4x4 Minutes of HIIT Per Week That's All It Takes For Already Well-Conditioned Individuals to Stimulate Mitochondrial Growth ➯ 15% Increase in VO2Max, Peak & Mean Power

HIIT is a builder, not a burner - it builds the powerplants you need to burn.

For you as loyal SuppVersity readers, the fact that HIIT is the #1 growth promoter for your mitochondria is no news. That 4x4 minutes of HIIT per week are yet already enough to promote significant increases in the mitochondrial counterpart of mTOR, PGC-1α - the master regulator of mitochondrial biogenesis (Wu. 1999) - will probably still comes as a surprise. This is all the more true in view of the fact that these observations have been made in young, healthy, recreationally active adult men - not fat rodents, frail heart disease patients or sedentary type II diabetics.

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

Triple Your Energy Exp.

The corresponding study, which was conducted by researchers from the Queen’s University, the Kingston General Hospital and the University of British Columbia Okanagan, involved four weeks of "tabata style" high intensity interval training. The 4x4 training sessions consisted of 8x20s intervals separated by 10 s of rest. The equipment of choice was a Monark Ergomedic 874 E stationary bicycle ergometer with the resistance being set to 170% of the individual subject's peak aerobic power at 100 rpm.

Figure 1: Changes in performance parameters and protein + enzyme expression (Ma. 2013)

When you take a look at the changes, I want you to keep in mind that 19%, 14% and 13% increase in VO2Peak, peak aerobic performance and mean power during the Wingate test were the result of exactly 43min* of active exercise distributed across a 4-week timespan (*excluding the rest periods)... now that you've digested that, ask yourself: Is my training regimen anywhere near as effective? I mean, what was the result you got from the last 43 minutes you've been sweating in the gym?

While you are pondering this question, let's briefly take a look at the way Jasmin K. Ma, Trisha D. Scribbans, Brittany A. Edgett, J. Colin Boyd, Craig A. Simpson, Jonathan P. Little, and Brendon J. Gurd evaluate the results of their latest study and the differences to previous low-volume HIIT interventions:

Suggested: "Cardio or Weights? What Do Lean People Do to Lose 20% Abdominal Fat in 10 Weeks?" | more

"While other low volume HIT protocols have reported non-significant (Burgomaster. 2005, 2006) or small (below 10%) increases in aerobic capacity (Burgomaster. 2008; Hazell. 2010) the current protocol induced rela- tively large increases in both VO2peak (+19%) and an- aerobic performance (+12% - 14%). These findings con- firm the results of Tabata et al.(1996) who reported ele- vated VO2peak at both 3 and 6 wks of training, and demonstrate that increases in VO2peak occur following 2 wks of training. Interestingly, while VO2peak is traditionally believed to be determined by cardiac output, a recent report demonstrated increased VO2peak without an accompanying increase in maximal cardiac output following treadmill sprint interval training (MacPherson. 2011)."

In other words: You don't necessarily have to do "cardio" training to improve what people usually call your "cardiovascular fitness", when they actually mean your overall conditioning. In the end, that's similar to sports cars. If you build a sports car or formula one racer, the best engine is useless, when the gear can't transfer its power to the wheels. For humans that's not much different. It is thus only logical to accept Ma et al.'s hypothesis that the "elevated aerobic capacity following low volume HIT may be result from peripheral [and not central cardiovascular] adaptations." (Ma. 2013)

Bottom line + important reminder:  Despite the fact that the increase in citrate synthase (CitSyn; cf. Figure 1) didn't reach statistical significance, the overall increase in mitochondrial protein (COX I and IV) will still allow for an increase in fatty acid oxidation during exercise. If you still believe that HIIT sessions were mainly used to lose body fat you are totally off track. The total calorie expenditure is way too low to have any effect on your body fat levels.

