on the myostatin inhibiting effects of sulforophane outside of the petri dish have yet to be conducted, a rodent study from 2009 did already observe another, likely related effect of sulforophane  supplementation in intact animals. Administered at dose of 25mg/kg (human equivalent: 4mg/kg ~ 300-400mg for an average adult) it exerted significant ameliorative effects on exercise induced muscle damage (Malaguti. 2009). Against that background it does not seem to be exactly unlikely that chronic sulforophane supplementation or cruciferous vegetable consumption could give you a slight edge over those who don't eat their greens.

Whether the digital broccoli munching Mr. O Popey will be able to bring more scientifically sound arguments to the table than his predecessor, popeye does however still have to be determined. After all, the scientists from the Animal Breeding and Husbandry Group at the University of Bonn in Germany did not study the real-world effects of sulforaphane (SFN), but only the in vitro effects the exposition of porcine satellite cells to, of which every SuppVersity reader knows that they function as skeletal muscle stem cells and support muscle growth and regeneration following injury or disease, when they found that...

"[...] 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." (Fan. 2013)

If you take a closer look at the data in figure you may notice that this increase in myostatin went hand in hand with a decrease in MyoD expression. With MyoD being a protein that is involved in the very first step of satellite cell recruitment (it stops the proliferation of stems cells and initiates their transformation to muscle cells) this may seem awkward at first.

In view of the MyoD promoting effects of trichostatin A, which basically stops cell development in its tracks it can however be explained by the fact that less new satellite cells are needed, because their survival is increased so that the proliferation rate does not actually suffer (figure 1, left).

Figure 1: Cell viability, proliferation, MyoD, Myostatin and (total) Follistatin mRNA expression in porcine stem cells (satellite cells) from semimembranosus muscles from 6 purebred Pietrain piglets after exposure to DMSO (control),  trichostatin A or different concentrations of sulforaphane (SFN; data based on Fan. 2013)

This explanation does not only stand in line with the previously reported increase in MyoD expression in aging muscle (in this case unfortunately in the absence of increased cell viability; Alway. 2013), but is also supported by the concomitant downregulation of the pro-apoptotic (=initiating cell death) caspase enzymes (not shown in figure 1) in the SFN treated satellite cells.

In conjunction with the decrease in myostatin, which is, as I am sure you all know the 'myocyte hypertrophy break' of your body, the data from this in vitro study clearly suggests that SFN treatment could well have a growth promoting effect on skeletal muscle, which is -- and this may be one of the most important messages here -- more prononce at lower concentration used in the study.

Figure 2: Appearance of SFN in serum (triangles) and its metabolite in the urin of one of 10 healthy, normal-weight adult (34 +/-13 y) male volunteers after the ingestion of 200g of raw (top) or cooked (bottom) as part of a warm meal (Vermeulen. 2008)

Bottom line: After you have read about the potent anti-adiposity effect of antibiotics which are used in poultry fattening, yesterday, and today's news about the myostatin inhibiting effects of cruciferous vegetables, or more precisely, their sulforphane content, the infamous 'chicken breast, broccoli and rice diet' does actually begin to shine in new splandor! I mean, if only 50% of the aforementioned in vitro effects could actually be achieved by eating like this day in and day out, these recent findings could well explain, why generations of bodybuilders thrived on these spartan foods. And in case you wondered why the guys get freakier year by year - that's simply the availability of broccoli extracts and the increased use of antibiotics in poultry fattening... ;-)

I am obviously just kidding. If we go by the bioavailability data of raw (figure 2, top) and cooked (figure 2, bottom) broccoli, 200g of broccoli served as part of a warm meal will get your blood SFN levels up to only 2.5% or 1.2% of the most effective dose (5µM) used in the study. So, it's pretty certain that you'd have to gobble copious amounts of red cabbage juice (see picture on top of the article) to get there.

In view of the fact that lower concentrations yielded greater effects, it is however not totally unlikely that even concentrations as low as 1µM would yield results. With additional supplements, it does therefore not appear to be unrealistic to achieve blood levels like that (although you should not expect the increase to be linear).... anyway, I will let you know as soon as the first pertinent rodent or even human trials are available.


