Will 2015 Be the Year You Pick up The Kettlebells? Find Out If Your Strength, Fitness & Physique Would Benefit

2015 may offer a chance to get spice up your routine with kettlebells.

"Moderate evidence indicates that kettlebell training may be safe and effective for increasing certain functional strength and power measures and may show positive results with postural control in young, healthy populations," says a recent review of the literature in Physical Therapy Reviews (Girard. 2014) and does thus sound positively optimistic, but by far not as euphoric as some kettlebell warriors on the Internet.

Those of you who know me are probably aware that I am not a fan of kettle bells, but I am true to the motto of being open to good scientific evidence, like the one from the previously cited review by Girard et al. (2014).

I won't lie to you: I believe there are better muscle builders than kettlebells

Tri- or Multi-Set Training for Body Recomp.?

Alternating Squat & Blood Pressure - Productive?

Pre-Exhaustion Exhausts Your Growth Potential

Full ROM ➯ Full Gains - Form Counts!

Battle the Rope to Get Ripped & Strong

Study Indicates Cut the Volume Make the Gains!

Speaking of which, the previously cited review found only five studies satisfied the eligibility criteria and were included in this review. The populations studied age range was 18–72 years old. Methodological scores based on the PEDro scale ranged from 3 to 7 out of 10. In those studies, ...

[k]ettlebell training demonstrated improvements for a number of strength measures: time 6 group for bench press ( P < 0.05) and back extension (P = 0.053), main effect for clean and jerk (P < 0.05) and certain power measures such as improved explosive strength comparable to a jump squat control (19.8% increase). Improved postural control was demonstrated in one study (P = 0.04)" (Girard. 2014).

What the kettlebells did not do in any of the five studies by Otto et al. (2012), Manoccia et al. (2013), Lake et al. (2012) and Jay et al. (2011 & 2013) was to have an effect on aerobic endurance as measured by VO2 Max.

Original photos from the study by McGill et al. (2014).

Isn't Kettlebell training bad for your back? No, it isn't. According to data from a 2012 study by McGill, kettlebell training rather than being bad for the back provides unique muscular pulses to the abdominals which, "[t]ogether with the muscle bracing associated with carries create kettlebell-specific training opportunities" makes McGill et al. conclude that the "unique loading patterns discovered during the kettlebell swing [...] which is opposite in polarity to a traditional lift" may in fact be the reason why "many individuals credit kettlebell swings with restoring and enhancing back health and function, although a few find that they irritate tissues" (McGill. 2014).

According to McGill et al. (2014) the "message for coaches is" that the kettlebell offers "several unique training opportunities", for example (a) the opportunity to train rapid muscle contraction-relaxation cycles emphasizing posterior chain power development about the hip. However, the large shear to compression load ratio on the lumbar spine created during swing exercises suggests that this training approach may be contraindicated for some individuals with spine shear load intolerance and (b) enhanced activation of the core musculature during the bottoms-up carry.

The non-significance of the oxygen uptake and thus the non-existence of conditioning effects may come as a surprise for those of you have already done kettlebell swings. Rightly so, as I would argue, because this result of the review is based mainly on the results of Jay et al. (2011) who invited 57 employees of a large pharmaceutical company for a physical examination. Of those only 43 showed up (motivation to work their assess off ↓) of whom 40 men and women in their mid-forties then trained for 20 minutes included a 5 –10 minute warm up and a 10–15 minute interval training consisting of 10 intervals of 30 seconds with rest period of 30–60 seconds which began with ZERO workload and was progressively intensified by the participants choice!

Kettlebell, weights, or ergometer, you have to work your ass off to make progress!

That's much in contrast to Fortner et al. (2014) who had their 14 young (18-25y), non-obese volunteers train three times a week for 8 weeks with 4.5kg and 8kg kettlebells for the female and male subjects, respectively in a "tabata style", i.e. at a twenty-second work to ten-second rest ratio and compared the VO2 response to a traditional protocol, consisting of four sets of work separated by ninety seconds of rest.

Figure 1: Subjective Borg RPE response to Tabata versus traditional kettlebell swing protocols in healthy, young adults. TAB- Tabata, TRADtraditional (left). % of peak VO2 value achieved during Tabata and traditional kettlebell swing protocols in healthy, young adults (right | Fortner. 2014).

As you can see in Figure 1 the response to the two different workouts was very different - despite the fact that the total number of swings from each individual's "tabata condition" (TBA) was equally divided into four sets for their "tradititional condition" (TRAD). From non-kettlebell studies, we know that training at an intensity like this, even if it's done for only a few minutes, will just as Fortner et al. say "safely and effectively provide multi-faceted exercise adaptations with a relatively short time investment" (Fortner. 2014) - an assumption that's backed by a 2011 study by Falatic et al. that used a 15s/15s protocol and elicited significant increases in VO2max in seventeen female NCAA Division I collegiate soccer players.

Figure 2: Energy expenditure during two-hand kettlebell exercise and graded treadmill walking (Thomas. 2014).

Furthermore, James et al.  (2014) were recently able to show that a KB routine consisting of 2-hand swings and sumo deadlifts with 3-minute rest periods produces similar metabolic responses to those of a moderate-intensity treadmill walking protocol designed for the improvement of aerobic fitness in 5 women, 5 men between 21 and 31 years of age - and, as you can see in Figure 2, it also burned a few extra calories.

A comparison with treadmill walking is yet not enough to confirm that kettlebell training is also superior to "regular" HIIT training. Personally, I suspect it isn't but it's at least a good way to diversify your training routines and create a new exercise stimulus that may even help you break through a plateau.

You're not interested in fitness? What about improve- ments in glucose tolerance, then? Samantha Leigh Greenwald found in her master thesis that kettlebell training can improve glucose clea- rance in young sedentary men" and concludes that the results of her study "suggest that kettlebell training may provide an inexpen- sive home-based approach for prevention or management of type 2 diabetes" (Greenwald. 2014).