The thing HIIT is good for is what you see in the study at hand. It's a mitochondrial builder that will ramp up PGC-1α, increases the mitochondrial firepower of your cells and promote the oxidative capacity of their power houses. How you use this increased "firepower", i.e. to run faster or longer or to burn a couple of additional calories while you are doing steady state cardio, play basketball or perform any other kind of aerobic activity to promote the baseline fat loss effects of your diet, is up to you, though.

References: 

• Burgomaster, K.A., Hughes, S.C., Heigenhauser, G.J.F., Bradwell, S.N. and Gibala, M.J. (2005) Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans. Journal of Applied Physiology, 98, 1985-1990.  
• Burgomaster, K.A., Heigenhauser, G.J.F. and Gibala, M.J. (2006) Effect of short-term sprint interval training on human skeletal muscle carbohydrate metabolism during
  exercise and time-trial performance. Journal of Applied Physiology, 100, 2041-2047. 
• Burgomaster, K.A., Howarth,K.R., Phillips, S.M., Rakobowchuk, M., MacDonald, M.J., McGee, S.L. and Gibala, M.J. (2008) Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. The Journal of Physiology,
  586, 151-160. 
• Hazell, T.J., MacPherson, R.E.K., Gravelle, B.M.R. and Lemon, P.W.R. (2010) 10 or 30-s sprint interval training bouts enhance both aerobic and anaerobic performance. European Journal of Applied Physiology, 110, 153-160.  
• Ma, J. K., Scribbans, T. D., Edgett, B. A., Boyd, J. C., Simpson, C. A., Little, J. P., & Gurd, B. J. (2013). Extremely low-volume, high-intensity interval training improves exercise capacity and increases mitochondrial protein content in human skeletal muscle. Open Journal of Molecular and Integrative Physiology, 3, 202.
• MacPherson, R.E.K., Hazell, T.J., Olver, T.D., Paterson, D.H. and Lemon, P.W.R. (2011) Run sprint interval training improves aerobic performance but not maximal cardiac output. Medicine & Science in Sports & Exercise, 43, 115-122.
• Wu, Z., Puigserver, P., Andersson, U., Zhang, C., Adelmant, G., Mootha, V., ... & Spiegelman, B. M. (1999). Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1. Cell, 98(1), 115-124.

Medium Intensity Interval Training (MIIT) Increases Fitness of Overweight Sedentary Women Slower, But Eventually Just As Effectively as HIIT. Neither Cuts Fat / Body Weight

It does not always have to be "all out", but 70% is probably the minimum for intervals - esp. for the non-obese.

If you know all SuppVersity articles by heart, the name Astorino may ring a bell. I mentioned a previous study by Todd A. Astorino in my 2012 article "Are You Still Burning Calories or Already Losing Fat? Study Shows: 5x15 Min HIIT Reduce Body Fat & Improve Fitness Twice as Effectively as 5x40min of Classic Cardio" (read more). In their most recent study, the researchers from the Department of Kinesiology at the California State University took another look at HIIT exercise for the average female US citizen, to be precise. And the observation they made is actually quite astonishing.

MIIT vs. HIIT: Can both be equally effective?

In this group of healthy sedentary (<1h/week of regular physical activity) women (n=30; age 18-40; BMI >35kg/m²) it did effectively not make a difference, whether the participants trained at a high or medium intensities.

As you can see in figure 1, over time, both workouts yielded the exact same increases in VO2Max (marker of cardiovascular fitness)., What is however significantly different is the slope and the general look of the VO2max graph.

Figure 1: Study design and results of the 12-week intervention; training was performed 3 days/week on a cycle
ergometer and consisted of 6–10 bouts of 1 min duration at the given intensities; the asterisk after the week # indicates that the intensity values were adapted to the increase in W-Max over the past weeks (Astorino. 2013)

While the latter is clearly logarithmic for the high intensity interval training arm (HIIT; intensities see figure 1, left), the MIIT (LO in figure 1) VO2Max development is much more linear and does not display the same ceiling effect you see in the HI group. It would thus be reasonable to argue that...