References:

• Alway SE, Degens H, Lowe DA, Krishnamurthy G. Increased myogenic repressor Id mRNA and protein levels in hindlimb muscles of aged rats. Am J Physiol Regul Integr Comp Physiol. 2002 Feb;282(2):R411-22.
• Fan H, Zhang R, Tesfaye D, Tholen E, Looft C, Hölker M, Schellander K, Cinar MU. Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells. Epigenetics. 2013 Oct 23;7(12).
• Totušek J, Tříska J, Lefnerová D, et al. Contents of Sulforaphane and Total Isothiocyanates, Antimutagenic Activity, and Inhibition of Clastogenicity in Pulp Juices from Cruciferous Plants. Czech J. Food Sci. 2011; 29(5): 548–556.
• Vermeulen M, Klöpping-Ketelaars IW, van den Berg R, Vaes WH. Bioavailability and kinetics of sulforaphane in humans after consumption of cooked versus raw broccoli. J Agric Food Chem. 2008 Nov 26;56(22):10505-9.

When Rodents Squat, Scientists Gain Insights into How Muscles Grow. IGF-1 Response to Exercise Does Matter - Locally, not Systemically, of Course!

You want to build big wheels? Look no further get yourself the "Squat T-Bar" with integrated 15mA electrical 'motivator' (Aguiar. 2013)

"A rodent study investigating strength workouts?" Yeah, I know it does not sound like that would be in any ways news-worthy, but if you take a look at the image on the right, you will immediately realize: This study is different! Instead of using a treadmill or simply stitching down (or rather up) one of the hindlimbs of the rodents to induce a chronic overload on the other one (don't laugh, many rodent studies have done just that), the study at hand (Aguiar. 2013), which is going to be published in the next issue of the International Journal of Sports Medicine, used a not innovative, but unfortunately largely forgotten (or overlooked?) torturing device that has been developed by Japanese researchers roughly 20 years a ago (Tamaki. 2013).

The rodent torture... ah pardon squat rack ;-)

After being fitted with a canvas jacket in a way that would enable the researchers to limit the twisting and flexion of their torsos (no, that was not a weight lifting belt ;-), the 32 male Wistar rats (80 days old, 250–300 g) were suspended in a standard position on their hind limbs and "encouraged" to exercise by "electrical stimulation [...] that was applied to the rat’s tail through a surface electrode"  (Aguiar. 2013).

Using their neat little toy, the eight researchers from the University Estadual Paulista, in Botucatu, Brazil, were able to submit the rats to a relatively realistic progressive resistance training regimen for either 8 or 12 weeks. Three times per week each rodent had to do 4 sets  of squats for 10-12 repetitions at 65-75% of its individual 1-RM (maximal weight the rodent could handle). During the study period, Aguiar et al. adjusted the weights twice a week to ensure the same training intensity throughout the experiment (something I would highly recommend to anyone of you, as well; try to pack on 1.25lbs - 2.5lbs at least every other week).

Figure 1: Body weight, muscle weight (plantaris, only) and food intake relative to body weight of the control (C8, C12) and trained (T8, T12) rats before and after the 8-week (C8, T8) and 12-week (C12, T12) intervention (data adapted from Aguiar. 2013)

As you can see in figure 1, this minimalist approach to leg training lead to an increase in both body weight and muscle weight that may initially look as if it was strongly linear. You do yet have to be careful about statements like that, because (a) the rodents did gain weight irrespective of whether they were training or not (80 day old rats are still growing!), so comparing the four bars next to each other and saying "yep, linear!" is not feasible, because this would mean linear as in not training for eight weeks < training for 8 weeks < not training for 12 weeks < training for 12 weeks, which is obviously nonsensical. That being said, there is simply (b) insufficient data to say anything about the linearity -- after all, we do have only three data points per group.

"All groups started the experiment with similar body weight. There was a significant increase (p < 0.05) in the body weight of the 4 groups in the resistance training program (C8: 35.5 %; T8: 27.7 %; C12: 46.9 %; and T12: 40.1 %) and final body weights were not significantly (p > 0.05) different between groups. Furthermore, no significant (p > 0.05) differences in the weekly food intakes were observed between the groups."(Aguiar. 2013)

What does yet stick out, is that the obviously age-dependent weight gain in the control groups C8 and C12 did not increase the weight of the plantaris muscle to a weight anywhere near to the muscle weight, the rats in the trained groups achieved.

Muscle gains and strength gains went hand in hand

In the rats who were subject to the three-times-per-week exercise regimen, on the other hand, those increases in muscle size went hand in hand with highly significant improvements in 1-RM squat power; While all groups had begun the training protocol with similar absolute 1-RMs of ~450g (that's about 130% body weight, pre) ...

