Treadmills in the Workplace, Say What?

Recently got this question on my forum and thought I’d post it here for all to see.

Question:

I’m interested in your opinion on the following and whether it would negatively impact strength gains or maintaining strength.

My employer has made a number of ‘treadmill desks’ available to us. Basically, a treadmill below a standing-height desk, the idea being you walk on the treadmill at some speed so low that it does not interfere with your desk work, but provides some ongoing activity during the day.

Answer:

I don’t foresee this being a big deal at all once you get used to it and I think this is analogous to “mail-man GPP”, i.e. the mailman walks 20,000 steps a day but can still train heavy after work because he’s gotten used to that volume of LISS, if you will. A person who just started at the post office gets wrecked from day 1’s 20K steps and because he’s not used to it, he needs to modify his training accordingly to allow a bit of transient performance drop off.

Perhaps the most poignant issue I could raise with this style of “cardio” is with it’s effectiveness to do anything useful at all. How can we expect a modality, frequency, and intensity of exercise that does not perturb our homeostasis much- as evidenced by fatigue, transient performance loss, etc.- to cause a beneficial adaptation? In other words, because the thing is so easy, I don’t know how much utility it has with respect to caloric expenditure, cardiovascular conditioning, etc. I highly doubt that your “net” caloric expenditure has changed over a 24-48hr period due to this type of exercise simply because the body is readily adaptive and there needs to be some critical threshold of “stimulation” that needs to be crossed to drive any and all adaptations.

On the other hand, I think the benefits of this type of intervention is more realistically applied to orthopedic benefits. Anything that gets you up out of the chair, into a better posture, pumps blood through the muscles, and moves the limbs, sinew, and soft tissue structures through their normal anatomical range of motion can only benefit the person doing it, in my opinion.

Rebuttal to “The Truth About Experts”

By Jordan Feigenbaum MS, Starting Strength Staff, CSCS, USAW CC, HFS

________________________________________________________________________

In general, articles on the Internet tend to come in three different flavors: a) chock full of useful information and analysis from a scientific viewpoint by a subject matter expert (self proclaimed or not), b) entertainment-based musings, or c) a blatant hatchet job written for the sole purpose of denigrating someone who’s well known in order to get your readership up. The article we’ll be discussing today falls into the latter category and both the author and publisher over at Juggernaut knew full well what they were doing. In response, I’ll appropriately be combing through this illiterate ignoramus’s article for the entire Internet to see in order to show just how bad it really is, why JTS should have higher standards for publishing, and how to present a counter analysis to another person’s viewpoint.

At this time, Mr. Mash has not responded to my email requesting his agreement to let the article be posted on StartingStrength.com for everyone to view. Additionally, I added if he’d like to discuss the article on the Internet or at our annual Starting Strength Coaches Conference he’s welcome to do so. We’re sincerely hoping Mr. Mash will regale us with his elite analysis of barbell training.

Since I do not own the article I cannot post it here in its entirety, but one of the joys of the Internet is the ability to see deleted pages through cache and I will link to a screenshot of the now-defunct page often as we take this journey through ad-hominem attacks, misinformation, and illogical arguments.

After a lot of self promotion and assertion that Mr. Mash is, indeed, a subject matter expert in the strength and conditioning world we arrive here:

“This long introduction is to explain why I cannot tolerate bogus information. My life is spent informing and helping people, so when I see someone giving out advice that is not only wrong but dangerous, it makes me furious.”

Just to be clear, we’re looking for why the subsequently argued viewpoints are safer and more correct.

“Mark Rippetoe is one such guy. Until recently I had never heard of Coach Rippetoe even though he is a self-proclaimed power-lifter and strength coach. “

So if you’ve competed in the sport of powerlifting at 40+ meets and been a gym-owner and coach for 35 years I think it’s safe to assume you’re not just a “self-proclaimed” powerlifter (1 word Mr. Mash, you elite typist you) or coach, rather actually are.

Also interesting that you say you’ve never heard of him until recently, yet you say in a comment (pic below) that “His book “Starting Strength is awesome.” Interesting.

Screen shot 2013-09-19 at 11.05.52 PMMr. Mash then goes on to say:

“His popularity surged from Crossfit HQ between the years 2006-2009 teaching basic barbell movements. (HQ really needs to be careful who they choose to represent their brand, but that is a topic for another article).

Below is a video of the way the Coach Rippetoe teaches the squat:

And here is a video that is correctly how to teach a squat:

In video 1 you have Rippetoe coaching a novice how to fix their hip drive, depth issues, and other technique issues as they present themselves throughout warm up sets with a lifter in REAL-TIME. There was no staging for this, as it was not a demo on squat technique nor was it a video on “how to teach the squat”, rather it was merely a “how to fix the hip-drive” during the execution of the low bar back squat. If we go through Mr. Mash’s video, we can get some real “pearls” of information:

At 0:18 Mr. Mash says this is how “true champions” squat, although I think Dan Green, Kirk Karwowski, Ed Coan, and Andrey Malanachiev would disagree with this depiction since none of them do the high bar back squat like Mash would insinuate.

From 0:31- 1:10 Mr. Mash insinuates that you “lead with your chest” out of the bottom, although I’m sure he understands that this is merely a cue for a lifter and not what is happening biomechanically, i.e. it is the hamstrings and gluteal muscles that are starting to extend the hip while the quadriceps muscles are extending the knee anteriorly to start the concentric portion of the squat. He continues to say that “you put yourself in a better biomechanical position”, though he does not say compared to what nor does he propose a mechanism or rationalization for how this occurs. We can assume that he means a better biomechanical position compared to a low bar back squat, but then we need Mr. Mash to tell us just exactly what he means, i.e. what joints are now in a more advantageous position for the relevant muscles crossing them to fire, how does this lead to increased loading (to get stronger) than the low bar back squat, and how does this lead to a better training effect. Then he continues to say that “If you’re doing the Olympic lifts, the snatch and the clean and jerk, you always want to keep a vertical spine and you only want to have a horizontal back angle during the pull.” Let’s take a look at Dolega’s would-be WR snatch (in training) and note the back angle change out of the recovery.

Let’s pause a second here. While it is increasingly important to keep a vertical torso when recovering from a clean so as not to let the barbell deviate too far forward of the midfoot, which would create an unnecessary moment arm between the weight and the lifter’s center of mass, this is definitively not the case for the recovery from the snatch. When you watch really heavy snatches being recovered from. Notice that we just saw “hip drive” and thus, a more horizontal back angle in a snatch recovery from a “true champion”. Could this be because it’s the most effective way to drive up (extend the hips) out of the bottom in the concentric portion of the squat? Notice also that I’m defining any ambiguity in my terminology so that people can fully understand my argument and position on the matter. Mr. Mash does not do this.

At 1:15, Mr. Mash starts to “teach” the low bar squat. Mr. Mash then cues his lifter to go “back, back, back, back”, to which the lifter properly ignores so his knees can travel forward enough to optimize tension on the quadriceps in addition to engaging the posterior chain to a high degree. Then Mr. Mash cues the lifter to come up out of the bottom and incorrectly states that “See, you lift your chest first” after his lifter actually used his hips to come out of the bottom, which will happen 100% of the time in a heavy squat that’s to depth regardless of what your “guru” tells you.

At 1:45 Mr. Mash says “If you bring your chest first it brings you to almost lock out anyway.” However, what we actually see in video analysis of lifters is that the bar speed craters when the chest gets lifted on the way up when the muscles of the hips (gluteal group, hamstrings, adductors, etc.) could still be actively contributing to hip extension. Lifting the chest or as Louie puts it “shove your hips forward out of the bottom slacks the hamstrings and causes force production to drop. I have seen many reps missed this way and this “phenomenon” has been corroborated by other coaches who know how to analyze a lift. For a rather dramatic example, see Scott Cartright’s Squat where he tries to “lift the chest and shoves his hips forward out of the bottom” (but he actually drives his hips upward) vs. Andrey Malanachiev’s squat. Which one is to better depth? Which one had better bar speed?

From about 1:50-2:00 Mr. Mash is almost incomprehensible as he talks in sentence fragments and does not really make a clear point except for telling us to watch a 2 year old squat because, children and that you shouldn’t lead up with the hips first then the chest, rather it should be one motion. Ironically, THIS IS HOW WE TEACH THE SQUAT AT ALL OUR SEMINARS, which we’ve been doing for years. Strange.

Then it’s time for some Johnnie Candito action, just for good measure because

“Here is another coach agreeing with me”

The focus for the video, as we find out at 0:16 is “Proper hip drive in the squat”. Notice that Candito uses Mark Rippetoe’s name in his video title so that he can get more views because, ya know, Rip actually has a pretty decent following and all. Mr. Candito has unfortunately disabled comments for this video as he was getting called out left and right for all of his misgivings, which we’ll address in order:

At 0:45 Mr. Candito posits that “Mark Rippetoe teaches the hip drive as driving back the hips” out of the bottom of the squat. He continues,

“Here is the problem that is not using your hips at all. What is really happening is knee extension.”

So first things first, we do not teach the hip drive as “driving back the hips” or moving the hips posteriorly out of the bottom of the squat and if Mr. Candito would have read the book by the person he’s trying to use to get views, he’d know this. Additionally, even if someone did move the hips backwards significantly out of the bottom of the squat on their way up, it is virtually impossible to move the hips and the rest of the attached lower limb posteriorly without also moving the damn things upwards, i.e. hip extension during the concentric portion of the squat. Knee extension in absence of hip extension from the bottom of the squat with any significant load is impossible, as the lifter would simply knock themselves over on their ass from the knee extension creating a moment arm between the barbell and the middle of the foot (with the barbell being behind the middle of the foot).

