ACSM Wrap Up Part II by Eric Cressey

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"Very Low Carbohydrate Ketogenic Diets and Metabolic Syndrome" (VLCKD) Jeff Volek, PhD, RD

Dr. Volek is not only a great guy, accomplished powerlifter, and highly-respected authority on carbohydrate-restricted diets, but he's also got the best damn Powerpoints you'll ever see. Comparing one of his presentations to "normal" Powerpoints is like hanging a Monet up next to a preschooler's finger painting… Sorry, I totally geeked out for a second there.

Dr. Volek started off with a "what they tell you and don't tell you" section. The so-called experts claim that saturated fat (SFAs) increases LDL cholesterol, insulin resistance and inflammation. Unfortunately, what gets back-burnered is that not all SFAs have these effects. Good examples of the healthier SFAs are stearic and palmitic acid.

The determining factors are the dietary intake of linoleic acid and the positional distribution of the saturated fatty acid on glycerol. Moreover, the healthier SFAs may increase HDL, reduce triglycerides and increase LDL particle size (this is a good thing; keep reading). SFAs only lead to insulin resistance in the presence of sugar, too. When carbohydrates are kept low, SFAs are "processed" differently.

Likewise, these experts claim that ketones are dangerous and that the brain needs glucose for fuel. What they don't tell you is that the level of ketones observed with VLCKDs is far below what one would see in a diabetic. Even so, ketones are indicators of accelerated lipolysis, and all cells can adapt to utilize ketones. Cellular glucose needs can be met through gluconeogenesis, and the ketones may actually be a "super fuel." Finally, research suggests that there may actually be therapeutic potential for ketones in the treatment of insulin resistance, seizures, Parkinson's and Alzheimer's disease.

Metabolic syndrome is at an all-time high. Currently, it affects 22%, 34% and 44% of Americans ages 40-49, 50-59 and 60-69, respectively. To "qualify," you either have to know the bouncer at the door to the Syndrome X night club, or have three or more of the following factors:

While all the experts agree on how to define and diagnose metabolic syndrome, a fierce debate rages on when it comes to treating it: low-fat or low-carbs? Dr. Volek is one of those leading the charge for the low-carb side, and he presented data from six studies done right here in our lab at UCONN that look at the blood lipoprotein responses to VLCKDs.

So what did they find in these studies? Well, essentially the same thing that 19 previous studies — studies people keep wanting to ignore, for some reason — found. Mean fasting triglycerides, postprandial triglycerides and total cholesterol/HDL ratio dropped markedly, while mean HDL was increased.

Interestingly, though, Dr. Volek pointed out that there's a significant amount of variability in individual responses to the VLCKDs. The drops in triglycerides are largely explained by starting levels, but the HDL increases weren't accounted for by weight loss or starting levels. It warrants mention that LDL values increased in four of the six studies. It's important to note, however, that not all LDL is created equal. In fact, a preponderance of small LDL particles (known as Pattern B) is highly correlated with cardiovascular disease. VLCKDs actually shift particle size to the larger variety, making people more "Pattern A." This shift's magnitude is largely explained by initial LDL sizes.

With his blood chemistry rationale complete (for now), Dr. Volek next addressed the question of whether or not VLCKDs enhance weight loss and, if so, whether this weight loss is only due to water and/or lean body mass. All the research verifies that low-fat diets are VLCKDs' whipping boy when it comes to weight loss. In the five studies cited, subjects generally lost twice as much (or even more) weight on VLCKDs than on low-fat diets after three, six and twelve months. The low-fat diet subjects also demonstrated noteworthy tendencies to hug trees, wear hemp, buy Enya CDs, and vote Libertarian.

Dr. Volek went on to present the results of eleven studies demonstrating that between 67% and 150% of weight loss with VLCKD interventions was actual fat mass. And yes, two studies actually saw increases in lean body mass simultaneously.

In the first one, an eight week treatment of morbidly obese adolescents, subjects averaged gains of 1.4 pounds in lean body mass while mean fat loss was 16.8 pounds. Blood chemistries improved, and the incidence of sleep abnormalities significantly decreased. These remarkable results were achieved with a diet of 650 to 725 calories and less than 25 grams of carbohydrates. Is there any chance we can replace vending machines with omelet bars in our high schools?

Just in case you're worried that children (or anyone, for that matter) can't get all the important vitamins and minerals with a low-carb diet, I should tell you that when caloric intake is held constant, you're slightly more likely to have vitamin and mineral deficiencies on a low-fat diet than you are on a low-carb diet. This statement takes into account fat and water-soluble vitamins as well as macro and trace minerals.