"[...] training for 8 and 12 weeks promoted a significant (p < 0.05) increase in the RM/BW ratio in the T8 (pre- vs. post-training: 35.7 % increase, p < 0.05) and T12 (pre- vs. post-training: 57.1 % increase, p < 0.05) groups, while no statistical (p > 0.05) difference was observed in their respective control groups." (Aguiar. 2013)

Consequently, the ratio of 1-RM to body weight was 36.1 % and 57.7 % higher in the groups who had been training fot the last 8 or 12 weeks than in the lazy controls and the time-effect yielded another +22% increase in strength in those rodents who trained for 12 and not just 8 weeks.

Figure 2: Strength gains (left) and increases in cross sectional area, as well as intramuscular IGF1, myogenin and myoD expression (data adapted from Aguiar. 2013)

Now you may have heard all that before, what really makes this study stand out, however, is the observation of statistically highly significant correlations of intra-muscular IGF1, myogenin and myoD  mRNA expression, which speaks in favor of my previous hypothesis (read up on that in the Intermittent Thoughts on Building Muscle) that muscle growth is triggered, driven and maintained almost exclusively at a local level.

What are myogenin and myoD? Both are myogenic regulation factors with myogenin actually being part of the myoD family of transcription factors that will make stem cells develop into myocytes (myo D is highest in recently activated satellite cells).

So, when you are looking for "hormonal" (or other pro-anabolic) ghosts (Phillips. 2013), it is imperative to look for them right where the spook, or, in this case, the muscle building magic happens. If you do just that (see figure 2) and correlate the intra-muscular mRNA expression of IGF-1, myogenin and myoD, you will find the "ghostly" explanation for strength and size gains, as well as the confounding structural changes in the architecture of the muscle, with corresponding correlations between the increases in muscle cross-sectional area (CSA) of r = 0.85 (p = 0.0001), r = 0.87 (p = 0.0001) and r = 0.88 (p = 0.0001) for myoD, myogenin and IGF-1, respectively.

Fiber type changes take their time and occur only within the type II spectrum

A neat side-finding, which is actually no news, though, pertains to the fiber-type conversions that took place in response to the exercise regimen. Firstly, the scientists confirmed the notion that these changes occur exclusively within a certain fiber type. In other words, while Aguiar et al. observed conversions from the metabollically more flexible type IIX/D to the highly glycolytic (power) IIA type, no conversions of the highly oxidative type I to type II fibers were observed. And though the results would generally suggest that fiber IIX/D-to-IIA type conversion, as they 

"[...] also appear to occur during endurance training in humans, so that it would [be] reasonable to think that any exercise stimulus (e. g., endurance or strength) that is sufficient in duration and/or intensity can potentially induce conversions within the fast fiber population from type IIX/D to type IIA" (Aguiar. 2013),

the time-frame in the course of which these changes took place -- namely 12 weeks -- would confirm that the common fear of strength and endurance athletes could provoke negative structral adaptations from doing a "cardio" or "strength" workout from time actually is actually unwarranted. Neither will the former turn a powerlifter into a weakling, nor will the latter make a marathon runner "bulky". Both powerlifter and marathoner are on the contrary going to benefit from the conditioning effect and increase in strength, respectively -- not to mention the important effects on overall health both and not as mainstream stupidity will tell you only the powerlifter can derive from, figuratively speaking, "killing some game in the other's territory"

Bottom line: More food for intermittent thoughts on building muscle ;-)

Figure 3: Correlations between acute GH (A), free testosterone (B), IGF-1 (C)  and cortisol (D) responses (area under the curve—AUC) and gains in type II fibre CSA (Burd. 2013).

Eventually, this study is an excellent example of a way to design a rodent study in a way that will render its results actually meaningful. And what's more, in this particularly case these results are not just meaningful, but can also help us to make some sense of a couple of things we have not fully understood / appreciated, as of yet.

What I am particularly thinking about here, is the contrast between the in-vitro effects of IGF-1 and the (more or less absent) real-world effects of the IGF-1 response to exercise (=systemic increase), as it was observed by West and Phillips in a 2013 study. In their well-powered longitudinal study, neither the acute increase in systemic testosterone, nor the exercise induced increases in systemic IGF-1 showed significant correlations with the gains in type II CSA in a cohort (n = 56) of young men in response to 12 weeks of resistance training (West. 2013; see figure 3).

Another interesting finding of the West study was that, contrary to the circulating testosterone and IGF-1 levels, GH and cortisol did show direct correlations with increased muscle cross sectional areas in type II fibers.