MIIT hits HIIT, but...

... it is VERY likely that this is a "overweight woman phenomenon". After all, the heart rate was essentially the same regardless of whether the ladies worked out at an average intensity of 176W (MIIT) or 202W.

Figure 2: Heart rate and workload develoment over the 12-week study period (Astorino. 2013)

At first that may seem odd, but to push your heart rate through the 200 mark, you actually need a pretty decent fitness level. If you have been sitting around your whole life, you will be up to 190bpm when you simply take the stairs instead of the elevator; and while this is no health benefit it makes the same walk in the park that's just a nasty way of locomotion for the average athletic person an intense workout for the morbidly obese.

And what do we know about "intense workout"? Right, those are the true "cardio workouts" adaptation does not happen in the comfort zone and it does not entail weight loss (!) - I don't know how often I have to repeat that, but weight loss happens in the kitchen. You can only steer and promote what and how much you lose by working out... but that's the topic of another article.

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"Men are different women, too..." We all know that, but can we still train together or will women have to do cardio first, while men would be better off starting out lifting weights? (learn more)

Bottom line: If you, family or friends are starting out to work out - keep things at a pace that's intense for YOU - not for whomever you are trying to emulate or you are training with. If there is one beauty of doing cardio in the gym instead of outside, it is that you can train right next to a friend at your personal intensity level.

So don't put a spoke into your own wheels by trying not too look bad in front of a friend. Stick to your own tempo and use yourself as a reference to judge your progress - and if the latter looks like the orange graph in figure 2 (right) you know you are on track, no matter what the absolute wattage (or RPMs) say.

References:

• Astorino TA, Schubert MM, Palumbo E, Stirling D, McMillan DW, Cooper C, Godinez J, Martinez D, Gallant R. Magnitude and time course of changes in maximal oxygen uptake in response to distinct regimens of chronic interval training in sedentary women. Eur J Appl Physiol. 2013 Sep;113(9):2361-9.

HIIT Economy: 30s Intervals + 2:1 Work-To-Recovery Ratio Allow For Maximal Peak Oxygen Uptake at Minimal Power Output During HIIT Exercises in Advanced Trainees

We all know and follow the fundamental rules of the marketplace, but when we are in the gym we tend to forget about profit maximization and the minimal investment, maximal returns principle.

It is quite funny that our gyms are among the few places in our economy-driven society where people tend to forget about the fundamental rules of the marketplace. The way many of weekend-warriors and fitness junkies train is in fact the exact opposite of the all-governing principle of profiteering. In their desperate and in many cases misinformed efforts to maximize their muscle gains, fat loss or overall fitness, many of them fail to realize that the "optimal" training strategy is not the one that leads to suboptimal results at a maximal level of exhaustion. Think about the 2h cardio sessions in the non-existent fat burning zone, for example, or the two hour resistance training workout with 10 different exercises per body part.

Even if you don't belong to this group of miserably misguided souls, I believe there is this innate masochistic side in all of us that makes us believe that the degree of post-workout exhaustion is an adequate measure of the efficacy of a given workout. It does not matter if we are talking about classic cardio training, weight lifting or the high intensity interval training - all of them could benefit from goal-specific modifications, such as those that researchers from the Lillehammer University College in Norway have recently tested in a small scale intervention trial involving 13 well-trained male cyclists (Rønnestad. 2013).

Note: Your Tmax is the time to exhaustion during continuously cycling to exhaustion at the minimal power output (MAP) that elicits peak oxygen uptake (VO2max).

The goal Rønnestad and Hansen had had in mind, when they came up with the study design  was to investigate the effect of interval durations of 30s, 50% of Tmax [Tmax = ], and 80% of Tmax on the corresponding time-periods the athletes would exercise at ≥90% of their peak oxygen uptake. The three workouts that were performed on three different occasions had a work-to-rest ratio 2:1 and the intensity during the active recovery periods was 50% of the minimal power output (MAP) that elicits peak oxygen uptake (VO2max).