From 0:54-1:10 Mr. Candito regales us with how he likes to teach the squat. He wants you to

initiate the squat by flexing the knee, then actively using your hip flexors on the way down to pull yourself into the bottom of the squat.

During the whole time of course, you should be actively flexing your glutes to “gradually sink back into the squat”. While I’m not sure what in the actual hell “gradually sink back into the squat” means, the preceding anatomy and biomechanics is complete and utter gibberish stemming from ignorance on the relevant topic. The hip flexors do not actively contract in order to flex the hip during the eccentric portion of the squat, just as the lats don’t actively contract in order to bring the bar back down from the press (overhead for the uninitiated). Gravity does a fine job at bringing things down and the only thing these muscles that are shortening do is relax in order to allow the movement to proceed. The only accurate thing mentioned here is the “flexing” of the glutes, as this eccentric braking resists “dive-bombing” the descent and getting out of position.

Next, Mr. Candito continues

“but this is not just simply bending forward, there is a difference between leaning forward and actually using your hip flexors and extensors.”

It’s hard to discern just what exactly Johnny is talking about, but this is nonsense. You lean forward, i.e. your back angle becomes more horizontal relative to the floor, during any variation of squat as the hips and the knees flex. How horizontal your back becomes is dependent on the bar position and segment length of the individual lifter. In the high bar position, the back angle will be more vertical compared to the low bar squat. If we consider the low bar back squat in an individual with a long torso, i.e. a long segment length between the SI joint and the barbell, he or she will have a more vertical torso than a person with a short torso. In any event, none of these squats will have occurred by the “hip flexors actively pulling the lifter downwards”, rather gravity will do that just fine. Similarly, the barbell will stay directly vertical to the middle of the foot and the intervening body segments, i.e. the torso and the femur, will accommodate any number of various configurations to make sure this happens. So what’s the take home? Forward lean is a function of segment length and bar position, the hip flexors don’t pull you down, and Johnny Candito should make less YouTube videos in his school library.

Next (at 1:22), it’s video time with Mr. Candito as he attempts to show us correct utilization of the hips. Mr. Candito says

“By using my hips properly I’m able to sit back, be explosive, while keeping my chest up.”

When watching his video, you can see that Mr. Candito has chosen to use a high bar variation of the squat, which is interesting because he’s claiming to want to show us how to drive the hips properly and hip drive is suboptimal in this variation due to slacking of the hamstrings relative to the low bar version. You’ll also notice, if you click through the video demonstration of his rep, that his hips do indeed move back as they start to go up out of the bottom. He actually writes “notice the knees are stagnate out of the bottom” when they are a) extending and b) moving posteriorly out of the hole. His chest also falls as he drives his hips because he didn’t keep his back locked in place well enough. So in effect, he’s doing exactly the opposite of all the things he told you that you shouldn’t do. Some of which are a misunderstanding of both the Starting Strength model of the squat and some are just form faults.

At 1:52, Mr. Candito says

“You might have noticed that my hips do not thrust forward immediately out of the hole. This is because your quads inevitably will be active throughout the entire movement. So mentally you need to counteract by thrusting the hips forward to remain in a neutral position.”

Typical gibberish. None of this makes sense except for the quads are active throughout the entire movement, which is correct in that they eccentrically lengthen during the descent and they concentrically shorten during the ascent.

At 2:29, Mr. Candito shows a clip of Rip coaching the low bar back squat (LBBS) to a novice lifter, which is the same video Mr. Mash referenced in the beginning of the article. Does the lifter shift his hips posteriorly out of the bottom in this video? Yes he does, as this was done when trying to coach a novice lifter who was not previously using the stretch-shortening cycle during his squat. Sometimes when you coach people, you have to get them to exaggerate the new behavior you’re wanting them to do in order to get the correction you want. This is not what we teach at the Starting Strength Seminars or in the book. We want the hips to drive straight up out of the bottom, as any other movement anterior or posterior is less efficient. Mr. Candito has not read the book, asked a question on the forum, or come to a seminar where he would learn he is mistaken. Rather, he is just running his mouth on the Internet because he can. Then we get a clip of Johnny squatting 500 about an inch high with really terrible hip drive. The hip drive is lost because he is high and he’s not thinking “hips up”.

The rest of the video is Mr. Candito stammering over his misinterpretation of the mechanics involved in the squat, what is actually happening anatomically and biomechanically, and in general, making himself look foolish. The hips do not go forward-optimally out of the bottom of the squat. Rather they go up via hip extension. If you look at heavy squats (including Cartwright who is trying to go “hips forward” out of the bottom) they will ALL come out of the bottom with a hip drive upwards. If you consciously cue “hips forward” after the initial hip drive, the bar speed slows markedly and this can be seen in video analysis of lifters who do this. On the other hand, if you “stay in your hips” (as in you do not exaggerate lifting the chest) all the way up the bar speed is better indicating increased force production and better mechanics.

Anyway, let’s move back to Mr. Mash now. He continues with:

“The problem with Rippetoe’s approach is that he is considering the hamstrings only, which is becoming a big problem in sports medicine in America.”

How in the world could one reasonably come to this conclusion when Rip spends pages talking about why we choose the stance we do in the squat, deadlift and powerclean, i.e. for more external rotator and adductor musculature to be used. Also, how are hamstrings only becoming a big problem in sports medicine in America? A quick review of relevant medical literature sources came up empty for “Subject matter expert only considers the hamstrings.” Maybe my search criteria was wrong or maybe Mr. Mash hasn’t yet defined his argument to anything intelligible. Here’s hoping he gets it together in a few paragraphs. Then, this useless nugget comes in:

“In contrast, Gray Cook, the best Physical Therapist, is changing all of that. Gray teaches movement and how muscles work synergistically. “

Synergy in the musculoskeletal system can be defined as the interaction of multiple muscles together to produce an effect greater than the sum of their individual effects. An example would be to use the low bar back squat with proper hip drive so you can use your hamstrings to a greater degree, whose force production will be added to the force created by the glutes, adductors, etc. Wow, this sounds almost exactly like what we teach at our seminars and what is written in the book that Travis claims is “awesome.”

Mr. Mash continues to provide us with other gems in his article:

“If you want to know how to squat properly, look at a two year old. They sit their butts between their ankles, maintain a vertical back, and they will not lift the butt or hips first.”

This is what’s classically known as an informal fallacy in that the structure of the argument is fine, but the conclusion is bogus. Is Mr. Mash really contending that the most optimal way to squat is the way in which a 2 year old squats? What does he consider optimal? We contend that the most optimal squat is the one that results in training the most amount of muscle mass, uses the most effective range of motion, and results in the highest force production and can subsequently be loaded the heaviest. Mr. Mash’s assertion that the way a 2 year old squats, which he defines as having the “butt between their ankles with a vertical back” results in decreased muscle mass usage, as at this depth the hamstrings are slacked to a much greater degree and cannot contribute to hip extension as effectively and thus, do not receive as potent a training effect. Moreover, because this style of squatting, i.e. ATG “2 year old style”, would undoubtedly lead to less weight on the bar, less force production can be trained and less strength-which is a general adaptation that can apply widely- will be accrued. The counter argument that is sometimes made to this when we go down this rabbit hole is why not use quarter squats then, as you can load them far heavier than a to-depth squat of any variety. We cannot forget about our first criteria for the most optimal form of each exercise, which is to train the most amount of muscle mass possible. A quarter, half, or other partial exercises result in decreased training of the hamstrings and glutes, which has been routinely demonstrated in published scientific literature.

So, Mr. Mash’s initial argument is bogus to begin with and just when you think it couldn’t get any worse:

“Not to mention we all learned in intro level Geometry that two levers are better than one, and Rippetoe teaches to shift all loads onto the hip lever. “

How exactly are two levers better than one and how did Mr. Mash come to the conclusion that Rip and Co. teaches the squat in such a way that “shifts all the loads onto the hip lever”?* If Mr. Mash had read the book, Starting Strength: Basic Barbell Training 3rd Edition, he would realize that his statements have no basis in reality. We properly define the levers as they apply to the trunk and lower limb as follows:

-The “trunk” lever- The horizontal distance between the barbell and the hip joint.

-The proximal femur lever- The horizontal distance between where the barbell bisects the femur and the hip joint

-The distal femur lever- The horizontal distance between where the barbell bisects the femur and the knee joint.

All these levers are defined and described in great detail in the book and Mr. Mash is incorrectly coming to the conclusion that because Rip talks about hip drive that he wants no distal femur lever arm and a maximal proximal femur lever. In actuality, these values are pretty much set in stone depending on the length of your femur, trunk, and where you place the bar. The argument that we make is that in the low bar back squat, the proximal femur lever is longer than it would be in the high bar back squat because IT IS. We further argue that we desire this long-er lever arm because the hip joint has more available musculature and soft tissue surrounding it so that it can both absorb the higher force values AND create more force during the concentric portion of the squat. In sum, we seek a long proximal femur lever by choosing the low bar back squat so that more of the stress is absorbed by the hips, which can create more force anyway. We do not actively seek the elimination of the distal femur lever and this does not occur in the version of the squat we teach anyway even with people of weird limb lengths.

In a high bar back squat, the proximal femur lever gets shorter (less force on the hips) and the distal femur lever gets longer (more force on the knees). Since there is a reduced moment arm acting about the proximal femur lever, the muscles acting on the hip cannot generate as much force and less weight is lifted. Concomitantly, the high bar squat also produces increased forces and shear on the knee, which may or may not be a training consideration to make when programming for your stable of lifters.