As you can probably imagine, fasting insulin levels also decrease with VLCKDs, although this increase is less pronounced in women. According to one study, overweight women saw a 9% decrease whereas overweight men experienced a 40% drop. This difference is most likely due to the fact that women have less insulin kicking around in the first place (which is why they tend to be more pear-shaped than apple-shaped).

Finally, VLCKDs lower leptin far more (50% vs. 17%, in one study) than low-fat diets. This difference can be attributed to the increased loss of fat mass with VLCKDs.

So, when taken collectively, all this data adds up to tell us that VLCKDs are a damn good means of preventing and treating metabolic syndrome. These dietary interventions allow for an amazing metabolic adaptation that provides for decreased triglycerides, insulin and fat mass while increasing LDL particle size and HDL.

Future research needs to move beyond the questions of "Do VLCKDs work?" and "Are VLCKDs safe?" Instead, research needs to look to figure out who responds best to these diets (Dr. Volek called it "personalized nutrition"), establish recommendations for optimal macronutrient breakdowns, and determine how such diets can be integrated with exercise, pharmaceutical interventions and OTC supplements.


"Ice Hockey Conditioning: The Science and Practical Application" David Harackiewicz, DPE, CSCS

Dr. Harackiewicz offered a very well researched presentation on the specific metabolic demands that performance enhancement coaches should understand in writing programs for hockey players. I really liked his general-to-specific approach, especially since he initiated this approach with the "Integrative Factors to Successful Performance," which was originally put forth by Cox et al. in 1995 (1):

Adapted from: Cox MH, Miles DS, Verde TJ, Rhodes EC. Applied physiology of ice hockey. Sports Med. 1995 Mar;19(3):184-201.

This model can easily be applied to success in any athletic venture, so consider each of these components as they relate to your own situation; you might very well stumble onto something you're missing and kickstart some new gains.

In terms of hockey-specific demands, here are some key points:

If someone tells you that hockey is an aerobic sport and encourages you to just do plenty of distance running to prepare, politely tell him that he doesn't know his ass from his elbow. Hockey is 70-80% anaerobic and 20-30% aerobic.

The typical shift can last anywhere from 30 to 80 seconds, during which time high-intensity sprints (anaerobic) are alternated with periods of gliding and light skating (aerobic). The aerobic energy systems do come into play in the recovery between shifts and periods, too, but if you're tired after a shift, it's due to phosphocreatine depletion and lactate/hydrogen ion accumulation — not because you aren't aerobically fit.

Although many teams use post-game "lactate clearance" protocols (light skating or cycling), research hasn't supported this practice as a means of enhancing subsequent performance or even lactate clearance in hockey (many players still swear by it). One study where hockey players were biopsied post-game found decrements, but not total depletion of muscle glycogen.

The authors suggested that complete depletion wasn't present because average ice time is only about 16 minutes per game, and the majority of the game (read: time on the bench and in the locker room) is played below lactate threshold — in spite of the fact that maximum heart rate averages 87-95% during shifts on the ice! Therefore, the assertion was made that "ingestion of large amounts of high caloric carbohydrate concentrated beverages may not be necessary."

I have several beefs with this statement:

With all that said, my feeling is that you should base carbohydrate type and amount on the task at hand. Let's move on…

Believe it or not, in terms of VO2 max, detraining usually occurs in hockey players during the season. One study was able to actually improve VO2 max in-season with supplemental interval cycling one to two times per week (each session lasted 48 minutes!) It didn't mention how it impacted their hockey performance, though. I bet that they were too exhausted to even play four times weekly with daily practices.

There are no universal international standards for physiologic assessment of hockey players, but several laboratory tests are common everywhere. They include height, weight, body fat percentage, anaerobic power and capacity (Wingate cycle test), strength (bench press reps — which isn't really maximal strength — and grip strength), power (vertical and broad jump) and endurance (sit-ups) tests, flexibility (sit-and-reach…good God!), and aerobic power (VO2max on a cycle ergometer).

It was interesting to note how the average physical profile of an NHL player changed from 1980 to 1991. Just imagine what's happened in the last 13 years!

Year

1980

1991

Weight (lb)

187.7

196.5

Height (in)

70.6

73.0

Body fat %

12.6

12.1

Combined Grip Strength (kg)

123.3

130.9

VO2max (ml/kg/min)

54.0

60.2

At any NHL combine, it's easy to tell the European players from the North Americans. The Europeans have monster legs, while the North Americans are top-heavy. This explains why North American players get more supermodels, though.