Speaking of diversification: Another recent study by Budnar Jr, et al. who investigated the testosterone, GH and cortisol response to kettlebell training, indicates that "the kettlebell swing exercise might [in fact] provide a good supplement to resistance training programs" (Budnar Jr. 2014).

So, in case you are just working on your 2015 workout routine, you may want to give kettlebells a chance. In that you may, for example, replace one of your regular HIIT training sessions with a brief, but intense tabata-style kettle bell workout as it was described by James et al. (2014): 2-hand swings and sumo deadlifts with 3-minute | Comment on Facebook!

References:

• Falatic, Jonathan Asher. "The effects of kettlebell training on aerobic capacity." San José state University (2011).
• Fortner, Howard A., et al. "Cardiovascular and metabolic demands of the kettlebell swing using a Tabata interval versus a traditional resistance protocol." International Journal of Exercise Science 7.3 (2014): 2. 
• Greenwald, Samantha Leigh. The impact of an acute bout of kettlebell exercise on glucose tolerance in sedentary males. Diss. State University of New York at Buffalo, 2014.
• Jay, Kenneth, et al. "Kettlebell training for musculoskeletal and cardiovascular health: a randomized controlled trial." Scandinavian journal of work, environment & health (2011): 196-203.
• Jay, Kenneth, et al. "Effects of kettlebell training on postural coordination and jump performance: a randomized controlled trial." The Journal of Strength & Conditioning Research 27.5 (2013): 1202-1209.
• Lake, Jason P., and Mike A. Lauder. "Mechanical demands of kettlebell swing exercise." The Journal of Strength & Conditioning Research 26.12 (2012): 3209-3216.
• Manocchia, Pasquale, et al. "Transference of kettlebell training to strength, power, and endurance." The Journal of Strength & Conditioning Research 27.2 (2013): 477-484.
• McGill, Stuart M., and Leigh W. Marshall. "Kettlebell swing, snatch, and bottoms-up carry: back and hip muscle activation, motion, and low back loads." The Journal of Strength & Conditioning Research 26.1 (2012): 16-27. 
• Otto III, William H., et al. "Effects of weightlifting vs. kettlebell training on vertical jump, strength, and body composition." The Journal of Strength & Conditioning Research 26.5 (2012): 1199-1202.
• Thomas, James F., et al. "Comparison of Two-Hand Kettlebell Exercise and Graded Treadmill Walking: Effectiveness as a Stimulus for Cardiorespiratory Fitness." The Journal of Strength & Conditioning Research 28.4 (2014): 998-1006.

No Time? No Excuse! Three Minutes (One Minute All Out, Only) Exercise Per Week Suffice to Increase One's Skeletal Muscle Oxidative Capacity and Improve Metabolic Health!

HIIT your weaker self hard, with a total of one minute all out cycling.

It's the most often heard excuse you get, when you ask your sick overweight neighbor if he'd like to accompany you to the gym to do something for his health, first, and his physique, second. "Ah, I don't have the time to work out!"

Obviously, this is a "perceived lack of time" that is not real for 99.9% of the people, even if we're talking about 30 minutes of exercise every other day. And even if it was not, the results of a recent study from the McMaster University in Hamilton, Ontario, will totally steal their non-existent thunder and provide you with convincing arguments to drag them to the gym for a quick HIIT session (Gillen. 2014).

Why? Well, as the headline of today's SuppVersity article says, the study shows that three (=3) minutes of all-out exercise per week (no typo or other mistake here!) will "Suffice to Increase Skelet al Muscle Oxidative Capacity and Improve Metabolic Health" (Gillen. 2014).

You can learn more about HIIT at the SuppVersity

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

HIIT Ain't For Everyone

Slackers, beware! The subjects of Gillen's study, fourteen overweight or obese men and women, who were recruited by poster advertisement from the McMaster Univerisity community, were not even as short in time as you were. While they still qualified as "sedentary based on their self-reported habitual physical activity", they actually did <2 data-blogger-escaped-u="">not "=zero" exercise sessions per week that lasted on average ≤ 30 min.

Participants were allocated into the male or female intervention group and matched for age, body mass index and VO₂ peak. The experimental protocol, itself consisted of familiarization and baseline testing that was followed by a 6 wk training intervention and post-training measurements. Over the course of the 6 week intervention period the subjects hit the gym only once a week, where they did

• 3x20 s all-out cycling efforts
• against a load corresponding to 0.05 kg/kg body mass,
• separated by 2 min of low intensity cycling (50 W)

The exercise was performed on an electronically braked ergometer (Veletron, RacerMate, Seattle, WA, USA). With the obligatory 2 min warm-up and 3 min cool-down at 50 W, the sessions lasted 10 minutes. That's more than just three minutes, but if you think about the exhausting part of the workout, only, it's actually not a three, not a ten, but a one minute workout.

Figure 1: Changes in BMI, parameters of blood glucose management (FPG - fasting peak blood glucose; FPI - fasting peak insulin; HOMA-IR, Gmax - maximal glucose levels in 24h; blood pressure (systolic & diastolic); MAP - mean arterial pressure; power output) in response to six weeks of once a week 3 min all out HIIT exercise (Gillen. 2014)

As you can see the once weekly workouts had a significant impact on both the parameters of glucose management and the cardiovascular and muscular fitness parameters (see Figure 1). The additional skeletal muscle biopsy samples the scientist obtained before and 72 h after training revealed that the above changes went hand in hand with an increase in maximal activity of citrate synthase and protein content of cytochrome oxidase 4 (p < 0.01, main effect) and increases in the maximal activity of b-hydroxy acyl CoA dehydrogenase in men only (p < 0.05).