As for your silly assertion that “two levers are better than one”:

Archimedes said :“Give me a place to stand and a lever long enough, and I shall move the world”, which refers to one lever. He’s probably a “rookie” too, right?

*Bonus points if you think Mr. Mash could correctly define the hip lever.

Next, Mr. Mash attempts to gain credibility by listing high level powerlifters who “know that the technique that Coach Rippetoe teaches is the very technique that we all avoid.” Let’s see who he lists:

“I have watched videos of all the great squatters in history: Ed Coan, Steve Goggins, Dan Green, Chad Wesley Smith, Shane Hammons, and Kirk Karwoski. “

Besides misspelling Shane Hamman’s name, does Mr. Mash realize that all of these lifters use the low bar back squat with hip drive? You know, the exact same technique that Rippetoe coaches and writes about? Does he know that Shane Hamman (fixed that one for ya’ rookie), Kirk Karwoski, and Ed Coan all have interviews on the Starting Strength site- seemingly lending credibility to idea that they agree with the technique advocated on the site.* Rip has even stated publicly that Dan Green’s squat is right in line with the hip drive he teaches, even if it’s not consciously done:

“No one ever said they were consciously thinking about driving their hips up. I’m sure that most of them are not. But they’re doing it anyway, because that’s how you get out of the bottom, and the longer you stay in the hip drive the more powerful the squat. My point is that they should be thinking about it, and that when you do you squat more efficiently. “

*This is me providing an informal fallacy of sorts, though it might actually be true as I haven’t asked them yet.

I’m not so sure that Mr. Mash’s assertion that the following is true at all:

“All great squatters know that the technique that Coach Rippetoe teaches is the very technique that we all avoid. “

Seems to me like they all use it whether they know it or not. A really poorly written article always needs some chest thumping and ad hominem attacks to keep readers interested and Mr. Mash did not disappoint:

“ I know all of these people, and I have talked squat with the best in the business. I have squatted 805lbs raw, 900lbs single ply, and 970lbs multi-ply and all at 220lbs.”

“ The position that he [Rippetoe] preaches is what we all call the “point of no return”, or where we are about to get crushed. At first I couldn’t believe that a power-lifter would preach this form, until I looked up his best numbers: Coach Rippetoe only squatted 611 lbs in a single ply squat suit at 220lbs. Rippetoe just doesn’t know any better. Rookie.”

Travis is a strong dude, no doubt about it. But how is it that having a better squat entitles someone to a better mechanical analysis, which is very cerebral in nature? While I’ll agree that a coach should have a good background in training him or herself, the degree to which these two coaches (Mash and Rippetoe) differ are not due to different “squat mechanics”. Rather the difference seen here, which is often under appreciated in people coaching high level athletes, is that some people are just very blessed in their ability to respond to a training stimulus. I could of course, opine about how Rip’s 611 was in a single ply squat suit from the 80’s which would pass for a singlet in comparison to modern-era equipment, but that’s not the point of showcasing how silly Mr. Mash’s belief is here.

He’s trying to make the case that because he “knows all of these people” and “has squatted 805 raw, 900lbs single ply”, etc. that his evaluation of the mechanics in the musculoskeletal system are better than someone else’s. I’d posit that a person with a PhD in kinesiology or biomechanics could easily analyze the barbell lifts and come up with a very sound analysis even if they have never trained. When you take a good chunk of training and coaching and put that on top of a knowledge base involving physics and human anatomy well, the analysis goes a lot smoother and additional insights will be made even if you never squatted 900. And let’s be real for a split second, while the gap between 611 and 900 is certainly vast, we’re still talking about the top 0.5% of human strength here, which is to say it really doesn’t matter if you squat 300lbs more provided you have actually trained your squat in the first place.

Let’s gear up for a couple more illogical arguments:

“I would like to coach Rippetoe myself, I could teach him how to have a decent squat.

You don’t have to have an elite squat to teach, but if you are going to be the self-proclaimed guru of the squat, then you need to be legit at least, not a rookie. (HQ should have checked him out first.) “

Let’s have a long hard look at this second sentence, shall we? Mr. Mash seems to contradict his earlier sentiments where he denigrated Rip’s 611 squat with the intent to assert himself as the subject matter expert, but then he turns around and says you don’t have to have an elite squat to teach- as long as you’re legit. So, I’m not sure exactly what “legit” is being defined as other than the fact that it’s not necessarily “elite”. I also don’t know how you can call a guy who has been doing this for 35+ years a “rookie”, but that seems to be his go to insult. Let’s see what other useful analysis Mr. Mash can provide:

“Even more infuriating is that this rookie is charging $600 per person to teach them how to squat incorrectly. Hey Crossfit community, stop giving your money to a phony rookie. “

If you’re going to try to bash someone, at least do it correctly. We’re currently charging 795-895 per slot at the seminar. See, if you only charge $125 like Mash does for his Learn to Lift Seminars you just know the info is bogus, right?* CrossFit charges $1000 a head for their weekend seminar where you don’t learn any technical analysis of the lifts, legitimate nutrition or programming information. On the other hand, you do get to see lots of Lululemon and do snatches with a PVC pipe so maybe that’s the real draw.

*Another illogical fallacy. Just keeping you guys awake here. Don’t worry we’re almost through so you can repost this 🙂

Moving along, Mash goes on to say:

“I know a lot of people are going to be upset about the harshness of this article, but this has to be said. If you are going to a seminar, watch some videos of professionals performing the movements. Then if the person teaching the seminar is teaching something completely opposite, leave the room immediately. World record holders and world champions lift weights a certain way for a reason: because it is the best way. There are a lot of seminars out there with great information, so do your research.”

“Here are three questions to consider about the presenters:

  1. What is their background?

  2. What is their education?

  3. Who have they coached?”

Here’s why 1 and 2 are good criteria, but 3 is not really helpful. 1 and 2 tell you how much legwork the coach/presenters have done and what kind of population they’re familiar with and who/what they cater to. Number 3 doesn’t help you because the people that get coached and perform at the highest levels often do well in spite of what they do. In other words, their coach is likely taking credit for their athlete’s awesome achievements even though the coach didn’t really do anything besides keep the athlete healthy. This happens all the time at the college and pro level, so it’s no surprise Mr. Mash feels this way. World record holders lift weights certain ways because they can, not because it’s optimal. There are great pitchers in the MLB who throw side arm, but no one would argue that this is the best way to throw a baseball.

And now, Mr. Mash wants a good ol’ fashioned high bar vs low bar argument:

“If your goal is to improve in Olympic weightlifting or athletic performance, the high bar back squat is best for maximal depth and range of motion. If your goal is maximal weight in powerlifting, then low bar is better for a center of gravity advantage.”

First you’d have to consider why an Olympic lifter is squatting in the first place, right? Hopefully the answer is to “get stronger” and the reason they use the back squat in addition to the front squat is because you can get stronger, faster, with the back squat as it can be loaded heavier than the front squat. The front squat is specific to the clean recovery whereas the back squat is not specific to the clean or the snatch (when high bar mechanics are used). So if we’re trying to use a squat variation that allows for the most efficient increase in strength we should use the LBBS for the following reasons:

-It uses more muscle mass than the HBBS or FS, as the hamstrings and muscles of the back get more training effect, which makes them stronger.

-The LBBS is more specific to the competition lifts than the HBBS. The HBBS does not replicate the receiving and/or recovery positions of the clean or the snatch with respect the angle of the torso. Nor do the torso and joint angles resemble the mechanics of the first pull. The LBBS, on the other hand resembles the snatch recovery position (see the earlier Dolega video) and the angle of the torso of in the competition lifts’ first pull. If specificity is your argument for use of the HBBS in addition to the FS, well…that’s not a very good one as you can see. Yes, the HBBS is more similar to the clean recovery than the LBBS, but the FS is more specific than that and you are training your front squat if you’re an Olympic lifter, right?

-The LBBS allows more weight to be lifted in training. Since the back squat is not a competitive lift or integral portion of either the clean or snatch recovery (unlike the front squat), then the variation of the other squat used in addition to the front squat should be the one that provides the most efficient increases in strength, since, ya know…that shit is important.

-Olympic lifters tend to get overuse injuries in their knees from aggressive receiving positions in the clean, snatch and the jerk. The HBBS puts more stress on the knees, as was discussed earlier and this might be an important training/programming consideration for an athlete, unless you’re a rookie.

Pretty standard argument really. You just need to think more and type less, Mr. Mash. It’s good for you. Let’s see what else we’ve got here:

“Absolutely lift your chest first when coming out of the bottom of a squat.”

Definitely don’t do this unless you want to kill hip drive and miss the rep. Wonder why Coan, Kirk, Mike T, Hamman, et. al don’t do this?

Here is a classic example of someone who has not read the material he is attacking:

“Knees and hips should lock out at approximately the same time; the last place that you want to be is with your hips as high as your shoulders or even close to that position.

When the hips shoot up like Rippetoe teaches, all the weight is shifted to the low back and most of the time the bar pulls the lifter forward, “the point of no return”

[bolded parts added for dramatic effect]

This is not actually what Rip and Co. teaches or writes about. We teach that the hip drive should be consciously focused on in such a way that produces the maximum force production out of the bottom of the squat. This maximal force production would ideally be transferred through a rigid spine so that no power leak occurs and the hips and chest rise together at the same rate. Doing it any other way, i.e. hips up without the chest or “lead with the chest without the hips” would result in suboptimal force production and lifting mechanics.