And while the former correlation may be explained by the influence of growth hormone (GH) on the local expression of IGF-1 (Hameed . 2004), there is another open question left: How does cortisol actually figure in here? I mean, the chronic elevation / exogenous adminstration of cortisol, has been show to do the exact opposite, i.e. it decreases the local IGF-1 mRNA expression (Inder. 2010).

Figure 4: Graphical summary of what you should have learned Intermittent Thoughts on Building Muscle ... you didn't 'cause you are new to the SuppVersity or simply forgot about it? No problem read the preliminary summary and browse the individual chapters here!

What was missing in the Inder study, however, was the exercise component: Working out does not just exert protective effects against the negative side effects of the provision of exogenous "cortisol" (in this case Dexamethason), as they were observed in the afore referenced study by Inder et al., exercise will also lead to profound increases in local IGF-1 mRNA expression (e.g. +60% in Bamann. 2001), despite the fact that it will also increase the release of the falsely vilified anti-inflammatory glucocorticoid, cortisol... acute vs. chronic, local vs. system, peak values and amplitudes vs. plateaus and AUC values - you got to keep all these contrastive, yet complementary pairs in mind, when you are thinking about the endocrine and intracrine (within the cell) mediators of skeletal muscle hypertrophy.... what? Sounds familiar? Well, you must have been following the Intermittent Thoughts on Building Muscle, then ;-)

References:

• Aguiar AF, Vechetti-Júnior IJ, Alves de Souza RW, Castan EP, Milanezi-Aguiar RC, Padovani CR, Carvalho RF, Silva MD. Myogenin, MyoD and IGF-I Regulate Muscle Mass but not Fiber-type Conversion during Resistance Training in Rats. Int J Sports Med. 2013 Oct 11.
• Bamman MM, Shipp JR, Jiang J, Gower BA, Hunter GR, Goodman A, McLafferty CL Jr, Urban RJ. Mechanical load increases muscle IGF-I and androgen receptor mRNA concentrations in humans. Am J Physiol Endocrinol Metab. 2001.
• Ding H, Gao XL, Hirschberg R, Vadgama JV, Kopple JD. Impaired actions of insulin-like growth factor 1 on protein Synthesis and degradation in skeletal muscle of rats with chronic renal failure. Evidence for a postreceptor defect. J Clin Invest. 1996 Feb 15;97(4):1064-75. 
• Inder WJ, Jang C, Obeyesekere VR, Alford FP. Dexamethasone administration inhibits skeletal muscle expression of the androgen receptor and IGF-1--implications for steroid-induced myopathy. Clin Endocrinol (Oxf). 2010 Jul;73(1):126-32.
• Phillips SM. Strength and hypertrophy with resistance training: chasing a hormonal ghost. Eur J Appl Physiol. 2013 May;112(5):1981-3-
• Sculthorpe N, Solomon AM, Sinanan AC, Bouloux PM, Grace F, Lewis MP. Androgens affect myogenesis in vitro and increase local IGF-1 expression. Med Sci Sports Exerc. 2013 Apr;44(4):610-5.
• Tamaki T, Uchiyama S, Nakano S. A weight-lifting exercise model for inducing hypertrophy in the hindlimb muscles of rats. Med Sci Sports Exerc. 1992 Aug;24(8):881-6.
• West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2013 Jul;112(7):2693-702. 

22g Baking Soda 60min Before a Old-School 4 x 12RM Leg Workout Allow for a 22 Rep Volume Increase on Hypertrophy Oriented Squat + Leg Press + Leg Extension Quads Routine

Image 1: Squats, 8 x 12, Leg Press 6 x 12, Leg Ext. 6 x 12; that's the Quads routine Serge Nubret trained twice a week in conjunction with chest – it stands out of question that this is the kind of workout that benefits most from an acid buffer like NaHCO(3)!

As a diligent student of the SuppVersity you are no stranger to the ergogenic value of sodium bicarbonate, NaHCO(3) or baking soda, and though I still believe that I have to do a lot of persuading in terms of its stand-alone benefits (click here to read more), many of you will at least have been impressed by its ability to boost the uptake and subsequent performance benefits from creatine supplements (cf. "Supercharging Creatine With Baking Soda"). And while I am not sure if the soon-to-be-published study by Carr et al. will be last straw that's finally going to break your back... ah, I mean your resistance, or I should say, unwillingness to accept that something as cheap and simple as baking soda could outperform 90% of the overpriced supplemental non-starters on the market and will not make you draw water or increase your blood pressure, although it has the bad word "sodium" in its name, I cannot tell, what I can tell you though, is that Benjamin M. Carr and his colleagues from the School of Human Performance and Recreation at the  University of Southern Mississippi in Hattiesburg are spot on, when they say (or write) that their "findings demonstrate ergogenic efficacy for NaHCO(3) during [hypertrophy-type resistance training]" (Kerr. 2013).