All the aforementioned changes in protein expression will allow the participants to burn additional amounts of fat during exercise and at rest and could, in conjunction with the improvements in glucose management that was brought about by increases in GLUT4 glucose transporter activity on the muscle specifically, slow down their weight gain - in conjunction with dietary lifestyle changes, they would even favor fat over muscle loss.

If you've missed Saturday's HIIT vs. LISS efficacy comparison, check the article out now! And/or learn more about HIIT at the SuppVersity.

Bottom line: There is no debating, the "[s]hort-term interval training using a 10 min protocol that involved only 1 min of hard exercise, 3x/wk, stimulated physiological changes linked to improved health in overweight adults." (Glenn. 2014) Changes that may pay off in form of a handful of additional years on earth, if the subjects (a) stick to their new exercise protocol and (b) stop eating everything in sight, relatively indiscriminately.

Without dietary intervention, though, I am not sure if the relatively small amount of exercise will do anything but turn a profoundly unhealthy overweight individual into a slightly more healthy overweight individual. Moreover, it's unlikely that the protocol will produce similar benefits in lean, athletic individuals. For them it probably requires some more effort to stimulate fitness gains | Comment on Facebook.

References:

• Gillen, Jenna B., et al. "Three Minutes of All-Out Intermittent Exercise per Week Increases Skeletal Muscle Oxidative Capacity and Improves Cardiometabolic Health." PLOS ONE 9.11 (2014): e111489.

L-Carnitine Works! Yet, Maybe More Subtly Than Thought: 1.2-5g L-Carnitine Increase Expression of Genes Implicated in Fatty Acid Oxidation, Glucose & Lipid Metabolism.

Image 1: This is you... well, not exactly. It's rather an animal model of human carnitine metabolis ;-)

As a faithful student of the SuppVersity it stands out of question that you have read my masterpiece *rofl* on the "Purported Ergogenics" in the "Amino Acids for Super Humans Series". You will thusly be familiar with the inconsistency of the mostly disappointing results of randomized, placebo-controlled trials. Whether it was for fat-loss, for increases in exercise performance or whatever else the producers of respective supplements promise would happen, when you buy and take their oftentimes profoundly underdosed supplements, in the absence of pathological (or severe dietary) carnitine deficiency the observed effects, if there were any, were negligible.

A soon to be published paper by Janin Keller and other researchers from the Institute of Animal Nutrition and Nutrition Psychology at the Justus-Liebig-University, in Gießen, the Institute of Agricultural and Nutritional Sciences at the Martin-Luther-University, in Halle-Wittenberg, and the Hans-Knöll-Institute, Research Group Systems Biology/Bioinformatic, in Jena (all in Germany, btw.), does now shed some light onto the more subtle, epigenetic effects of l-carnitine supplementation (Keller. 2011).

Image 2: The calculation of human equivalent doses is a constant (unreliable) pain in my ass - either you don't have the adequate conversion ratio or you do not know how much an animal eats. weighs etc...

Note: While my calculation (see below) indicates that the equivalent dose of the dietary enrichment used in the study should be ~4-5g, Keller et al. use a different method to calculate dose equivalents that is based on the ~500g of feed the pigs consumed per day. According to their calculation the daily dose of l-carnitine on a per kg body weight base for the piglets (final body weight: 17kg) was 15mg/kg body weight l-carnitine. If we now take a look at our conversion table (cf. table 1), where this specific type of big obviously is not listed, we probably have to divide that by 1.1 to get the Human Equivalent Dose - but since this is for "Mini pigs", we will just leave it with 15mg/kg and would thus have a dose of only 1.2g for an 80kg human being.

Keller et al. fed a group of 16 male crossbred pigs (body weight at study begin: ~10kg) a standardized diet with a naturally occurring amount of <5mg/kg carnitine. Half of the pigs, did receive additional 500mg/kg carnitine in their feed. In view of the fact that this effectively centuplicated (x100) the carnitine content of the diet, and considering the fact that the average human dietary carnitine intake ranges from ~47mg in men to ~30mg in women (Lennon. 1986), this would translate into an additional dose of roughly 4-5g of supplemental l-carnitine per day for humans. If you buy your carnitine in bulk (currently ~5$ per 100g) mimicking the supplement regimen used in the study would cost you about 25cents a day... but I guess before you do that you will rightly want to know what the potential benefits would be.

Figure 1: Liver free and total l-carnitine levels (in nmol/g) in growing piglets after 21-days of normal or carnitine supplemented feed (data adapted from Keller. 2011)

As you can see in figure 1 the liver of the animals literally squirreled the l-carnitine away (this could also be the reason, why most of the previously cited studies saw only transient increases in serum l-carnitine levels and almost no increases in muscular carnitine stores). An increase of +915% in free and +937% in total liver l-carnitine content is - I probably don't have to mention that - more than significant and was not without consequences... consequences of which scientists probably would not have even thought about 10 or even 20 years ago - epigenetic changes of which Keller et al. write:

we observed that 563 genes were differentially expressed by L-carnitine. This shows that supplemental L-carnitine influences gene expression in the liver of piglets and indicates that at least some of the biological effects of L-carnitine are mediated by altering gene transcription. [...] Gene term enrichment analysis revealed that the most frequent biological processes associated with L- carnitine supplementation were dealing with metabolic processes. This was not surprising considering that the main function of L-carnitine is to stimulate energy metabolism by acting as shuttling molecule for long-chain fatty acids which also enhances the metabolic flux of glucose through the glycolytic chain. This was also confirmed by clustering analysis showing that 6 out of the 10 top-ranked clusters were dealing with metabolic processes. Representative genes from one of these clusters dealing with metabolic processes (carboxylic acid metabolic process, oxoacid metabolic process, organic acid metabolic process) encoded proteins or enzymes involved in cellular fatty acid uptake (SLC27A6, solute carrier family 27/fatty acid transporter, member 6), fatty acid activation (ACSL3, Long-chain-fatty-acid-CoA ligase 3) and fatty acid β-oxidation (ACADSB, Acyl-CoA dehydrogenase, short/branched chain specific), and most of these genes including SLC27A6, ACSL3 and ACADSB were found to be significantly up-regulated by L-carnitine supplementation.