We do not teach “hips up first”, which you would know if you would’ve read the book, come onto the forums, or done any sort of research at all before you began your intentional character assassination designed to increase you and Chad Wesley Smith’s readership. More on that later, we’ve got more bro to flame here:

“Muscles were designed to work synergistically, and in the squat the quadriceps are attempting to extend the knees while the hamstrings and glutes are extending the hips. The muscles were designed to work together at the same time, maintaining two fulcrums at the knee and hip until completion. They were never designed to work independently.”

Muscles weren’t designed to do anything besides contract. They’ll do so in isolation and they’ll do so as part of a complex movement. They’ll synergistically contract if they share a common function or movement, i.e. the glutes’ force plus the hamstrings’ force in getting out of the bottom of the squat. I’m not sure why you’re under the impression the Rippetoe teaches that muscles should work independently because again, this is not even close to what is written in the book or presented at our seminar.

And to finish, some stuff is so good that I couldn’t even make up if I tried:

“I spent last Monday night Skyping with one of the best Olympic weightlifting coaches in America (I will leave him anonymous to protect him from the fallout of this article). He agreed that this article needed to be written because this Rippetoe thing has gone way too far.

Ah, good, you talked to Glenn Pendlay who undoubtedly gave you the low down. Nevermind the personal feud between them and ignore that Glenn is an Internet troll who has been making up fake aliases and talking to himself online for years in order to bolster his own credibility.* Seems like a good place to get an unbiased opinion from in order to get all your ducks in a row for presenting your carefully thought out argument. Please read this thread to see Glenn trolling and getting caught just a few months ago.

*See, that was what an ad hominem attack looks like.

Wow, look how far we’ve come! I really didn’t want to have to write this article and in truth, I wasn’t going to because after reading the comments on the JTS site on the article it was very apparent that anyone with half a brain saw how poorly this article was written and the fallacies inherent to literally every single one of Mr. Mash’s “points.” It’s rare that you can’t find anything good in an article or video so I’ve got to hand it to Mr. Mash and Mr. Candito for doing a smash up job on their contributions.

In writing this, however, I got to thinking about how it would be possible for such an experienced lifter and coach to actually believe the nonsense he was writing. I mean, he did squat 800 raw, which clearly makes him an expert here, right? I ended up coming to the conclusion that Mr. Mash actually wrote this drivel incorrectly on purpose in order to get more traffic to the JTS site and his own website. Then I started thinking that the only reason CWS would put this up knowing that people aren’t in fact brain dead, is because he knew it would blow up over the Internet and that’s good for business. CWS ended up writing a poorly worded apology after he took the article down and then he had the balls to take the apology down after he started deleting comments criticizing the article or questioning the author. Basically they’re trying to cover the whole thing up, which is a cowardly move if I’ve ever seen one. Listen folks, when you screw up- you screw up, but you have to face the music and take your lumps as you own up to your mistakes. Time to face the music, fellas.

-thefitcoach

Booze and Barbells Part II

By Jordan Feigenbaum MS, Starting Strength Staff, CSCS, HFS, USAW CC

In case you missed part one of this three part series, click here. In today’s blog entry we’re going to talk about how alcohol affects skeletal muscle and the sex steroid, testosterone. Things can get pretty complicated in a hurry here, but what I aim to do is provide some basic science background for my readers as well as how a certain stressor, i.e. alcohol, can alter the internal milieu. I actually just used the words “internal milieu”, which describes the internal environment of the human body just so I could provide the following quote to pay homage to my previous physiology professors:

“The stability of the internal environment [the milieu intérieur] is the condition for the free and independent life”- Claude Bernard

The concept of the internal environment being important for physiological normalcy and a rationale for the human body’s homeostatic underpinnings was later expanded upon by Walter Canon’s characterization of homeostasis in 1932. He [Canon], proposed four characteristics of homeostasis as follows:

  1. Constancy in an open system, such as our bodies represent, requires mechanisms that act to maintain this constancy. Cannon based this proposition on insights into the ways by which steady states such as glucose concentrations, body temperature and acid-base balance were regulated.
  2. Steady-state conditions require that any tendency toward change automatically meets with factors that resist change. An increase in blood sugar results in thirst as the body attempts to dilute the concentration of sugar in the extracellular fluid.
  3. The regulating system that determines the homeostatic state consists of a number of cooperating mechanisms acting simultaneously or successively. Blood sugar is regulated by insulin, glucagons, and other hormones that control its release from the liver or its uptake by the tissues.
  4. Homeostasis does not occur by chance, but is the result of organized self-government.

It is important to appreciate the homeostatic mechanisms that the human body possesses in order to maintain an “even keel”, as without redundant pathways in place things can go awry in a hurry. At any rate, while the overall concept of the internal milieu and it’s influences on homeostasis are critically important, further discussion of it would preclude our look at just how alcohol/ethanol can alter skeletal muscle metabolism and testosterone levels. To begin, let’s talk a bit about skeletal muscle.

One of the most common effects of alcohol on striated muscle, i.e. skeletal and cardiac muscle, is fiber atrophy or reduction in size. Skeletal and cardiac muscle are both striated, as they have repeating sarcomeres and appear (under the microscope) to have alternating “light” and “dark” bands.

Screen shot 2013-06-12 at 6.07.19 PMSmooth muscle on the other hand, which is found in lots of places like the walls of the vascular system and the GI tract, do not appear striated under a microscope because they lack the organized, repeating structure of the sarcomere.

At any rate, striated muscle size is a result of the balance of protein synthesis and protein breakdown. In other words, the net flux of protein reflects the protein being built (synthesized) and deposited minus the protein being broken down and metabolized. If something were to either increase protein synthesis or inhibit (prevent) protein breakdown, their would be a net gain in protein levels. On the other hand, if the rate of protein breakdown is increased OR the synthesis of new protein is inhibited, there will be a net loss of protein. In general, a net gain of protein within muscle tissue results in hypertrophy (increased size) and a net loss of protein in the muscle tissue results in atrophy.

Ethanol tends to decrease striated muscle protein synthesis [1]. Interestingly, the resulting atrophy appears to be greatest in Type IIB fibers, which are a subtype of the fast-twitch muscle fibers that produce high amounts of force, contract rapidly, and are anaerobic. Some researchers actually classify type II muscle fiber atrophy as part of a diagnostic criteria of alcoholic myopathy, however this selective decrease in size also occurs in other issues like calorie malnutrition, neuropathy, etc. Additionally, only about 33% of chronic asymptomatic alcoholics show significant type II fiber atrophy without malnutrition, neuropathy, etc. although other studies report 40-60% of alcoholics presenting with significant atrophy [1]. Urbano et al. goes head to head with Preedy et al in the following quotes:

In fact, it [ethanol] is the most frequent cause of toxicity to striated skeletal and cardiac muscle in adults in dose dependent fashion [1].

“Due to the ethanol-induced reduction of muscle phosphorylase activity, decreased rates of protein synthesis and whole-body protein metabolism by 15–30%, predominantly in type II fast-twitch anaerobic fibers that utilize glycolytic metabolism.Type I fibers were not overly affected and there was no clear decrease in muscle protein breakdown [5].

As far as how this occurs on a cellular level, it appears as though ethanol consumption disrupts the translation of would-be muscle-protein RNA, but not it’s transcription. For background information, muscle protein synthesis signalers (like eating a protein-rich meal or training) increase the transcription of certain DNA to muscle protein RNA. Muscle protein RNA is then translated into muscle protein, which is shuttled to it’s target and deposited as muscle. Through increased binding of a variety of different regulatory sites on the muscle protein RNA, translation is decreased and total muscle protein synthesis decreases [2].

Measuring decreases in total muscle protein synthesis can be tricky in the laboratory settings, as most of the time a total nitrogen balance measurement is used. Remember, protein is the only macronutrient with nitrogen as a component. Therefore, it intuitively makes sense that the amount of nitrogen taken in minus the amount of nitrogen excreted can give insight into the nitrogen balance of a person or animal. Unfortunately, some people take this sort of information as definitive with regards to what is actually happening in the muscle specifically. Remember, all tissues (lungs, gut, kidney, visceral organs, etc.) are made up of protein, which are also turned over regularly and thus influence total body protein and nitrogen balance. Lang et. al. provide a nice quote describing this:

However, whole body measurements represent the sum of many vastly different organ systems (e.g., muscle and nonmuscle protein synthesis and hepatic secretory protein synthesis) and provide little information concerning individual processes or tissues.

So while total body nitrogen balance tells us what’s happening on a body wide or systemic level, it does not tell us what’s happening in just the muscle tissue. Muscle protein turnover, in sum, makes up less than 30% of total body protein turnover anyway [3]. Other studies, however, have shown that with acute alcohol intoxication muscle protein synthesis decreases in skeletal muscle, heart, intestine, bone, and skin. Additionally, chronic ethanol exposure has been demonstrated to decrease skeletal muscle protein synthesis in rats [4, 5]. It appears that ethanol exposure is potentially harmful to overall protein synthesis, as described in the following quote:

“However, experimental and clinical studies have clearly demonstrated that ethanol itself is a direct noxious agent to heart and skeletal muscle in a progressive, cumulative, and dose-dependent manner, an effect independent of nutritional, vitamin, or mineral factors.”-[Nguyen et al. (6)]

There are only a couple of things left to discuss with respect to actual skeletal muscle function and ethanol. First, muscle glycogen concentration tends to increase in chronic alcohol patients because glycogen cannot be degraded as efficiently. This is due to a partial inhibition of the biochemical pathway for glycogenolysis (glycogen breakdown) as well as glycolysis (glucose breakdown) [5]. In contrast, acute alcohol exposures tend to decrease glycogen storage, especially post workout as some of the mechanisms used to store glycogen in skeletal muscle are inhibited and instead fatty acid production is increased. These effects are independent of acetaldehyde toxicity, which was discussed in part one of this series [5].