The latter, i.e. the time spent at a minimal power output that elicits peak oxygen uptake, was obviously also the criteria to define the "optimal" HIIT workout. After all, it can be expected that the "cardiovascular" (=fitness) benefits and the corresponding increases in the max. VO2 will be most pronounced, when you work out close to your individual VO2max without subjecting yourself to a potentially detrimental strain.

Figure 1: Maximal rate of perceived exertion, lactate levels and rtime at >90% heart rate in % of the total exercise time (left); VO2 levels at different timepoints expressed as percentage of time to exhaustion (Rønnestad. 2013)

As the scientists point out, their observation that their interval protocol using 30 s work periods induced a longer time ≥90% of VO2peak, longer time ≥90% of HR peak, and longer work durations at MAP intensity than the interval protocols using work periods of 50% of Tmax and 80% of Tmax

"diverge somewhat from the findings of Millet et al. (2003) [who] compared, amongst others, intermittent runs at MAP with a work duration of 30 s and 50% of Tmax with a 1:1 work:recovery ratio and a recovery intensity of 50% of MAP [and] found that work intervals lasting 50% of Tmax resulted in greater time ≥ 90% of VO2peak than work intervals of 30 s (~ 8 min vs. ~ 2.5 min, respectively)." (Rønnestad. 2013)

According to the authors this difference is probably a direct consequence of the extended active rest periods in the Millet trial. While the study at hand used rest periods of 15s (50% of the time spent ad MAP intensity), the participants in Millet's study rested for 30s. Enough time for the heart rate to recover and the "workout economy to decline".

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Suggested read: "Eight HIIT Sessions on the Rowing Ergometer Cut Body Fat, Increase Adiponectin, VO2Max & Performance in National Level Rowers - Workmatched Classic "Cardio" Does Nothing" | read more

Bottom line: "Cardio" as in "cardiovascular exercise" is supposed to be a form of training that is challenging enough to elicit beneficial adaptation processes that will results in increased exercise performance and/or VO2max. For most advanced trainees, a conventional "cardiovascular training" at say 70-80% of the individual VO2max is not going to deliver the stimulus that would be necessary to elicit significant adaptation processes.

For the advanced trainee looking to increase his cardiovascular capacity, high intensity interval training should thus be the training method of choice and as the study at hand confirms, the most economic form of HIIT is one that maximizes the time spent in the magic >90% of your HR peak training zone, at minimal intensities.

References:

• Millet, GP, Candau, R, Fattori, P, Bignet, F, and Varray, A. VO2 responses to different intermittent runs at velocity associated with VO2max. Can J Appl Physiol 28: 410-423, 2003.  
• Rønnestad BR, Hansen J. Optimizing interval training at power output associated with peak oxygen uptake in well-trained cyclists. J Strength Cond Res. 2013 Aug 12. [Epub ahead of print] 

Unexpected Performance Increments in Elite Wrestlers in Response to Well-Timed Arginine Supplementation: 5.8% Increased Time to Exhaustion, No Recution in O2 Cost!

Science is still wrestling with evidence in favor vs. against l-arginine

Actually the study at hand is not really exciting, the researchers from the Near East University Medical School in Cyprus recruited nine male national and international level wrestlers put them on more or less standardized diets, forbid them to work out and or use caffeine, stimulants or other ergogenic supplements and fed them 1.5g arginine per 10kg body weight (that's 12grams for someone with a body weight of 80kg).

Aside from the dosage, which would be on the higher side compared to the average arginine trial, there were no significant differences to study protocols you know.

Lear more about L-arginine at the SuppVersity!

No N.O. W/ Arginine

Arginine vs. High Lipids

Arginine Blunts GH?!