The benefits of baking soda start at high intensity aerobic exercise, and end right where your willpower ends ;-)

That baking soda can be an effective ergogenic aid, especially when it comes to high volume workouts has actually long been established. Still many, if not most of the trials involved sprinters or cyclists performing HIIT-esque protocols on the track or cycle ergometer (e.g. 11.5% increase in sprint performance in Price. 2003), whereas researchers such as Portington et al. or Webster et al. totally missed the boat or, I should say, what it means to train, when they had their study participants perform laughable 5 sets of leg presses and measured nothing but a (yet significant) difference in blood pH in response to pre-supplementation (105 min before the test) with sodium bicarbonate (Webster, 1993; Portington. 1998).

Figure 1: Overview of the experimental protocol that was used in the study (based on Carr. 2013)

With four sets of three exercises at the 12RM (not yet Serge Nubret style, I know; see image 1 ;-) and the king of all leg exercises, the squat being one of them, as well as resistance trained study participants who were actually able to lift a weight that would be taxing enough to see a difference, the study design of the Carr study (see figure 1) is yet more of what I would expect to yield results with real world significance for trainees who are not at the gym to chat and show off their latest gymwear, but to train... and as the data in figure 2 goes to show, the results were what these very trainees are looking for:

Figure 2: Lactate, pH, ratio of hydrogen carbonate ions to NaHCO(3) and base excess in blood after, as well as number of total reps performed during the leg workout (data adapted from Carr. 2013)

I freely admit, an overall plus of ~22reps, in other words 1.83 reps per set does not sound like much, but if you think about how long you would have to train to achieve this improvement and/or compare it to the median effect size of weeks of beta alanine supplementation, of which you can hardly say that it was one of the aforementioned supplemental non-starters, and still offers a performance increment of only 2.87% (Hobson. 2013), the 22 +/- 13 reps or 4% increase in total volume the participants in the Carr study achieved within about 2min (by drinking their 22-32g of baking soda) are more than just a bit of alright.

"But isn't the increase in lactate a bad thing?"

"Lactate...?" I knew this would be your next question. I mean it is already hard enough to believe that anything that has the word "sodium" (by the way you Americans are the only ones who don't get that this ought to be "natrium" and not "sodium" ;-) in its name is not per se bad for you, and now the guys in the baking soda group had higher lactate levels!

Image 2: "Cholesterol is the devil and sodium is his little brother!" Everyone who still believes everything the medical orthodoxy says, please raise your hands!

A note on the dangers of "salt": Firstly, baking soda is "only" ~28% sodium, which means that for every 4 grams you ingest you get roughly 1 g of sodium. Secondly, it is arguable how much of the sodium is effectively taken up and will be floating around in your blood. As T. Lakhanisky points out in his dossier for the Belgian government: "The uptake of sodium, via exposure to sodium carbonate, is much less than the uptake of sodium via food. Therefore, sodium carbonate is not expected to be systemically available in the body." (Lakhanisky. 2002) And thirdly, there is more and more evidence that suggests that the chloride rather than the sodium content of common table salt (NaCl = Natrium + Chloride) is the root cause of "sodium induced hypertension" in "sodium sensitive" individuals / animal models. Only recently, a study by Schmidlin et al. showed that chloride loading induced hypertension in the stroke-prone spontaneously hypertensive rat despite profound sodium depletion (Schmidlin. 2010). So, if you asked me, rather than pointing at salt as the #2 on the list of greatest evils (obviously cholesterol is still #1, here) the medical orthodoxy would be better advised to address the imbalances between sodium and potassium (click here to learn more about the ratios), which are so characteristic of the western diet, instead of painting yet another black and white picture where sodium is the bad guy and potassium the dangerous mineral that cannot be sold OTC in dosages >80mg.... but hey, this would be the topic for a whole new blogpost and as gross as it may sound, the chance that you get diarrhea from the baking soda is probably 1000x higher than the remote possibility of increases in blood pressure. A 1990 study by Luft et al. even found that the blood pressure of 10 mildly hypertensive and normal subjects decreased by 5mmHg after 7 days in the course of which they drank 3 liters of sodium bicarbonate containing water per day (Luft. 1990)

Now, you would have reason to be concerned if we were talking about lactic acid, which is basically lactate + a proton (you can also say, lactate is the negative ion of lactate acid if you want to). Contrary to the latter, which increases during exercise when the acid buffer of your musculature is exhausted, lactate is however not just benign, but actually beneficial.