Ethanol and acetylaldehyde also tend to increase formation of reactive oxygen species due to their effects on vitamin metabolism. Reactive oxygen species (ROS) tend to increase cellular damage and stress in the skeletal muscle, thus increasing damage to cells of the muscles which may increase atrophy.

Moving along, let’s start our discussion about alcohol and testosterone production by covering the general overview of testosterone production in vivo (in the body). This will give us some background to what is normal so we can consider the effects of ethanol on the internal milieu and homeostasis.

Gonadal-AxismennewestNormally, males produce testosterone in the Leydig cells of the testes from cholesterol via increasing leutinizing hormone (LH) activity within the testes. LH increases an enzyme called cholesterol desmolase, which is responsible for converting cholesterol to pregnenolone. Pregnenolone will go on to be converted through various enzymes to testosterone and thus, but first it needs to be formed from cholesterol. Thus, increasing the enzymatic activity of cholesterol desmolase helps to increase testosterone production.

Naturally, one would ask well what increases LH? Gonadotropin releasing hormone (GnRH) is secreted by the hypothalamus in the brain. GnRH is released into blood vessels that carry this peptide to the anterior pituitary gland (hypothalamic-hypophysial portal system). GnRH is normally secreted in a pulsatile fashion, i.e. it is not constant. It acts on certain cells in the anterior lobe of the pituitary gland (gonadotropes) to cause them to manufacture and release LH, which is also released in a pulsatile fashion. LH is released into the systemic (body-wide) circulation where it ends up traveling to the testicles and causing the Leydig cells to pump out testosterone, as described above.

As discussed at the beginning of this post, most, if not all of the body’s pathways are tightly regulated to keep it on an “even-keel”. Let’s explore this now that we know the testosterone-producing pathway. Testosterone produced by the Leydig cells provides what’s known as “negative feedback” on the hypothalamus and cells of anterior lobe of the pituitary, effectively decreasing secretion of GnRH and LH. Thus, when testosterone levels are high, GnRH and LH levels are low. Conversely, when testosterone levels are low, the frequency and amplitude of GnRH pulses are increased. A downstream effect of this is increased LH release and thus, increased signaling to the Leydig cells to produce more testosterone because the negative feedback signaling is removed.

As we’ll see in the upcoming discussion of ethanol’s effects, perturbation at any level of this pathway can result in deleterious effects. So, how does ethanol affect testosterone production and/or signaling?

As it turns out, ethanol exposure appears to lower GnRH levels, which leads to reduced LH secretion from the anterior pituitary and reduced testosterone production by the Leydig cells of the testes [7]. Mechanistically, this occurs because a hormone normally produced in the testes and hypothalamus at very low levels, β-endorphin (an endogenous opiod), normally only slightly suppresses testicular testosterone production and release. In the hypothalamus, β-endorphin results in decreased GnRH release. Adams and Cicero have shown an increase in β-endorphin after acute alcohol exposure [10]. Naltrexone, a treatment currently used in alcoholism to decrease alcohol cravings, blocks B-endorphin activity and may prevent reduced testosterone levels. Three other ways ethanol affects active GnRH levels is through acetalaldehyde, which is toxic, disturbing nerve impulses outside the hypothalamus that signal GnRH production WITHIN the hypothalamus, and finally, ethanol appears to interfere with processing of the inactive GnRH precursor to the active GnRH form according to Uddin et al.

LH levels actually decrease with alcohol exposure, which is not what we’d expect. Harkening back to our homeostatic mechanism discussion, if testosterone production falls, we’d expect GnRH and LH levels to increase to “right the ship”. However, as discussed above GnRH levels actually decrease and so do LH levels. Mechanistically, the decreased LH levels appear to be due to the toxic affect of ethanol directly on the anterior pituitary gland where LH is released by interfering with GnRH’s signaling of LH production in the cells that they act on (gonadotropes). Another effect of ethanol on LH that causes it’s decrease is that alcohol in the blood tends to result in the anterior pituitary gland’s production of less potent LH variants, thus decrease the level of LH in the blood and the quality of LH in the blood too.

A study done by Steiner and colleagues in 1996 found that when males were given a 15-percent alcohol solution that was administered every 3 hours, around the clock, together with a diet replete with protein, vitamins, folic acid, and minerals (total daily alcohol dose was 220g or 3g/kg body weight, which equals 15 drinks) that the testosterone levels in the men’s blood declined 5 days into the study and continued to fall over the entire period. This was attributed to a decrease in testosterone production in the Leydig cells of the testes and increased removal rate of testosterone from the blood via catabolic processes. On the other hand, Southren et al. found that the increased testosterone catabolism or breakdown is only present in men without liver disease, whereas the clearance is decreased in men with liver disease.

Numerous studies in human and animal models have since confirmed reduction in testosterone levels after either acute or long term alcohol exposure. Acute alcohol ingestion appears to result in a significant reduction in testosterone levels that lasted for 96 hours in a rat model [9].

Sarkola and Eriksson actually found that testosterone can increase in men exposed to a low dose of ethanol, although this is a transient effect due to the predomination of decreased liver clearance of testosterone from the blood compared to the decreased testosterone production in the testes. Unfortunately, during the latter stages of elimination of alcohol or when alcohol has been completely eliminated, testosterone production decreases even more. Similarly, in higher doses of alcohol consumption, e.g. 1.5g/kg, the decreased production of testosterone predominates over the transient decreased clearance rate of testosterone. This has been confirmed by experiemental evidence from Välimäki et al in 1990 and Ylikahri et al. in 1974 [10].

Another interesting finding is that alcohol abuse and subsequent impaired testosterone production tends to result in testicular atrophy/shrinkage, which occurs in about 75% of men with advanced cirrhosis [10]. The atrophy most likely results from the toxicity on the testes, decreased LH and FSH production, and other confounding factors causing decreased sperm cells and sperm production.

Finally, and perhaps one of the more important ways alcohol effects testosterone’s activity and blood levels is that ethanol exposure tends to increase aromatization of testosterone and testosterone precursors. Aromatase is an enzyme that converts testosterone to estrogen and thus, increased aromatization results in increased conversion of testosterone to estrogen. Additionally, the immediate precursors to testosterone, androstenedione (Mark McGwire?) can be “aromatized” to another estrogen subtype called estrone. Scientific evidence points to this “increased aromatization” as a byproduct of increased estrogen production and not a decrease in estrogen clearance [10]. Aromatization is not a good thing above physiological normal (homeostatic) levels in men, as the authors conclude:

“In addition to causing breast enlargement, estrogens appear to exert a negative feedback effect on LH and FSH production and may thereby contribute to alcohol’s suppression of those key reproductive hormones.”

While alcohol certainly has some benefits, which we’ll get to I PROMISE, it’s important to know the deleterious effects that alcohol can have on the internal milieu, especially as it pertains to training. Again, I’ll leave you with my favorite axiom related to alcohol consumption and training:

“If you’re drinking enough to get drunk, you’re drinking enough to mess with your results.”

 

Until next time.

-thefitcoach

1)  Urbano-Marquez, A.; Fernandez-Sola, J. Effects of alcohol on skeletal and cardiac muscle. Muscle Nerve 2004, 30, 689-707.

2) Lang, CH, Wu, DQ,  Frost, RA. Inhibition of muscle protein synthesis by alcohol is associated with modulation of eIF2B and eIF4E. American Journal of Physiology-Endocrinology and Metabolism 1999, 277, 268-276.

3) White JP, Baynes JW, Welle SL, Kostek MC, Matesic LE, et al. (2011) The Regulation of Skeletal Muscle Protein Turnover during the Progression of Cancer Cachexia in the ApcMin/+ Mouse. PLoS ONE 6(9)

4) Preedy V. R.,Peters T. J.,Patel V. B.,Miell J. P. (1994) Chronic alcoholic myopathy: transcription and translational alterations. FASEB J. 8:1146–1151

5) Preedy V. R., Peters T. J. (1990) Changes in protein, RNA, DNA and rates of protein synthesis in muscle-containing tissues of the mature rat in response to ethanol feeding: a comparative study of heart, small intestine and gastrocnemius muscle. Alcohol Alcohol. 25:489–498.

6) Nguyen VA, Le T, Tong M, Silbermann E, Gundogan F, de la Monte SM. Impaired Insulin/IGF Signaling in Experimental Alcohol-Related Myopathy. Nutrients. 2012; 4(8):1058-1075.

7) Vatsalya Vatsalya, Julnar E. Issa, Daniel W. Hommer, and Vijay A. Ramchandani. Pharmacodynamic Effects of Intravenous Alcohol on Hepatic and Gonadal Hormones: Influence of Age and Sex. Alcohol Clin Exp Res. 2012 February; 36(2): 207–213.

8) Sarkola, T. and Eriksson, C. J. P. (2003), Testosterone Increases in Men After a Low Dose of Alcohol. Alcoholism: Clinical and Experimental Research, 27: 682–685

9) Steiner, J., Halloran M.M., Jabamoni K., Emanuele, N.V., Emanuele, M.A. Sustained effects of a single injection of ethanol on the hypothalamic-pituitary-gonadal axis in the male rat. Alcoholism: Clinical and Experimental Research 20:1368–1374, 1996.

10) Emanuele, N.V., Emanuele, M.A. (1998) Alcohol’s Effects on Male Reproduction. The Alcohol and Other Drug Thesaurus. Vol. 22, No.3.