Moreover, the researchers found that a whole host of genes (e.g. GLUT8, GCK and GPD1 more than 4x elevated) related to glucose metabolism (glucose transport, conversion of glucose into glucose 6-phosphate, and glycolysis, and hexose biosynthetic processes, like gluconeogenesis) and triglyceride metabolic and triglyceride biosynthetic processes were elevated, as well. Taken together this lead the scientists to conclude that the epigenetic changes that were induced by 21 days of (relatively) high-dose dietary l-carnitine supplementation suggest that the "conditionally essential" amino acid l-carnitine

1. ... exerts its "well-known stimulatory effect [...] on fatty acid β-oxidation" at least partly by stimulating the transcription of genes involved in "cellular fatty acid uptake, fatty acid activation and β-oxidation"
2. ... has profound beneficial effects on glucose metabolism and utilization, which are mediated "not only by [a genetically triggered] stimulation of glycolysis but also suppression of gluconeogenesis in the liver", and
3. ... triggers genetic modifications which lead to an "inhibition of glycerolipid biosynthesis and stimulation of lipoprotein secretion and fatty acid catabolism", which contribute to its overall beneficial effects on lipid metabolism.

Now that you have all the facts, I'll leave it up to you to decide whether those "hidden" genetic changes are worth the 0.25$ (or 0.06$ if you use the 1.2g dose, cf. red box above) you would have to pay for your share of supplemental l-carnitine per day... and by the way: don't ask me if whatever other form of carnitine will do just as well, better or worse. This is a question only a separate study could answer!

When Timing Matters - Melatonin: Incorrectly Timed it Ruins Your Glucose Metabolism - Studies Show Acute Increases in Glucose Excursions During OGTT of 186% With 5mg

Melatonin is one of the few supplements where timing is everything.

As of late the nutrient and supplement timing craze has started to abate. People begin to realize that timing doesn't always matter, and that you can still make gains if you don't consume your whey protein shake 2 minutes, but rather 60 minutes after your workout.

For some nutrients and supplements, timing does yet matter and with melatonin I want to introduce you to an example, where the beneficial effects are not just attenuated, but will actually turn against you.

Want to learn more about melatonin? The SuppVersity is the place to be.

Melatonin as potent as Letrozole

Melatonin for Bone & Tooth Health

M. Sleep Aid W/ Anti-Alzheimer's Effect

Melatonin vs. Fructose Overloads

Melatonin as Anabolic On-Switch

M. Anti-Alzheimer + Anti-Body Fat Agent

As a SuppVersity reader, you are well aware of the beneficial metabolic "side effects" of melatonin. Effects that are mostly related to its ability to re-align the circadian rhythm (learn more). As a SuppVersity reader, you will also know that circadian misalignments have been shown to augment markers of insulin resistance and inflammation, independently of sleep loss (Leproult. 2014). And, as a SuppVersity reader, I want you to be aware of the fact that taking melatonin at the wrong time points is going to induce just that: a circadian misalignment with all the negative consequences on your insulin sensitivity that messes with your internal clock is going to have.

Actually, I believe I've mentioned the seminal paper by Angelo Cagnacci et al. which is - at least to my mind - the first one to show that using melatonin the way only a dumbass would do, i.e. taking 1mg early in the morning, is going to ruin the insulin sensitivity of postmenopausal women.

Figure 1: Taken in the AM right before an oral glucose tolerance test, melatonin ruins postmenopausal women's insulin sensitivity. Glucose area under the curve, insulin and the amount of C-peptide that's required are increased (Cagnacci. 2001)

Just a couple of days ago a study from the University of Murcia in Spain confirmed that this problem is not one that occurs only in postmenopausal, but also in 21 young, healthy women (24 ± 6 y; body mass index: 23.0 ± 3.3 kg/m²). In said study, the oral glucose tolerance test (OGTT) was performed on four occasions: In the morning (9 AM), and evening (9 PM); each occurring 15 minutes after melatonin (5 mg) and placebo administration on 4 non-consecutive days.

And what Patricia Rubio-Sastre and her colleagues found clearly confirms the results Cagnacci et al. presented 13 years ago:

"Melatonin administration impaired glucose tolerance. When administered in the morning, melatonin significantly increased the incremental area under the curve (AUC) and maximum concentration (Cmax) of plasma glucose following OGTT by 186% and 21%, respectively, as compared to placebo; while in the evening, melatonin significantly increased glucose AUC and Cmax by 54% and 27%, respectively. The effect of melatonin on the insulin response to the OGTT depended on the time of day (P < 0.05). In the morning, melatonin decreased glucose tolerance primarily by decreasing insulin release, while in the evening, by decreasing insulin sensitivity."

If that's not enough to scare you away from stupid experiments that involve using melatonin as an "anti-oxidant" supplement at other time-points during the day than 1-2h before bed, you probably cannot be helped ;-)

Suggested: Melatonin the anabolic on-switch | learn more

Bottom line: Taking melatonin before a meal and / or anytime but 1-2h before bed is not just going to ruin its beneficial metabolic effects, it's actually going to ruin your insulin sensitivity. So, if you want to use it, make sure you do so at the correct time point.

Melatonin is not the only supplement, where timing appears to matter, by the way. If you want this post to be the first in a series of articles on supplements and other things where timing matters, let me know on Facebook - I may be inclined to write a couple of additional articles ;-)

References:

• Cagnacci, Angelo, et al. "Influence of melatonin administration on glucose tolerance and insulin sensitivity of postmenopausal women." Clinical endocrinology 54.3 (2001): 339-346.
• Leproult, Rachel, Ulf Holmbäck, and Eve Van Cauter. "Circadian misalignment augments markers of insulin resistance and inflammation, independently of sleep loss." Diabetes 63.6 (2014): 1860-1869.