"So lactate is a bonus... really?"

Figure 3: Mean plasma lactate, GH, and prolactin responses to intravenous infusion of 250ml 1M sodium lactate in 7 untrained healthy volunteer; note: the respective increase in GH is more pronounced with natural = exercise induced increases in lactate.

While it's still debated whether lactate is only a beneficial co-factor in the mitochondrial energy chain, as Van Hall proposes in his Y2K review of the research (Van Hall. 2000) or rather a mitochondrial energy substrate in its own right that cannot be used only in the mitochondria of your skeletal and heart muscle but also in your brain, as Pellerin et al. suggest (Pellerin. 2007), it is indisputable that the decreased formation of lactic acid, due to the perseverance of an overall higher alkalinity in the presence of a 4% higher workout volume is a beneficial things. Not the least, by virtue of the its ability to trigger the release of growth hormone (cf. figure 3; Luger. 1992), which could - in conjunction with the increased workout capacity and the supposedly faster post-workout recovery give trainees on a hypertrophy-oriented volume training regimen an edge over the salt-o-phobic competition.

In view of the fact that Carr et al. arrive at the exact same conclusion, before they state that the "ergogenic efficacy" of sodium bicarbonate during "hypertrophy-type resistance exercise" would "warrant further investigation into chronic training applications" (Carr. 2013), we can expect to see a future trial investigating exactly that: How much more will you gain if you repeat this practice for 6-8 weeks? ... I guess, I don't have to tell you that the SuppVersity is going to be the place, where you are going to read about the results of that study, first!

References:

• Carr BM, Webster MJ, Boyd JC, Hudson GM, Scheett TP. Sodium bicarbonate supplementation improves hypertrophy-type resistance exercise performance. Eur J Appl Physiol. 2013 Sep 4.
• Lakhanisky T. Sodium Bicarbonate. OECD SIDS. UNEP Publications. 2002.
• Luger A, Watschinger B, Deuster P, Svoboda T, Clodi M, Chrousos GP. Plasma growth hormone and prolactin responses to graded levels of acute exercise and to a lactate infusion. Neuroendocrinology. 1992 Jul;56(1):112-7.
• Luft FC, Zemel MB, Sowers JA, Fineberg NS, Weinberger MH. Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man. J Hypertens. 1990 Jul;8(7):663-70.
• Pellerin, L., Bouzier- Sore, A.-K., Aubert, A., Serres, S., Merle, M., Costalat, R. & Magistretti, P. 2007. Activity-dependent regulation of energy metabolism by astrocytes: an update. Glia 55, 1251–1262. 
• Price M, Moss P, Rance S. Effects of sodium bicarbonate ingestion on prolonged intermittent exercise. Med Sci Sports Exerc. 2003 Aug;35(8):1303-8. 
• Portington KJ, Pascoe DD, Webster MJ, Anderson LH, Rutland RR, Gladden LB. Effect of induced alkalosis on exhaustive leg press performance. Med Sci Sports Exerc. 1998 Apr;30(4):523-8.
• Schmidlin O, Tanaka M, Sebastian A, Morris RC Jr. Selective chloride loading is pressor in the stroke-prone spontaneously hypertensive rat despite hydrochlorothiazide-induced natriuresis. J Hypertens. 2010 Jan;28(1):87-94.
• Van Hall G. Lactate as a fuel for mitochondrial respiration. Acta Physiol Scand. 2000 Apr;168(4):643-56.

Adelfo Cerame & Mr C: A Basic Workout + Nutrition Plan for Average Joes Trying to Get Stronger, Leaner & Healthier

Image 1: Don't worry, since this is a new series, you will soon know who "Mr C" is ;-)

I assume you will be wondering about the title, right? "Adelfo Cerame & Mr C"? Who the f*** is 'Mr C'?" Well, I guess you will have to read the whole post to find out who this mysterious rookie is, but before you do so, I just want to point out that I was really happy that so many of you took the chance, last week, and asked Adelfo for advise, questioned why he does this and not that and asked him to comment on your own training routines. I know that many bloggers either don't have the time or are simply not willing to reply to the inquiries of their visitors. Even I sometimes miss comments or file them in my infamous "to-do" folder ... long story short: Don't be shy and pick Adelfo's brain and if you like what you read, share this and other blogposts on Facebook, Twitter, Google+, Digg, Reddit and co.!