Several on-ice tests are also valuable for assessment of anaerobic and aerobic power as well as performance drop-off with repeated efforts. In a study comparing elite and non-athlete hockey players, significant differences were noted in full speed, drop-off time and the sum of six repeated trials (factoring in drop-off time).

The superior drop-off times in elite players suggest that these athletes had enhanced cardiovascular systems that enabled them to more rapidly recover from high-intensity exercise. Interestingly, no significant differences were noted between groups on agility, acceleration and average speed. Elite players also demonstrate superior performance on cycling tests of aerobic capacity and anaerobic power.

The most valid off-ice predictor of on-ice speed is the 40-yard dash. The "40" and vertical jump were both good predictors of anaerobic capacity, and vertical jump also correlated with acceleration and speed. Nonetheless, according to Harackiewicz, if NHL scouts could only use one factor to assess players' potential, it would be body fat percentage.


"Functional Rehab of an Injured Firefighter: A Work Hardening Approach!" Peter Ronai, MS, CSCS, RCEP & Heidi Shamansky, MS, PT

Ronai and Shamansky offered a complete overview of the rehabilitation of a firefighter who tore his rotator cuff in the line of duty. For those who don't know, firefighting is an extremely demanding job — so demanding, in fact, that it ranks among the top five occupations in job related injuries and illness. We aren't just talking burns here; more than half of these injuries are musculoskeletal in nature, as the job has a broad array of physical demands. Ronai likened training a firefighter to training a wrestler; they require contributions from both anaerobic and aerobic energy systems, both muscular strength and endurance, and a significant amount of active flexibility. In other words, they have to ride several horses with one ass — and with roughly 80 pounds of gear on their backs!

Every good physical therapist should start with a comprehensive assessment of the task at hand. Beyond simply noting the injury and related functional impairments, one should do the following:

Only once these duties have been fulfilled can one adequately design a truly functional and individualized rehabilitation program. This program should eventually progress to utilization of work-related implements in work-related settings with work-specific biomechanical and metabolic demands. If you go to a PT, ask if they're doing something similar. In fact, while you're at it, request that they explicitly state in writing what their goals for your rehabilitation are. A good physical therapist will appreciate your enthusiasm, concern and proactive mindset. If yours doesn't, find someone else.

Rather than detail the full 12-week program Ronai and Shamansky utilized, I'll highlight the broad guidelines and goals to which they adhered to rehabilitate the tear:

In terms of other key points, read on:

Ligaments are the static restraints to excessive motion of the humeral head, while the rotator cuff kicks in as a dynamic restraint. Because the muscles of the rotator cuff have limited effectiveness in positions of combined external rotation, abduction and horizontal abduction (think of where your upper arm is on a squat or behind the neck press), traumatic rotator cuff injuries commonly occur in these positions.

As Mike Robertson and I detailed in our "Neanderthal No More" series, postural distortions are a major risk factor for a variety of injuries and conditions. Ronai validated our assertions with a simple test: internally rotate your shoulders and assume a hunchback position. Now, try to get your arms overhead. It ain't happening, is it?

Now, stand up straight and make sure that your scapulae are tight to your rib cage; try it again, noting how much further overhead your arms go. You need to be able to posteriorly tilt the scapula to give the humeral head space to track upward in the subacromial space during overhead activities.

Now, assume the same hunchbacked position, take a deep breath, and forcefully exhale. Again, stand up straight and repeat the test. Notice any difference? Poor posture can actually mechanically compromise diaphragmatic function, reducing the overall effectiveness of your pulmonary system. Considering how crucial proper breathing patterns are to lifting success, chalk this up as one more way that bad posture can sabotage your efforts in the gym.

One of the most common scapular dyskinesis patterns a clinician observes is the upper trapezius substitution with abduction and flexion. It closely relates to the aforementioned posture problems, as individuals with limited posterior scapular tilt need to try to find an alternate way to increase the subacromial space. Rather than using the appropriate serratus anterior-lower trapezius-upper trapezius force couple to posteriorly tilt, they simply "hike" the scapula with the upper trapezius and levator scapulae.

This pattern is easily identified, as the shoulder girdle will rise before the humerus; you'll see it all the time in the gym when people do lateral raises. This hike will usually be accompanied by scapular winging due to a weak serratus anterior. Ronai actually likened this muscle to the transverse abdominus and vastus medialis in that all three tend to "shut down" when dysfunction is present. Finally, you'll likely see an underdeveloped/atrophied mid-back, as the lower traps won't be up to par.