Arginine for Satiety?

Arginine vs. T2DM

Arginine for Fat Loss?

The subjects reported to the laboratory fasted in the AM, they have followed identical diets before both the active and the placebo trial and they had to perform one of those arduous pedal until you drop exercise tests on a cycle ergometer...

There was one difference, however. The subjects were not allowed to start working out immediately after they'd washed down the arginine / placebo supplement. Instead, they had to wait for sixty minutes for the arginine peak in plasma (Gannon. 2002).

Figure 1: Time to exhaustion and lactate levels increased, the VO2 costs of which you could expect that they decreased and would thus allow for the increased time to exhaustion, on the other hand, didn't change (Yavuz. 2014)

And voila! As you can see in Figure 1, Yavuz, Turnagol and Demirel observed a significant performance increase in the arginine trial.

In that, it is quite astonishing that these improvements occurred in the absence of changes in VO2 consumption. A reduction in O2 cost, as it was reported by Bailey et al. (2009) would after all be the most obvious explanation of the ergogenic effects of arginine.

Suggested Read: Arginine a BAT Building WAT Killer & Repartitioning Agent? Plus: The Arginine Enriched Biscuits Diet ;-) | read more

Bottom line: Previous results of studies with arginine supplementation on performance are rather inconsistent and it is difficult to say whether these differences can be explained by the length of the supplementation period, the combination of arginine with different components, different doses of arginine, different exercise protocols, different fitness levels of subjects (endurance trained athletes, physically active healthy men, or combat sports athletes as in the study at hand). Even the hitherto overlooked exact timing of supplementation and workout could make all the difference - so in case you still have a truckload of arginine lying around at home, remember to take it on an empty stomach and 60 minutes before your workouts.

Reference:

• Bailey, Stephen J., et al. "Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans." Journal of Applied Physiology 107.4 (2009): 1144-1155.
• Gannon, Mary C., Jennifer A. Nuttall, and Frank Q. Nuttall. "Oral arginine does not stimulate an increase in insulin concentration but delays glucose disposal." The American journal of clinical nutrition 76.5 (2002): 1016-1022.
• Yavuz, H. U., H. Turnagol, and A. H. Demirel. "PRE-EXERCISE ARGININE SUPPLEMENTATION INCREASES TIME TO EXHAUSTION IN ELITE MALE WRESTLERS." Biol. Sport 31 (2014): 187-191.

Resveratrol from 100l of 1994 Pinot Noir Could Increase Fat Oxidation by 71%, Strength by 18-58% and Endurance by 20% - At Least, If You Could Afford and Drink It Every Day!

Image 1: Itadori (Japanese Knotweed) and selected varieties of red wine are the best yet vastly 'underdosed' sources of resveratrol (see red box, below)

At least in rodents, resveratrol, the red-wine polyphenol, has been shown to act as an exercise mimetic, exerting profound effects on PGC-alpha expression which protect muscle from wasting due to mechanical unloading (also know as extreme couch-potato-ing ;-) and rodents from the negative side-effects of obesogenic diets by directly modulation gene expression, lipid transport and fatty acid oxidation in skeletal muscle (Chen. 2011; Momken. 2011). Still, most of the oftentimes publicly puffed up data on resveratrol comes from in-vitro studies with dosages of which even the researchers often believe that they are not attainable via oral supplementation.

Rodents or petri dishes? Humans would be too expensive...

Compared with the aformentioned in vitro data, the numbers and gene essays in a recently published study by scientists from the University of Alberta are actually of great practical relevance (Dolinsky. 2012), because Dolinsky et al. administered their resveratrol orally* (4g in 1kg chow) to healthy rats and - what's even more important for the average trainee - 50% of those rats were exercised for 60min, 5x per week on a treadmill (10m/min to 20m/min; cf. Fenning. 2003) for 12 weeks.