Another New Week a Whole New Endeavor

Things seem to be coming along quite well as far as my efforts to broaden my horizons and gain more experience and expertise not just as a trainee, but also as a trainer within the nutrition and fitness game are concerned. As I mentioned in my post last Thursday, I intend to use the current off-season not just to grow physically, but also mentally - to accumulate knowledge, to learn how to better myself and how to help others find and make their way to a leaner and healthier self.

Image 2: Should no be too difficult to locate Adelfo among the huge team of fitness professionals, at Epic Inc.

I knew that to achieve these goals, I had to find new endeavors, something different from my previous day-in-day-out schedule of eating, training, sleeping and spending some time with family and friends ...and as of last week, I was hired on as a nutrition coach for a company.

No, I am not working for Herbalife, now ;-)

It’s a fitness-based company called Epic Inc. They do everything from strength and conditioning programs for the general public, to football training camps, and also have a program that helps student athletes with the opportunity to receive scholarships and I'm honestly pretty excited to be part of a coaching team that consists of ex-collegiate and professional athletes that have played abroad professionally and in the NFL.

Basically I’m going to be getting paid to hold nutritional workshops every other week, and offer nutritional advice for their clients, and at the same time a great opportunity to build my own clientèle.

Dear SuppVersity Student, Meet Mr C - The Subject of Our First "Case Study"

Speaking of clientèle, Adel (Dr. Andro) suggested that instead of just talking about me, I could tailor my  blogpost a little more to the non-bodybuilder average Joe who does not necessarily ever want to step on stage by presenting something he aptly called a "case study" - coincidentally I happen to actually have a new client. We will start to work together in about two weeks and he agreed that I could use him (without mentioning his name) as the subject of this new mini-series.

Mr. C's Stats

• Age: 32, 
• Height: 5’8’’, 
• Weight: 175, 
• Waist: 36"

Details (before):

• works from 9am-5pm at a hospital
• eats only twice a day (lunch & Dinner)
• lunch consists of cafeteria food, such as tuna melts, chicken sandwiches, and the occasional salad
• dinner consists of fast food and take-out – McDonalds, Jack in the box, Taco bell...
• trains rarely, but if he does, it is at a friend's makeshift gym in a garage at about 7pm-8pm

I’m sure you guys would be interested to see how an average Joe (and when I say "average", this just implies that we are not talking about your typical physique athlete or your hardcore gym rat or fitness enthusiast -  so, by no means "average" with a depreciative connotation, though!) transform his physique. Just a regular guy like you (and me, back in the day) trying to improve his health and physique who hardly knows where to start. An honest, hard working family guy that does the daily 9-5 grind - that's Mr. C.!

It's going to be hard work, for both of us!

I must admit that this is the first time I am working with a real "rookie". Almost all my previous clients had already some experience with training and nutrition - not so for Mr. C, though. For me that means that I will have to teach him everything from scratch: From how you can easily keep track of your macronutrient intake to how to perform a bench press. And above all, I got to keep things simple and practical.

His goals, my goals, our goals!

"Every journey has a destination!" As stupid as this may sound, you may remember from either

• Adel's vastly popular Intermittent Thoughts on Intermittent Fasting, e.g. "Programing Success: Goalsetting & Tracking") or his 
• more recent "Step by Step Guide to Your Own Workout Regimen", e.g. "Chose the Right Training Style for your goal"

that one of the most common mistakes trainees make is not to define clearcut goals for themselves.

Trainer or trainee - always know you goals!

Too many of my colleagues approach their clients planless, in the most literal sense of the word, and with a cookie-cutter-plan in their hands, let alone in an automated email they had an assistant write for them, as Carl Lanore mentioned it in his Super Human Radio interview with Molly Galbraith, yesterday....but I am getting derailed, here. Let's get back to my plans for Mr. C:

• Starting him off slowly - I got to work his new regimen into his everyday obligations and old habbits, but only for as long as those will not hinder or sabotage his progress; this means he will have to meet me halfway, so that we can create a plan that will work for him for more than the initial 2-4 weeks of dopamine driven enthusiasm and outstanding results.
• Finding the optimal nutrition regimen - Although you may say that this is just my interpretation of "intermittent cookie cutting", given his work-schedule and current primer on fatloss Intermittent Fasting is simply the logical and best choice here, so that’s what I’ll structure his schedule on.
• Writing a custom-tailored workout program - With a primer on simplicity and a challenging, yet manageable workload we will be starting with a 3-4x/ week. Moderate volume (5-6 exercises), moderate intensity workout regimen that's structured around the most fundamental movement patterns: Pressing, squatting, rowing.