Booze and Barbells Part 1

By Jordan Feigenbaum MS, CSCS, HFS, USAW CC, Starting Strength Staff

And I hate running...

And I hate running…

One of the most common questions I get with regards to nutrition and/or training pertains to alcohol and how it effects potential performance, health, or aesthetic outcomes. I get asked this question so often that I’m dedicating an entire chapter of my book to the stuff. Instead of sharing part of the manuscript on here, I thought I’d post up a truncated version of my thoughts and findings on the subject, which will actually be broken up into three separate blog posts on this blog as well as my new website. Consider this advertising for what sort of cool things go on over on that site. You should join, methinks, to get some good information 🙂 Now, let’s talk about booze!

Let’s begin by defining alcohol as a dietary component. An average “drink” has approximately 14 grams of pure alcohol (ethanol) within it, which is in addition to all the other stuff in the drink, i.e. mixers, flavorings, etc. At any rate, a drink is defined by the volume of substance that has 14g of alcohol in it. This metric equates to the following serving sizes:

Screen shot 2013-06-02 at 12.02.08 PMor equivalently:

  • 12-ounces of beer.
  • 8-ounces of malt liquor.
  • 5-ounces of wine.
  • 1.5-ounces or a “shot” of 80-proof distilled spirits or liquor (e.g., gin, rum, vodka, or whiskey)

So now that we have defined our terms of what an actual drink is, what exactly happens to the good stuff when we’re out at happy hour? Orally ingested alcohol is transported through the proximal digestive tract intact, i.e. it is not broken down, metabolized, or otherwise changed until it gets into the stomach. The amount of alcohol that gets to the stomach is very high compared to other parts of the digestive system like the duodenum or other parts of the small intestine. Due to this high concentration, approximately 40% of alcohol is metabolized (broken down) in the stomach within the first hour following initiation of drinking. Within about 2 hours, up to73% of the total alcohol that was ingested has been metabolized in the stomach [1]. Alcohol absorption, on the other hand, takes place in both the stomach (slow) and small intestine (rapid). The total amount of alcohol metabolized and absorbed in the stomach depends on the rate of emptying of the stomach, which is influenced by lots of things. At any rate, the stomach’s metabolism of alcohol in humans plays an important role in First Pass Metabolism.

Some of you science-minded folks might be thinking, Wait, the STOMACH metabolizes and absorbs alcohol? I thought that absorption occurred in the small intestine! Yes Virginia, this is normally correct. However, it has been shown that the stomach’s lining, more appropriately termed the gastric epithelium, contains a version of the enzyme alcohol dehydrogenase (ADH). This version, σ-ADH, is not present in the liver. breaks down ethanol into acetylaldehyde, which is the metabolite in the overall metabolism of ethanol. Different types of alcohol dehydrogenase (ADH isoforms) are present in the liver, but σ-ADH is only found in the gastric epithelium.

So how do we know that alcohol is actually metabolized and absorbed in the stomach and what sorts of things affect this? Blood alcohol levels, i.e. the amount of intact ethanol in the blood after ingestion, changes under certain conditions. When alcohol is ingested orally, lower blood alcohol levels are seen than when alcohol is given intravenously [2]. This is due to the first pass metabolism occurring in both the stomach and liver, as both of these organs have high levels of alcohol dehydrogenase. Because the ethanol is metabolized and degraded into acetylaldehyde, as mentioned above, there is less of it that actually enters the blood stream and thus, less alcohol in the blood. These facts, however, do not tell us the importance of the stomach’s metabolism of ethanol. For that, we must dig deeper.

Aspirin and H-2 blockers (histamine receptor blockers) both decrease σ-ADH activity in the stomach, which results in less ethanol being metabolized to acetylaldehyde. These drugs also increase the rate at which the stomach’s contents are emptied into the small intestine. Both of these factors, i.e. less ADH activity and faster emptying, result in higher blood alcohol levels in humans. Interestingly, Japanese persons have lower σ-ADH activity naturally and thus, first pass metabolism is significantly compromised and blood alcohol levels are higher at a given dose than their non-Japanese counterparts [2].

You might be wondering what other sorts of things influence stomach emptying, you know, in case you wanted to see higher blood alcohol levels get drunk quickly. Fasting accelerates emptying, which results in less exposure of ethanol to the σ-ADH in the stomach and more rapid absorption of ethanol in the small intestine. On the other hand, consuming a high fat meal alongside alcohol significantly delays emptying and absorption of food. In general, the effect of food on alcohol metabolism and absorption, i.e. increasing metabolism and delaying absorption, is primarily due to the slowing down of gastric emptying. Alcohol content also influences rate of absorption, with maximum absorption occurring  with consumption of a drink containing approximately 20-25% alcohol  on an empty stomach. The absorption rate may be less when a 40% alcohol solution is consumed on an empty stomach. The rate may also slow down when high fluid volume/low alcohol content beverages, such as beer, are consumed.

So we know that a varying amount of ethanol is metabolized in the stomach and a small amount is absorbed there as well. What happens to the ethanol that remains untouched and makes it to the small intestine? Ethanol in the small intestine, which is made up of the duodenum, jejunum, and ilieum from proximal to distal, is generally absorbed by diffusion from the inside of the GI tract’s lumen into the cells lining the tract, the enterocytes. Mechanistically, this likely occurs due to the high permeability of cells to pure alcohol/ethanol and it also appears that certain simple sugars (monosaccharides and disaccharides) like glucose, galactose, sucrose, etc. also increase the rate of absorption of ethanol in the small intestine. Carbohydrates are all eventually broken down into glucose, galactose, and fructose and are absorbed via sodium-dependent transport, i.e. sodium is concomitantly transported with the sugars. Carbohydrate absorption likely increases alcohol absorption through electrochemical gradient changes. This means the sugar containing margarita likely gets into your bloodstream faster than pure ethanol. Unfortunately, lactose, the main carbohydrate in milk, does not increase absorption rates [3].

Ethanol moves from the lumen of the GI tract, into the enterocyte, then into the veins supplying the gut, which drain into the liver as the portal circulation.

Ethanol moves from the lumen of the GI tract, into the enterocyte, then into the veins supplying the gut, which drain into the liver as the portal circulation.

Once into the enterocyte, ethanol diffuses into the veins suppying the enterocyte and is carried to the liver as part of the hepatic (liver) portal circulation. Once in the liver, ethanol diffuses from the venous blood into the liver cells, aka hepatocytes, where the majority of ethanol metabolism will finally occur. In the liver cell ethanol will encounter another isoform of alcohol dehydrogenase and get oxidized into acetylaldehyde. This enzyme, alcohol dehydrogenase, can become saturated at certain levels of ethanol ingestion and thus, extra ethanol will spillover into other metabolic pathways in order to be eliminated from circulation. While not particularly important to our discussion on the effects of booze on training, for the sake of completeness these other liver pathways include Microsomal Ethanol Oxidized System (MEOS)/Cyp2E1 (functions primarily during high levels of ethanol intake) and catalase (minor). An important take way from this is that ethanol must be metabolized or eliminated from the body, as  it cannot be stored and serves no particular purpose. That should beg the question, why do we even have mechanisms and pathways in our body to eliminate ethanol anyway?

Alcohol dehydrogenase and the downstream pathways used to eliminate ethanol from circulation are believed to originate out of necessity due to the small amount, i.e. 3g or so, of ethanol produced daily by resident bacteria in the intestinal tract via fermentation and other biological processes [4]. Similarly, only a small amount (2-10%) of ethanol is eliminated through the lungs and kidney, so the rest must be metabolized in the liver, stomach, etc. Maybe booze isn’t so Paleo after all? 🙂

paleo_smallSo now, after all that rigamarole, we have two things that we’re dealing with that can cause potential downstream effects, ethanol and acetylaldehyde. Acetylaldehyde will eventually get metabolized acetate, which will get metabolized into acetyl-coA and contribute to one of the following pathways depending on what else is going on:

  1. Fatty acid synthesis (if insulin is elevated)
  2. Cholesterol synthesis (if insulin is elevated)
  3. Be used for fuel by the heart and skeletal muscle (and turned into co2 and water)

So, if you’re drinking alongside some carbohydrates or a mixed meal, the end products will be different than if you’re just boozing solo. Ethanol will, at some point, get metabolized as described before although while it’s floating around in the blood stream it will certainly exert some effects that will discuss during the rest of this article.

With all the background information out of the way now, we can get down to the business of actually talking about what drinking does performance and health-wise. To begin with, let’s talk about alcohol’s effect on metabolism, i.e. does it have a negative, positive, or neutral effect on you getting lean?

In general, ethanol carries about 7.1-7.5 kCal per gram. A “drink”, as defined by the 14g/ unit metric, therefore contains about 99kCal per “unit” just from alcohol. Remember how we talked about ethanol not being able to be stored and requiring almost immediate metabolism? Well, it turns out the ethanol becomes the “preferred fuel” of the liver and decreases liver fat oxidation by about 70% and protein oxidation by about 39%. It also almost completely abolishes carbohydrates being use for fuel even after an infusion. Normally, when carbohydrates reach the bloodstream their oxidation (metabolism) increases by about 2.5x. In the presence of ethanol, however, carbohydrate’s oxidation for fuel stays at baseline and storage of carbohydrates as fat increases [4].