Short Bursts of High Intensity Circuit + Plyometric Training Keeps Blood Sugar "In the Zone" - No Matter If Your Parents Were Obese Diabetics, Or Lean Athletes!

Circuit Train Your Way Out of the Type II Diabetes Trap - High Intensity Resistance Training + Plyometrics Work Regardless of "Bad Genes" | It's your Lifestyle not your destiny that determines whether you'll become and insulin resistant lifestyle diabetic or not.

While many people still believe that "cardio" training was the only way to keep your blood sugar levels under control, anyone who knows something about exercise physiology will argue that a highly anaerobic exercise regimen, just like high intensity resistance training, for example, should be a way more powerful blood glucose normalizer than a 20-40 minute jog.

I guess this was what Ryan D. Russell, Arnold G. Nelson, and Robert R. Kraemer must have had on their minds, as well, when they planned their most recent experiment. An experiment that was designed to (1) determine the clinical benefits of "high intensity-resistance-focused" exercise training (HIRFT) in  healthy young people (age 23.5; BMI 24.25kf/m²) and (2) elucidate whether these effects would differ between young people with and without a family history (FH) of type II diabetes, if the baseline fasting glucose levels were identical (6.67 mmol/L in the study at hand).

Using HIIT you can achieve similar results as in the study at hand

Never Train To Burn Calories!

Increase GH, Lower Body Fat

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

Triple Your Energy Exp.

The study consisted of three main parts: (A) a pre-training test day including fasting blood glucose measurement followed by determination of an estimated one-repetition maximum (1- RM) for bench press, squats, and dead-lift, and twopost-workout blood glucose measurements; (B) 7-weeks of short, HIRFT using fast-paced superset circuit training, body core, and plyometrics training; and, (C) a post-training test day including fasting and post-exercise blood glucose and re evaluation of calculated maximal strength. Participants were instructed not to perform strenuous exercise, nor consume alcohol or caffeine at least two days prior to either test day.

Table 1: Overview of the weekly training schedule (Russel. 2014)

Fasting blood glucose was measured in order to establish at baseline to ensure participants are evenly matched and not pre-diabetic. In order to determine if HIRFT is an effective means of resistance training, a sub-group was randomized to perform traditional multi-set resistance training instead of the fast-paced circuits, and strength gains was compared.

"Building the Jack-of-All-Traits Legs Workout With Squats, Jump Squats and Body Weight Plyometrics?" | more

"Individual resistance exercises were the same between both modes of training, and included: squat, bench-press, lateral pull down/seated row, shoulder press, push-up, bicep curl, triceps extension, and dead-lift exercises performed in that order.

Time to complete each session of multi-set training was 40-minutes, including 1-minute of rest between sets; while each circuit training session was limited to 10-minutes excluding warm-up and cool-down with no rest between exercises.

All subjects completed the same plyometric and body core exercises. Core and plyometrics continually changed with increased fitness. Core was performed in less than 15 minutes, using weighted/resistance techniques including, but not limited to: dumbbell sit-ups, medicine-ball toss, rolling on ab wheel (or barbell), and plank positions.

Plyometric workouts were completed in 50 minutes, and utilized short bouts of explosive movements with several minutes of rest between. Some workouts included: stadium sprints, clapping push-ups, box jumps, obstacle hops, ramp-runs, and various fast medicine ball and dumbbell movements.

The participants were encouraged to drink water ad-libitum before, during, and after workouts. Training progression was continuously monitored and load adjusted for all participants in both exercise groups to ensure continued progression, enabling all participants to continue to work out at 65-85% of 1RM (8-12 reps; to failure on last set) throughout training.

Figure 1: Strength gains (righ) and blood sugar reductions (left) correlate negatively (Russel. 2014)

While the specific HIRT circuit training showed significant reductions in fasting blood-glucose (p < 0.05), there were no differences in fasting, post-exercise, and 10-min recovery blood glucose concentrations between FH and CON.

Strength increased from pre to post training similarly in both groups, while fasting blood glucose concentrations decreased with training overall (p = 0.0054), with no differences between FH and CON groups (p = 0.7). Last but not least, the scientists found an inverse correlation between percent strength gains and decreased blood glucose concentrations from pre- to post-training (r= -0.519, p = 0.05), which indicates that the strength gains and thus eventually the training success determined the health improvements (measured as reductions in blood glucose levels).

Suggested read: "Isn't High Intensity Interval Training (HIIT) For Everyone? Study Puts "!" Behind "Personalized Training" - Fitness, Fatness, Age & More Determine Its Effective- & Usefulness" | read more

Bottom line: The study at hand demonstrates having a family history of type II diabetes is a lame excuse not to avoid having blame yourself for developing diabetes, when you are too lazy to go to gym to give your body a chance to burn off some of the sugary garbage you're shoveling down your piehole whole day, just like your sick relatives did.

Apropos "burning glucose", I am not sure why people still believe that it would always take endless, boring cardio sessions to ward off diabesity, when it's resistance training that depletes your intramuscular and hepatic glycogen stores to make room for the dietary glucose that would otherwise build up in your bloodstream until your organs are sugar-coated.

Reference:

• Russel, et al. "Short bouts of high-intensity resistance-style training produce similar reductions in fasting blood glucose of diabetic offspring and controls." Journal of Strength and Conditioning Research (2014). Publish Ahead of Print - DOI: 10.1519/JSC.0000000000000624

Raspberry Ketones? Why, if Two Grande Caffe Americano Could Suffice To Keep Your Belly & Liver Fat Free and Your Heart Healthy, Even on a +40% Hypercaloric Crap Diet?