As you can see below, I have already done my homework! I do yet have to admit that the nutrition and workout routine below is still a "work in progress" and will probably change even before Mr. C. and I are going to start to work together in two weeks; and they are certainly going to change in the weeks let alone months to come - I mean, why would the "new", transformed Mr. C. of say December 2013 train the same way as the slightly chubby rookie Mr. C. trains now?

Mr C's First Real Nutrition Plan

As I mentioned earlier, I want to keep things as simple as possible, so no caloric zigzagging – I would just risk to confuse him with all these numbers and that for an (at the moment) negligible benefit; maybe later down the road but not yet - here are the main features of the plan

Whole Foods, no fast-food!

Training days	PRO	CHO	FAT
Meal 1	65	50	16
Pre-workout	65	50	16
Post-workout	65	100	16
Total	195	200	50

---

Non-training days	PRO	CHO	FAT
Meal 1	65	50	16
Meal 2	65	50	16
Meal 3	65	100	16
Total	195	200	50

• Energy deficit of ~20% - we’ll play with these numbers for the first 2 weeks and adjust as we go in order to find set numbers that allow him to lose about a 1 lb. to 1.5 lb. / week 
• Similar meal frequency as before - the timing is more rigorous and the structure will make it easier for him to get along
• Food quality over quantity - more whole “real” foods, no more McDonalds and Jack in the Box on a daily basis
• Macronutrient awareness over calorie counting - based on his newly acquired knowledge of the average macronutrient content of whole foods Mr C will have to learn to estimate portion sizes and combine foods to "meet his macros" (at this point still only roughly)

The structural elements and the similarity to his previous habits will make compliance easier. Compared to the meticulous calorie-counting, the quality over quantity approach is a sustainable way of tracking your food intake. And with given ratios and a primer on whole foods, Mr C is going to see changes in his physiques within 2 weeks (4 weeks from now, as you may remember)

Mr C's First Real Workout Plan

Just as with the nutrition routine, I also tried to keep the workouts simple. Keep in mind that Mr. C is a beginner. This means that he will probably be struggling to perform the lifts properly, but it is now that I am working with him, when he can and has to learn how to do the muscle building compound movements I packed into his workout routine right! Now, or never, so to say ;-)

5x5 - Push	Sets	x	Reps
Flat bench	5	x	5
Dips	5	x	5
Squats	5	x	5

5x5 - Pull	Sets	x	Reps
Pull or chin ups	5	x	5
Deadlifts	5	x	5
Dumbell rows	5	x	5

---

Hypertrophy - Push	Sets	x	Reps
DB bench press	3	x	6-10
Military press	3	x	6-10
DB side laterals	2	x	12
Leg press	3	x	6-10
Leg extensions	2	x	15
Skull crushers	3	x	10-12

Hypertrophy - Pull	Sets	x	Reps
Bent over barbell row	3	x	6-10
Lat pulldown	3	x	6-10
DB reverse fly	2	x	12
Straight legged deadlift	3	x	8-12
Barbell curls	3	x	6-10
DB Hammer curls	2	x	15

That being said, his workout regimen resides on two pillars, I picked according to his goals to get stronger, leaner and more muscular:

1. 5x5 fundamental strength workouts - since one of Mr. C’s goals was to increase strength, the first part of his routine has a clear focus on building just that; with 5 sets of 5 reps on three basic lifts, there is no way, Mr. C. is not going to see magnificent strength gains within weeks
2. Push / pull hypertrophy workouts- the foundational strength regimen is compounded by hypertrophy-specific work later in the week to make good use of the strength gains in order to pack on a few lbs of muscle aka "metabolic currency" in the weeks to come

When you look at the workout on the right, you got to keep in mind that this is still work in progress. Especially the fact that Mr. C. trains at his friend's makeshift gym in a garage, could become a problem, because, as of now, I simply assumed that he will have all the equipment available. When this is not the case, we will have to tweak things accordingly, but those and other tweaks will have to wait until we are starting to train together.

It's going to be an exciting time for Mr C. for me and - as long as you don't forget to come back every Thursday for my weekly updates - for you, as well! So, stay tuned!