"Functional Single Nucleotide Polymorphisms Affecting Muscle Size and Strength: Report of the FAMuSS Study" William Kraemer, PhD, FACSM; Rick Seip, PhD, FACSM; & Monica Hubal, MS

Hands down, this was the convention's most intriguing presentation for me. In case you haven't heard of the FAMuSS study, it's an NIH-funded collaborative effort among eight universities that's been ongoing for several years now, and the primary focus is to examine the genetic component of muscular performance and individual responses to resistance-training.

According to the primary investigators, "FAMuSS should help identify genetic factors associated with muscle performance and the response to exercise training. Such insight should contribute to our ability to predict the individual response to exercise training but may also contribute to understanding better muscle physiology, to identifying individuals who are susceptible to muscle loss with environmental challenge, and to developing pharmacologic agents capable of preserving muscle size and function (2)."

From microgravity induced atrophy and strength loss, to disease progression, to athletic performance, to getting hyooooge, this study has all the makings of a classic. The presentation was only the preliminary findings report, as approximately half of the subjects have completed the intervention and had their data analyzed. The final results will be presented at the ACSM National Conference in 2005.

Dr. Kraemer "headlined" the presentation as somewhat of a guest speaker. Who better to ask to give a presentation on all the factors that could impact muscle size and strength that are not directly controlled by genes? Dr. K cited age (chronological), training age (i.e. available window of adaptation), gender, diet, behavioral (e.g. alcoholism), and health status as overt factors that affect neuromuscular plasticity. Moreover, program variables such as exercise selection, intensity, rest interval, sets and reps dictate the training effect. In other words, different programs require unique motor unit recruitment, and a tissue will only adapt if it's actually activated. It goes without saying that some protocols (cough, cough…not Super Slow) activate tissues better than others. Different protocols will yield different hormonal responses, too.

To emphasize the varying effects of different training styles on the fibers themselves, Dr. Kraemer spoke of a typical marathoner having approximately 100 muscle fibers/cm2 compared with 300/cm2 in an Olympic lifter. He also noted that powerlifters are even more "densely packed" than O-lifters, and that bodybuilders fall somewhere in between marathoners and O-lifters. Finally, he cited obvious protein accretion difference between type I and II fibers; you'll get a whole lot more size from the type II denominations.

From a dietary standpoint, Dr. Kraemer validated that lifters need more protein, as increased protein consumption enhances the hypertrophic response to resistance training. He cited one study in which subjects trained the knee extensors and consumed a fixed amount of protein. A small amount of hypertrophy was noted (as would be expected from a single session).

However, when the protein intake was held constant and the subjects trained the entire body, the hypertrophic response was virtually non-existent; there wasn't enough protein to go around. Does anyone else find it sad that we have to keep justifying eating more protein to uninformed laypeople? Part of me wanted to cannibalize a few of the food-guide pyramid nutritionists in attendance just to prove a point.

Dr. Rick Seip of Hartford Hospital spoke next, describing the protocol. Over 1000 men and women (ages 18-40) are training (or have trained) only the non-dominant arm for twelve weeks with a series of isolation exercises in a periodized program. Pre and post-intervention assessments of size and isometric and dynamic strength are taken. Those subjects whose baseline values or response to training deviate by 1.5 or more standard deviations from the mean are defined as outliers and examined for genetic variants.

Monica Hubal offered some background on the concept of single nucleotide polymorphisms (SNPs). Phenotypes are the characteristics an individual displays independent of genotype (genetic makeup). Our genotype for a specific trait is composed of two alleles (one is inherited from each parent); for instance, AA, BB, or AB.

Now, a polymorphism is a mutation in a gene that may be inherited from one or more parents. With this single substitution, you may wind up with AA, AX, or XX. Normally, genotype is significantly correlated with phenotype. However, in some people — such as men who gain more than 10cm2 on their arm in only twelve weeks of training — things aren't acting as one would expect; that's where the FAMuSS folks come in to review the X alleles (SNPs) that may be present. These genetic anomalies may be the difference between an elite marathoner and the Incredible Hulk.