Image 1: If I had the choice to have a tasty cup of coffee with the beautiful young lady or a couple of overpriced  raspberry ketone caps with Dr. Oz, I would not even need scientific studies to make my choice ;-)

I am a huge fan of innovation, but when the name of the innovation begins with “raspberry” and ends on “ketones”, is pimped by TV doctors and sold on the 24h shopping channels, I can do well without it and better drink another cup of coffee and eat a couple of lycopene-laden tomatoes, whenever I feel the need to prevent hepatic steatosis on an obesogenic diet. I know this may not be as hip as investing 30-50 bucks in an underdosed “scientifically proven” (by exactly two dubious rodent trials, i.e. Miromoto. 2005, Wang. 2012) raspberry ketone supplement, but, on the other hand, it is also half as stupid and probably at least as efficient (Bahcecioglu. 2010; Vitaglione. 2010; Birerdinc. 2011; Molloy. 2011).

And what's more, picking cafeine over raspberry ketones would not only protect me and my virility from potential anti-androgenic effects of the latest nutraceutical rip-off (Ogawa. 2010), it could, according to a recently published study from the Department of Biological and Physical Sciences at the University of Southern Queensland in Toowoomba, Queensland, Australia, also help me to stay lean by simply blocking fatty acid synthase (FAS) in my adipose tissue (Panchal. 2012).

Caffeine? how boring is that!?

Contrary to the, as of late, often-cited study by Wang et al. on raspberry ketones (Wang. 2012), which is by the way one out of two peer-reviewed in vivo studies (the other one is Morimoto. 2005) to support the claim that raspberry ketones do anything, when they are not administered in unrealistic amounts to cells in a petri dish, Panchal et al. did not just measure a couple of serum markers, but investigated a host of metabolic parameters and structure and function of the heart and the liver of their 6-8 week old male Wistar rats that had been randomly assigned to what you might jokingly call the “pest or cholera” diets for 16 weeks: Corn starch diet (control), corn starch diet plus caffeine (CC), high-carbohydrate, high-fat diet (H), or high-carbohydrate high-fat diet plus caffeine (caffeine supplementation with 0.5g per kg chow took place only in the last 8 weeks of the 16-week study period).

Figure 1: Final body weight and body composition after 8 weeks without and another 8 weeks with caffeine supplementation (based on Panchal. 2012)

If we assume that the cornstarch only diet is pest and the high fat high carbohydrate diet is cholera, the data in figure 1 clearly indicates that 28.1mg/kg body weight caffeine ARE sufficient to reverse the effects of the pest and that 47.9mg/kg body weight caffeine are potent enough to survive any cholera epidemic; or put straight, the rodents on the

• standard cornstarch diet, which consumed 28.1mg caffeine per kg body weight (~360mg for a human being) per day, were leaner than their peers in the “control” group and that despite a 20% increase in energy intake
• high carbohydrate + high fat diet, which consumed 47.9mg caffeine per kg body weight (~612mg for a human) per day, were about as lean as the rodents on the standard diet and that despite a 40% higher energy intake (3% more than their peers in the high carbohydrate high fat diet without caffeine supplementation)

I guess none of you but maybe a few less educated minds could now reply: "Whatever... Dr. Oz said raspberry ketones are healthy; and everyone knows caffeine is not!" So, is this another case where Dr. Oz was at least partially right (cf. "Every Dog Has His Day: Dr. Oz Was Right, Exercise Does Not Just Make You Hungry, But Reduces Energy Intake!")? The increased glucose clearance and the reduction in visceral fat pad weight do speak a different language (cf. figure 2):

Figure 2: Parameters related to glucose and lipid metablism as well as visceral fat depot weight expressed relative to the non-supplemented rodents in the cornstarch control level (based on Panchal. 2012)

The same goes for the cardiovascular and liver parameters who give a damn about the increases in total cholesterol, free fatty acid and triglyceride levels, if those are the result of increased lipolysis (release of fattty acids from aidpose tissue), decreased fatty acid deposition in adipose tissue and an overall increase in metabolic rate, which is a long-established consequence of methylxanthine (=caffeine) intake in rodents and human beings (Bracco. 1995):

"[...] there was removal of fat from the abdominal area, and this fat was not transported to the
other fat-storing areas, including subcutaneous fat [...] The increase in plasma lipid components, especially NEFA, reflects the removal of fat from the abdomen [...with] the excess plasma
lipids are being metabolized rather than stored in the organs [...]" (Panchal. 2012)

The fact that the fat is simply "burned off" also explains that the increased non-esterified fatty acid concentrations, scientists usually associate with cardiovascular dysfunction and hepatic steatosis (fatty liver) did not lead to any of these complications in the study at hand. On the contrary, ...

[...] despite much higher plasma concentrations of NEFA in the caffeine-supplemented rats [..t]hese rats showed decreased infiltration of inflammatory cells, decreased collagen deposition, and decreased diastolic stiffness in the left ventricle, attenuation of non-alcoholic steatohepatitis [...]

Now, the question still remains: Why, are not all Starbucks customers lean then? The answer is pretty simple and "visualized" in image 2, it carries names such as "Peppermint White Chocolate Mocha" contains the sugar equivalent of 8½ scoops Edy’s Slow Churned Rich and Creamy Coffee Ice Cream and is "America's Worst Espresso Drink" - at least according to foodfacts.com. And while you can easily make it worse by adding some caramel syrup or junk, the average normal weight woman (if those still exist today) would almost get the +40% caloric intake the rodents in the high fat high carbohydrate diet consumed from that one "coffee" alone!

2-3 cups of black coffee would suffice!