Ethanol metabolism also requires a coenzyme, NAD+, that gets reduced to NADH when ethanol is converted to acetylaldehyde by alcohol dehydrogenase. NADH levels tend to rise during metabolism of ethanol and NAD+ levels tend to fall, thus increasing the NADH:NAD+ ratio. This increased ratio does a number of things metabolically, like increasing fat storage synthesis and causing damage to the mitochondria. Remember, mitochondria are the “energy powerhouses” of the cell and are very important [4]. Some training protocols we use, like high intensity interval training and weight training increase “mitogenesis”, i.e. the creation of new mitochondria to burn fuel (carbohydrates and fat). Ethanol and acetylaldehyde exposure to mitochondria decreases mitochondria activity, increases reactive oxygen species creation (which can damage other tissues), and can eventually cause mitochondrial dysfunction and death.Decreased mitochondrial activity can have negative impacts on basal metabolic rate, as it will decrease in response to lower levels of mitochondrial density or functioning.

This isn’t meant to be a scare tactic, as with most things, the poison is in the dose. On the other hand, the level of alcohol intake required to become inebriated far exceeds the levels of ethanol and acetylaldehyde that were used experimentally to demonstrate deleterious changes in mitochondrial activity.

Actual metabolic rate based on measuring oxygen consumption will increases upon ingestion of alcohol, as it also does with food alone [5]. Some people have taken this out of context and said that alcohol will increase metabolic rate to a greater degree than an isocaloric diet sans alcohol. Unfortunately, this has not been shown as of yet.

Another important metabolic issue as it pertains to ethanol, is that ethanol reduces the activity of muscle phosphorylase in human skeletal muscle [6]. Muscle phosphorylase, i.e. glycogen phosphorylase that breaks down muscle glycogen into glucose, is an important enzyme needed for the muscles to use stored carbohydrates as fuel. A disease of this enzyme, McCardle’s Disease, presents with exercise intolerance, early fatigue, and excessive muscle breakdown products (myoglobinuria) that may lead to rhabdomyolosis. In any event, in addition to decreased muscle phosphorylase activity, ethanol exposure also decreases rates of muscle protein synthesis and whole body protein metabolism by 15-30% [6]. The worst part is, these affects are primarily seen in type II fast-twitch fibers that we need for high level anaerobic performance!

To wrap up part 1 of this series, which was admittedly science-heavy (sorry), I’d like to state how I’d start to apply all these things practically. I do not believe it’s necessary to cut out all alcohol in the quest for ultimate performance and especially not for health, as we’ll discuss next time. On the other hand, I think many people are way too liberal with having a “few” drinks per day. That being said, I’m a proponent of counting the calories in liquor as carbohydrates, as they both demand preference for use as the primary metabolic substrate. What I mean by that is if ethanol is present, it will be metabolized first and foremost. Other calories and energy containing things will be stored so as not to compete with alcohol metabolism, in general. Carbohydrates are similar in that way, as they will be preferentially used by most tissues when the diet provides high levels of them. Additionally, both promote fat storage in the short term. Whether or not this leads to long term fat accumulation depends on the rest of the diet, i.e. total calories, macronutrients, etc.

So, yeah, count the alcohol as carbs and if it fits within your macronutrients and fiber goals for the day, it’s probably fine. On the other hand, I really like this soon-to-be-famous axiom:

“If you’re drinking enough to get drunk, you’re drinking enough to mess with your results.”

That’s it for part I. Sorry for the science primer, but it will pay off big time in parts II and III.

-thefitcoach

1) Cortot A, Jobin G, Fucrot F, et al. Gastric emptying and gastrointestinal absorption of al- cohol ingested with a meal. Dig Dis Sci 1986;31:343–8

2) Frezza M, Di Padova C, Pozzato G, et al. High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. N Engl J Med 1990;322:95–9

3) Broitman SA, LS Gottlieb, JJ Vitale Augmentation of ethanol absorption by mono- and disaccharides  Gastroenterology 1 June 1976 (volume 70 issue 6 Pages 1101-1107)

4) Lieber Charles S. Metabolism of Alcohol. Clinics in Liver Disease, Volume 2, Issue 4, Pages 673-702

5) Rosenberg Kathryn, Durnin J.V.G.A. The effect of alcohol on resting metabolic rate. British Journal of Nutrition (1978). Vol. 40. 293

6) Urbano-Marquez, A.; Fernandez-Sola, J. Effects of alcohol on skeletal and cardiac muscle. Muscle Nerve 2004, 30, 689-707.

 

 

The Ultimate Top 5 List

By Jordan Feigenbaum MS, CSCS, HFS, USAW CC, Starting Strength Staff

I’ve been doing a lot of work with clients, the new website,  and others (see Reddit AMA #1 and #2) and it’s got me thinking: What are the most important things in training that people are doing wrong?

Facepalm_1

Obviously this also tends to include things like nutrition, lifestyle factors, etc., but I’ve really been seeing a lot of common threads amongst people who need some help. So, without further ado here’s my Ultimate Top 5 List:

  1. Eat More Protein
Mom, where's the protein?

Mom, where’s the protein?

All things being equal, more protein is better from a performance and aesthetic standpoint with the following caveat: if you’re weighing and measuring all your food anyway, this does not apply. Most people eating ad libitumdo not eat enough protein. This also includes people who are specifically looking to increase their protein intake on a daily basis, however, this generally results in 4-5 days of a decent protein intake but 2-3 days of sub optimal protein intake. It’s just not that palatable in and of itself and few people actually crave protein unless they haven’t had some animal flesh in a while.

That being said, I’ve consistently seen better results when it comes to strength increases, better body composition, and compliance on a dietary strategy when it has more protein in it. Don’t get this confused with me telling you that you need 400g a day to make gains, as this is hardly the case. What I’m saying is that most people, male or female, should be between 200-300g of protein/day based on their age (older=more protein), size (bigger=more protein), sex (females=more protein), and training status/frequency (more frequency/harder training= more protein). In addition, if you suffer from compliance issues, i.e. you fall off the wagon frequently, then more protein tends to help this as it is very satiating. Above all else, hit your protein numbers for the day and most other things will take care of themselves.

Lifestyle Hack: Immediately after training drink a protein shake. Repeat again before bed. This get’s you at least halfway there.

2) Do The Correct Conditioning Work

What's better, walking on an incline or this?

What’s better, walking on an incline or this?

Most people undertaking a body recomposition phase in their life immediately start to do some sort of conditioning work concomitantly. Unfortunately, this often tends to be of the low to moderate intensity variety, i.e. walking on a treadmill, jogging, riding the bike, etc. While I applaud people for making healthy-ish changes in their lives, I think they could do a better job MORE EFFICIENTLY with some well structure high intensity interval training (HIIT).

The argument most people make about low intensity cardio being > HIIT is that “it burns more fat calories” and “burns more calories total”. Here’s the rub, low intensity cardio only burns a higher percentage of calories from fat than HIIT does. It does not burn a greater number of fat calories unless the total work done is grossly disproportional, i.e. someone is comparing doing 1 hour of cardio vs. 5 minutes of HIIT. Additionally, I’ll concede that traditional cardio burns more calories during the actual activity, however HIIT burns more calories over the course of the next 16-48 hours (+/- 8 hours) via metabolic increases systemically.

The only really good rationale for incorporating low to moderate intensity cardio in someone’s regimen (who isn’t an endurance athlete) is to just provide a calorie burn without expending the effort of HIIT (it’s much harder so you can’t do it all the time, especially if you’re on a massive deficit), or the person simply cannot muster the requisite effort or drive to push themselves to the limit during the HIIT. The magic is in the intensity. If the intensity isn’t there, then don’t bother.

Lifestyle Hack: On your off days (optimal) or at the end of your training sessions (okay) do the following protocol: 5 minute warm up, then 7 rounds of 30 second sprints followed by 3 minute rest periods. Cool down with 10 minutes easy effort.

3) Train Economically

Most people screw the pooch on this one, thinking they need to hit all sorts of variety and complex training to reach their goals when in fact, some form of either linear progression or rudimentary periodization will work just fine (outside of competitive lifters).

If you’re a beginner/novice, all you need to do is hit the big exercises 2-3 times per week and add weight to the bar each week, BECAUSE YOU CAN. If you can no longer do this, you’re not a novice anymore and thus, should not be on a novice program.

After the novice program ends, you do not need a 4 day split with all sorts of fancy accessory exercises in order to drive progress. What you need is consistent exposure to the movement at various levels of intensity (weight) and volume (reps x sets). Complexity can come later, when you need it.

Lifestyle Hack: Pare down your training template to the bare bones: squat, deadlift, press, bench press, chins, and power cleans. If you’re going to add anything, it better be a curl variation, a triceps exercise, and some abs. Everything else can stay in everyone else’s crappy program.

4) Eat the Right Amount of Energy

Bacon vs. Pasta? Easy. Bacon by unanimous decision

Bacon vs. Pasta? Easy. Bacon by unanimous decision

This should go without saying, but it’s not fat OR carbs that make you fat. It’s too much of either, or more often, too much of both. For the strength or anaerboically inclined athlete, carbohydrate is a much more effective fuel bioenergetically and I’d try to persuade this population to shift to a high protein, moderate to high carb, and low fat style diet. On the other hand, someone who’s not really into strength or is an endurance athlete would benefit from being efficient at using fat as a fuel in addition to carbohydrates, as fat is very important in long endurance efforts. For this population, I’d lean towards a high protein, low to moderate carb, and higher fat style diet. The biggest takeaway from this is that if overall energy is high, i.e. both carbs and fat are high, this will likely lead to unwanted “changes” in the body unless you’ve specifically added small amounts of carbs and fats to the diet incrementally.

Note: both diets are high protein

Of course, all of these recommendations are in relative amounts and not exact. High carb to one person might be low carb to another and vice versa. The important thing is to choose which way you’re going to go and choose appropriately based on what you do and what you can comply with.