To give us a taste of how profound the FAMuSS results may be, Hubal highlighted ?-actinin 3, a skeletal muscle protein that anchors myofibrillar actin to the Z-line and assists in coordinating myofibrillar contraction. There are three ?-ACTN variations (1, 2, and 3); ?-ACTN3 is specific to fast twitch muscle fibers and has a positive effect on generating high forces and velocities. Yang et al (2003) demonstrated that "the skeletal-muscle actin-binding protein ?-actinin-3 is absent in 18% of healthy white individuals because of homozygosity for a common stop-codon polymorphism in the ACTN3 gene, R577X."

Hi, I don't understand any of this either. But aren't you glad you scrolled all the way to the bottom of the article?

In plain English, we aren't just talking about the same old "more fast-twitch fibers" argument; we're talking about better fibers, too. These elite Australian sprinters had significantly higher 577R allele frequencies than their non-elite (translation: slow!) counterparts (3).

Oh, and the good news for strength and power athletes is that the current FAMuSS figure for this SNP is 27%, although they're still seeking more data to improve their statistical power. This genotype alone appears to be responsible for 2% of the variability in 1RM change in the data reported thus far. This number might not seem like much, but when you consider that the most widely recognized SNP in terms of breast cancer predisposition accounts for 5% of one's risk variability, 2% seems pretty appreciable.

The ?-ACTN3 is just the tip of the iceberg, too, as they claim to have identified several SNPs, including ones that are specific to certain ethnic groups. We may finally find out why some guys just won't grow as quickly as their training partners when everything else is held constant, or why some kids ought to give up distance running and get into deadlifting.

I've never been all that enthusiastic about genetics discussions or coursework, but I'll be the first to admit that this presentation really piqued my interest. Rarely will you find a single study with so much potential to answer a broad array of questions.


Free Communications of Note

Effects of Instruction on Abdominal EMG During a Bench Press (4)

Have you ever been struggling to complete a rep, and then someone shouts out a cue that reminds you to make a technical adjustment that ultimately allows you to make the lift? Ever wonder if constant feedback can actually impact muscle fiber recruitment?

Quinnipiac University researchers found that EMG values were higher for the upper and lower rectus abdominus and external obliques when participants were instructed to "maintain abdominal contraction" during a bench press than when they lifted without the cue. It's hard to appreciate how valuable the core is on the bench until you really know how to use it to transfer strength from the lower body to the upper body.

However, these results indicate that it'll be much easier to do so with some continued verbal reinforcement from a spotter or the little voice inside your head.


Effect of Post-Exercise Ethanol Intoxication on the Free Androgen Index Response to Resistance Exercise (5)

Subjects were involved in three separate conditions: a three to five RM whole-body circuit plus ethanol, the circuit without ethanol, and neither of the two. The researchers found that post-exercise intoxication didn't lead to a change in the serum free androgen index.

Although I'm sure that Surge would still taste good with vodka, it probably isn't a good idea to get hammered after you're done squatting, as there are a lot of other potentially detrimental consequences (e.g. impaired glycogen synthesis) of intoxication post-training. Plus, the blood measures only occurred up to five hours post-exercise, so the longer-term effects of such intoxication aren't considered.

All that said, I'm sure that many of you will find comfort in knowing having a beer a few hours after a lift won't totally negate the benefits of what you just did in the gym.


Conclusion

It's not easy to cram two days worth of knowledge bombs into a two-part article, so this is far from exhaustive. Hopefully, you'll walk away from this conference report with some new perspectives on how to improve on what you're doing, as well as an appreciation for what us New Englanders have to offer… you know, besides clam chowder.


About the Author


References

1. Cox MH, Miles DS, Verde TJ, Rhodes EC. Applied physiology of ice hockey. Sports Med. 1995 Mar;19(3):184-201.

2. Thompson PD, Moyna N, Seip R, Price T, Clarkson P, Angelopoulos T, Gordon P, Pescatello L, Visich P, Zoeller R, Devaney JM, Gordish H, Bilbie S, Hoffman EP.

Functional polymorphisms associated with human muscle size and strength. Med Sci Sports Exerc. 2004 Jul;36(7):1132-9.

3. Yang N, MacArthur DG, Gulbin JP, Hahn AG, Beggs AH, Easteal S, North K. ACTN3 genotype is associated with human elite athletic performance. Am J Hum Genet. 2003 Sep;73(3):627-31. Epub 2003 Jul 23.

4. Tenenhaus, B, Whitney, J, and Straub, SJ.

5. Vingren, JL, Kosiris, LP, and Kraemer, WJ.

 


Submitted by DMorgan on Sun, 09/09/2007 - 11:25am.

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