Image 2: Starbucks Peppermint White Chocolate Mocha with Whipped Cream, 660kcal, sugar equivalent: 8½ scoops Edy’s Slow Churned Rich and Creamy Coffee Ice Cream (foodfacts.com)

If you pass those diabolic sugar bombs and pick up one Grande Caffe Americano (225mg caffeine per serving) in the AM and another one in the afternoon or before your workout (cf. "Pre-Workout Caffeine: Fat Liberator, Substrate Modulator, Trans-Fatty Acid Eliminator & Performance Upregulator!"), make sure to get your 20g+ of protein with every meal and refrain from drinking 100 bottle of Pinot Noir every day, to make sure to  get your share of fat-burning, strength building and endurance enhancing resveratrol (cf. "Resveratrol from 100l of 1994 Pinot Noir Could Increase Fat Oxidation by 71%, Strength by 18-58% and Endurance by 20%"), your liver, heart and metabolic health will thank you for that. Your belly and the raspberry ketone producers and snake oil vendors, on the other hand, will probably be offended - but I guess, you can live with that, right?

References:

1. Bahcecioglu IH, Kuzu N, Metin K, Ozercan IH, Ustündag B, Sahin K, Kucuk O. Lycopene prevents development of steatohepatitis in experimental nonalcoholic steatohepatitis model induced by high-fat diet. Vet Med Int. 2010
2. Birerdinc A, Stepanova M, Pawloski L, Younossi ZM. Caffeine is protective in patients with non-alcoholic fatty liver disease. Aliment Pharmacol Ther. 2012 Jan;35(1):76-82. doi: 10.1111/j.1365-2036.2011.04916.x. Epub 2011 Nov 7.
3. Bracco D, Ferrarra JM, Arnaud MJ, Jéquier E, Schutz Y. Effects of caffeine on energy metabolism, heart rate, and methylxanthine metabolism in lean and obese women. Am J Physiol. 1995 Oct;269(4 Pt 1):E671-8.
4. Molloy JW, Calcagno CJ, Williams CD, Jones FJ, Torres DM, Harrison SA. Association of coffee and caffeine consumption with fatty liver disease, nonalcoholic steatohepatitis, and degree of hepatic fibrosis. Hepatology. 2012 Feb;55(2):429-36. doi: 10.1002/hep.24731. Epub 2011 Dec 22.
5. Morimoto C, Satoh Y, Hara M, Inoue S, Tsujita T, Okuda H. Anti-obese action of raspberry ketone. Life Sci. 2005 May 27;77(2):194-204. Epub 2005 Feb 25.
6. Ogawa Y, Akamatsu M, Hotta Y, Hosoda A, Tamura H. Effect of essential oils, such as raspberry ketone and its derivatives, on antiandrogenic activity based on in vitro reporter gene assay. Bioorg Med Chem Lett. 2010 Apr 1;20(7):2111-4. Epub 2010 Feb 21.
7. Panchal SK, Wong WY, Kauter K, Ward LC, Brown L. Caffeine attenuates metabolic syndrome in diet-induced obese rats. Nutrition. 2012 Jun 19. [Epub ahead of print]
8. Vitaglione P, Morisco F, Mazzone G, Amoruso DC, Ribecco MT, Romano A, Fogliano V, Caporaso N, D'Argenio G. Coffee reduces liver damage in a rat model of steatohepatitis: the underlying mechanisms and the role of polyphenols and melanoidins. Hepatology. 2010 Nov;52(5):1652-61.
9. Wang L, Meng X, Zhang F. Raspberry ketone protects rats fed high-fat diets against nonalcoholic steatohepatitis. J Med Food. 2012 May;15(5):495-503.

Zinc: 15mg Are Plenty - After 120 Days Rodents on Diets Containing 2xRDA of Zinc Develop Metabolic Syndrome

Image 1 (scipop): Physicists and battery specialists know that copper and zinc make a galvanizing couple. If you put too much copper into your "battery" it will however stop working.

A recently published study from the Panjab University in India clearly suggests that doubling or quadrupling your zinc intake, a common practice in the health and fitness community, could do more harm than good. After only 4 months on a low phytate, high zinc diet (2x or 4x more zinc than in the standard chow), the rodents in the medium and high zinc intake goups showed a couple of unsettling metabolic changes (Taneja. 2012):

• 20-40% increase in food intake
• 20% increased body weight
• 2x or 2.7x elevated blood sugar
• 3.75x or 6x elevated insulin levels
• 100% increase in cortisol
• 2x or 2.5x elevated leptin levels

In short, while the Wistar rats that consumed the basal diet with the "rodent RDA" of 20mg zing per kg diet (0.53mg/day, 1mg/kg; HED ~0.17mg/kg or 8014mg/day) those with a two (human equivalent: 30mg) or four times (HED: 60mg/per) higher intakes developed all the classic symptoms of the metabolic syndrome

• insatiable hunger despite overabundant energy intake
• uncontrolled weight-gain => obesity
• high blood sugar, insulin resistance => type II diabetes
• constantly elevated cortisol levels
• leptin resistance

Interestingly, these highly undesirable effects of long-term were precipitated by profound morphological changes in the structure of the mucosal epithelial cell layer of the intestine:

Figure 1: Mean microvillus height and number/unit surface area of mucosal epithelial cell of intestine in normal zinc (control) or high zinc groups (Taneja. 2012)

The TEM studies of intestinal segment revealed a significant increase in the absorption surface area of the absorptive mucosal epithelial cells. It was reflected as increase in mean height and number/ unit surface area of the microvillus (figure 1). Their mean height (nm) was calculated as 506.1 ± 2.30 in control group-I, 749 ± 1.22 in group-II and 942 ± 1.30 in group-III. Their  number/unit surface area (µm) was found to be 10.4 ± 0.51 in group-I, 13.2 ± 0.33 in group-II and 15.4 ± 0.36 in group-III (figure 1).

The increases in height and number/unit surface area were suggestive of increased capability of the intestine to absorb the nutrients per unit area than the control group-I.