Lifestyle Hack: Eat lean proteins and veggies at most meals of the day. Add starch pre and post workout. Add enough fat to suit your needs at meals outside of the periworkout window.
5) Eat Enough Fiber

We’ve heard for so long from the mainstream medical community that we should “Get more fiber in!” Surprisingly, I’m mostly on board with this statement. Here’s why:

The rationale behind having a “fiber goal”  is multifactorial. One, fiber is thermogenic in that it requires lots of energy to move it to the large bowel where the resident bacteria ferment it into a short chain fatty acid. Two, three, and four it tends to be very satiating, all things considered, lowers the glycemic index of meals, and controls for how much junk you can eat and still be compliant, i.e. 200g of carbs is different from 200g of carbs with the caveat you’re getting 35g of fiber/day too. Five, fiber levels have been linked to many healthy outcomes. Whether or not this is correlation, i.e fiber within the diet means you’re eating “healthy”, or causation, e.g. fiber ingestion itself is healthy, is unknown to me but it is what it is. Finally, fiber just eliminates one more variable in macro recs. If fiber intake is changing but carbs stay the same then the two inputs are not exactly equal in effect.

So there you go, the five things you and your friends need to be doing to take your performance and aesthetics to the next level! I’d love to hear from people reading this blog. What do you want to hear about next??

-thefitcoach

2013 USAPL/IPF Raw Challenge @ The Arnold Report

Calm before the storm.

Calm before the storm!

Hey everyone!! Thanks for all the support and for checking up on me. It was a fun day at the Arnold and although things didn’t go as well as planned I still had a blast and learned a lot. Additionally, I saw some super impressive lifters.

Jennifer Thompson (NC) benches 300 raw at 132lb bodyweight!

Jennifer Thompson (NC) benches 300 raw at 132lb bodyweight!

Here’s how the day went:
Wake Up Call: 530am. Headed to the convention center for the 6 am weigh in. Probably got about 4hours of decent sleep last night, but that was fine. I had to make sure all my gear was legal, i.e. shirt, singlet, shoes, etc. (not kidding). They told me my Brute Strength t-shirt was illegal, but that I could purchase a t-shirt to comply with the rules at their vendor conveniently located in the other room. Strike 1 IPF.

Anyway, I got to weigh in around 645 and was 82.9 kg (182.3 lbs). Slammed my super top secrete shake, 32oz gatorade, BCAAs+ water and was ready to roll.

Squats: Warm ups felt fine, hit my last warm up @365 but then they were screwing around around taking so much time to start my flight, so I hit 315 again to stay warm. Here’s how my attempts went:

190kg: Easy. Got 1 red light because apparently I fidgeted after given the squat command. Idk, they make me feel like I’m hyper extending my knees to get the squat command, so then I intuitively unlock them but this is frowned upon. The judges were super strict, per usual, at this meet and were red lighting people on depth (some people even bombed out of the meet due to this), but luckily in training I always squat deep. This rep was easy and I felt way better mentally after I hit it. Got it and called for 205kg.

On the way up with 425.

On the way up with 425.

205kg (452): Didn’t feel particularly hard or grindy. Just hit depth stood up, and got 3 whites.

452, buried alive!

452, buried alive! Note the knee position. My toes need to be angled out more though.

212.5kg: Either I didn’t have enough chalk on my back or I set up incorrectly because the bar rolled up my back out of the hole. Missed it ~1/3-1/2 way up. I didn’t fight it for too long because I didn’t wanna waste all my energy. I’m confident 210 would have gone, but 212.5 just wasn’t there today. I hit heavier than both (470) in training, but this was also after a full night’s sleep and without any added pressure from being at the Arnold. At this point, I wasn’t bummed at all, but I wish I could have gotten set up better so I could give it a real go without the bar rolling up my back.

Break #1: Took down some sliced turkey, rice cakes, and a bunch of water. Feeling good.

In the warm up room with JD.

In the warm up room with JD.

Bench: My last warm up, 300, felt pretty slow so I backed down my opener from 145 to 142.5 just to make sure I got into the meet. This was a smart move.

Attempt 1: 142.5- this was way slower than it should have been, as the bar went forward (towards my feet) off my chest. The pauses weren’t exceptionally long at all but I just executed this rep wrong. I was pretty pissed at myself since I hit 340 in training and even that didn’t feel this hard. I called for 147.5 for my 2nd.

(If you listen closely you can here the bar actually come to rest on the pins. The safeties were too high turning this into a pin press, essentially).

Focused.

Focused.

Attempt 2: I took down an entire gallon (literally) between attempt 1 and attempt 2. This extra hydration and me realizing I pushed the bar forward made this attempt a whole lot smoother. This felt super easy and was a 2.5kg meet PR. I also realized at this attempt that I never was setting my back and chest and my setup was essentially shit for all of these attempts since I failed to correct for them. Also, at the bottom of the rep before the pause, the bar kept hitting the safety pins and this was annoying as hell and distracting. I had them move the safety pins down 2 notches to try and get them out of the way.


Attempt 3 152.5: Drank a bunch more water and felt pretty confident going into this attempt. Unfortunately, I made the same mistake and didn’t set my shoulders on the bench after unracking it (the lift off sucked but that’s not an excuse). I also pushed the bar forward on this attempt too, which is why I missed it. I really though this was gonna be a smoke show but I cannot make technical errors at circa maximal attempts at huge meets and expect to get away with it. Ughhh.

Good handoff? Nope.

Good handoff? Nope.

Break 2: More turkey, more rice cakes, and water. Pull time. At this point I was pretty sure my elite total was out the window, but I still wanted to hit a 585-600lb pull, which would have been 3 PRs and big meet total PR. I was OKAY with this, as I wasn’t executing perfect technique at all, which is unacceptable.

Deadlifts: All warm ups were stupid easy. Very confident going into the pulls.

535 easy.

535 easy.

Attempt 1: 242.5 (535): Total smoke show. Felt like a speed pull, honestly. Something weird happened before this attempt though backstage. I started shivering and shaking violently, like I was soooo cold. I put on my heat gear (thermal shirt , jacket, and stocking cap) and tried to stay warm. When I was pulling this deadlift I also got this strange sensation that my arms were going to rip off, like both biceps were cramping or tearing or something. Totally weird.

Attempt 2: 265 (585 or something): The set up was okay, although my back was not as tight as it should have been, but it came off the floor fast and I thought it was game over until it cleared the knees. The bar moved away ever so slightly and the bar speed cratered. I kept pulling and from what the video shows, I shrugged it back against my legs. I did not feel myself rebend my knees, and the video shows this (will post it when my friends send me both angles) but I know the pull certainly didn’t feel normal. I’ve never hitched in my life so the weird feeling of the top of the pull makes me believe the call was accurate and hitchy, although all the dudes backstage told me it was a good pull. Who knows though. This was an expensive rep, that’s for sure. I called for the same attempt for my 3rd but was still shaking and shivering back stage even in full thermal gear. It was the strangest damn thing.

Swinging for the fences.

Swinging for the fences.

 

Locked out.

Locked out.

My best blue steel.

My best blue steel.

3rd Attempt: No gas, no chance. There could have been 280kg on the bar and it would have moved the exact same distance, zero inches.

Total: 1313 (or 1312), 9th overall for <93kg men.

Feelings: I’m kinda bummed about the deadlift since I really felt good about my training cycle coming into the meet. In retrospect, I should have called for 260-262.5 or not mess up the pull by being technically proficient in the lifts and just smoked it. If I would have hit 262.5 I think I would have ended up with a better placing in the overall standings. On the other hand, I didn’t come to the Arnold to necessarily put up a big total, but rather I just wanted to go for PRs. I set two meet PRs and missed a 3rd (deadlift).

So I weighed in at 182.3 and before anyone says anything, I was 198 after stepping off the platform for my 3rd deadlift attempt. I have no doubt in my mind as to why my performance wasn’t what I wanted, I plain screwed up on every max effort attempt. No excuses, I just either set up wrong or did the movement incorrectly on my 3rd Squat and Bench (also my 1st one here) and 2nd pull. I cannot expect to get away with compromised technique and set crazy PRs on the biggest stage in powerlifting. I thought the judging was fair and I felt fine all day except for the shivering/shaking thing before deadlifts.

I can’t tell you how overwhelmed I am at the support of the Internet community and my friends for my meet Friday on here, Facebook, and Twitter. It was a really cool meet that was run extraordinarily well, yet I can’t help but be disappointed in the overall outcome due to technical miscues. If I would have missed weights because they’re just too heavy that’d be one thing, but to miss attempts because I did them wrong bums me out.

Going forward, I’m definitely moving up a weight class, adjusting my peaking schedule, and will probably pick a meet to do that’s more low key. I’ve only done one small meet (my first one ever a little less than a year ago) and then the other meets were Raw Nationals, USAPL NE Regionals (huge meet), and the Arnold. I need to work my technique more and fine tune it so I can display my strength better. I have no doubt that the weights I missed today would have fallen on a different day or if I had better technique, but it wasn’t in the cards. I still had a blast competing at the Arnold, although I must say the place is packed full of weirdos. I just changed my flight back to VA to tomorrow instead of Sunday because all the strange folks really put me off to the whole thing. I’ve never seen more steroids, fake tans, makeup (on both genders), and peacocking going on in one place. It was overly stimulating for sure!

Again, thanks for all your support everyone. I’m not down on myself at all. I know I could have easily deadlifted 260 no problem and put up a much bigger total, but that wasn’t the goal for this meet as mentioned before.

-thefitcoach