Now what is interesting about these observations is not just that it is 100% logical (at least for a physicist like me) that an increase in epithelial surface area will increase the nutrient absorption, but also that scientists knew about them and their beneficial side-effects in people with Crohn's disease, a damaged  or "leaky" gut all along (Sturniolo. 2001) and still nobody ever even thought about the downsides of subsequently increased nutrient assimilation. Instead, it was once again simply concluded that what helps the sick, obese and pre-diabetic cannot hurt normal people - and that despite the absence of ample evidence for consistent beneficial effects of  zinc supplementation as a protective, let alone curative means in sick people (Beletate. 2007), or zinc (+ magnesium) supplementation in athletes (Wilborn. 2004)

Double or quadruple your zinc intake, avoid phytates and turn from athletic to diabetic!?

Figure 2: After only 120 days the rodent in the high zinc groups exhibited all the typical symptoms of the metabolic syndrome (Taneja. 2012)

In view of the fact that still way too many gymrats adhere to the false belief that a zinc supplement (just like a "high performance" multivitamin) was an absolute staple supplement everybody striving to build a better physique should consume, it is no wonder that supplement vendors like to put copious amounts of this cheap ingredient into their products. Even if you are cheap (or smart) and avoid buying one of the "performance" multis, the 15mg of zinc every standard multi has plus the 30-50mg of your "nightly" ZMA, would take you right into the danger zone and even beyond and assuming that you follow another currently often proffered advice, which is to avoid phytate containing foods like a plague, your additional dietary zinc intake would probably get you right into the 60mg/day zone, which was so detrimental to the metabolic health of the rodents in the Tenja study.

In the defense of zinc supplements it should yet be mentioned that the chow the rodents were fed in the course of the experiment was not exactly what you, as an educated SuppVersity students would consider healthy, let alone "optimal". After all the diet was deliberately composed of "semi-synthetic" ingredients such as refined sucrose instead of the regular "grainy" pallets you would find in standard rodent chow, "to rule out the possibility of Zn-interaction with fibres and phytates" (Taneja. 2012), so that it would not take so long for the effects of the exuberant zinc intake to manifest.

"But my ZMA works! I feel so much better on it and if I drop my multi I get sick!"

"Artificial diet, rodent study, no real world implications", I hear ya! A 2004 study by Xiang et al. is yet only one out of many examples which suggest that you should not be so sure that will get away with taking your zinc-laden "staple supplements" (and in the case of the "multi" not just because of the zinc) for years: Increased lipid oxidation after 2 weeks, and increases in total cholesterol, triglycerides, LDL-C, ApoB100 and decreased in HDL and ApoA1 after 8 weeks of 50mg zinc per day in formerly healthy men are likewise clear indices of developing metabolic syndrome (Xiang. 2004). A result, by the way, that does not stand in contrast to studies on the effects of dietary zinc intake on glucose management such as Kanoni et al. (2011), where the highest dietary zinc intake of all subjects was 12.4mg (!) and thus still below the RDA and right on par with what the "average" American gets from his junkfood diet and supplements (see figure 3)!

Figure 3: I would not hope that you are eating like the "average American", are pre-diabetic and / or obese, but the data from the NHANES study is another puzzle to the picture that explains why Mr./Mrs. Average's health may benefit, while yours may suffer from supplemental zinc - they just don't get enough in their diet (Briefel. 2000)

If you are not constantly wreaking havoc on your gut lining and want it to regrow, are obese or diabetic (we do have some studies that suggest that at least in certain subgroups supplemental zinc can ameliorate this condition, yet mostly at the expense of higher insulin levels), you may want to reconsider if those staples of yours are really necessary, at least beneficial or maybe detrimental to the way you look feel and perform. And in the, as the guy at your local supp store would probably say, "totally improbable" case that despite taking all the staples he recommended, your blood glucose levels are getting out of whack, your cortisol is skyrocketing and your HDL is plummeting towards zero, you better not take his advice that all that will resolve once you introduced the latest (R-)ALA based nutrient partitioner into your supplement regimen (cf. "Lean & Muscular With Alpha Lipoic Acid?" ;-)

References:

1. Briefel RR, Bialostosky K, Kennedy-Stephenson J, McDowell MA, Ervin RB, Wright JD. Zinc intake of the U.S. population: findings from the third National Health and Nutrition Examination Survey, 1988-1994. J Nutr. 2000 May;130(5S Suppl):1367S-73S.
2. Beletate V, El Dib RP, Atallah AN. Zinc supplementation for the prevention of type 2 diabetes mellitus. Cochrane Database Syst Rev. 2007 Jan 24;(1):CD005525. Review. 
3. Kanoni S, et al. Total zinc intake may modify the glucose-raising effect of a zinc transporter (SLC30A8) variant: a 14-cohort meta-analysis. Diabetes. 2011 Sep;60(9):2407-16.
4. Taneja SK, Jain M, Mandal R, Megha K. Excessive zinc in diet induces leptin resistance in Wistar rat through increased uptake of nutrients at intestinal level. J Trace Elem Med Biol. 2012 Jun 8.
5. Sturniolo GC, Di Leo V, Ferronato A, D'Odorico A, D'Incà R. Zinc supplementation tightens "leaky gut" in Crohn's disease. Inflamm Bowel Dis. 2001 May;7(2):94-8.
6. Wilborn CD, Kerksick CM, Campbell BI, Taylor LW, Marcello BM, Rasmussen CJ, Greenwood MC, Almada A, Kreider RB. Effects of Zinc Magnesium Aspartate (ZMA) Supplementation on Training Adaptations and Markers of Anabolism and Catabolism. J Int Soc Sports Nutr. 2004 Dec 31;1(2):12-20. 
7. Xiang Y, Yang X, Bian J, Wang L. [Effects of high level Zn intake on metabolism in man]. Wei Sheng Yan Jiu. 2004 Nov;33(6):727-31.