Figure 1: Resveratrol content of selected red-wines and Itadori (Japanese knotweed) tea (based on Burns. 2005; equivalent consumption based on dose used in Dolinsky. 2012)

*Can I get my resveratrol from wine or food: I cannot emphasize enough that with ~75% of orally administered resveratrol being excreted via feces and urine and an oral bioavailability of resveratrol of almost ZERO (Vitaglione. 2005; Wenzel. 2005), there is no reason whatsoever to cope with any of the ~100 in-vitro studies that are published on a monthly basis hailing resveratrol for this and that and praising it as the god-sent natural remedy for every ailment, except the consistent ignorance towards the profound difference between a cell in a petri dish and a complex organism that is so prevalent among the human lab rats in their white coats, these days. And the data in figure 1 should make it pretty clear that similar benefits as they were observed in the study at hand are not just unlikely, they are simply impossible to be achieved without highly concentrated supplements - or do you want to drink 105+ liters of wine a day to get your daily dose of ~2g of resveratrol?

Let's assume you got the ~350$ for your 2g/day of resveratrol powder** to mix with your food (**calculated based on the current price of >90% pure bulk powder in Europe), what would be the results? Would you lose weight? Unlikely. Would you lose body fat? Possible! Would you gain muscle? Very unlikely. So what's all the fuss about then?

Figure 2: Body weight (in g), time to exhaustion (in min) and distance covered (in m) during a treadmill exercise test at the end of the 12-week study period (based on Dolinsky. 2012)

Much ado about nothing? Not really, no. After all, the ~20% increase in endurance (time to exhaustion and distance covered; cf. figure 2)  did not come out of nowhere and do - and this is actually the main reason this study did actually make it to SuppVersity - add to the benefits of regular training. The "resveratrol rats" had ...

Image 2 (ADAM): Resveratrol has already been shown to prevent pathological hypertrophy of the heart muscle by AMPK / AKT modulation (Chan. 2008)

• greater strength gains +18% tibialis anterior twitch force and +58% and +22% tetanic and twitch force, respectively, in soleus vs. training alone
• improved cardiac function as assessed by statistical significant improvements in left ventricular ejection fraction and decreased isovolumic relaxation time, as well as increased ratio of the peak mitral flow velocity (E-wave) to the peak velocity of the late filling wave of atrial contraction
• decreased cardiac stress due to a -30% reduction in left ventricular wall stress vs. training alone
• higher VO2 ~10% during the active period 
• increased PPAR signalling and fatty acid metabolism in the heart (+8.8% and +10.3% respectively; p < 0.00001)

Sexier than the strength gains and the utterly unsexy (but vitally important) improvements in cardiac performance are yet the statistically significant reduction in triglycerides which should help insulin sensitivity (not measured in the study) and are probably a beneficial downstream effect of the  resveratrol induced shift towards higher fatty acid and lower glucose oxidation (-6% respiratory exchange ratio, RER; cf. figure 3) that went hand in hand with a highly significant +71% increase in fatty acid oxidation:

Figure 1: Triglyceride levels, free fatty acids, respiratory exchange ratio (higher values = lower fat oxidation, higher glucose oxidation) and total fat oxidation at the end of the 12-week study period (all data expressed relative exercised control; based on Dolinsky. 2012)

Along with the +50% increase in AMPK (vs. exercise alone) and the 20% increase in the "mitochondrial builder" PGC1-alpha (cf. "Two days on High Fat Diet Increase the Activity of Irisin Releasing Transcription Factor PGC1-α") it is obvious that, taken at the right dosage, resveratrol is not the supplemental non-starter everyone is let to believe who spent $30 for 60 100mg caps of resveratrol and took a 3-day dose (3x 2g!) spread across a whole month - obviously without the desired outcomes result.

At the moment resveratrol is still an expensive toy for scientists

Table 1: Significant changes in heart muscle gene expression (based on Dolinsky. 2012)

As a tool to study (epi-)genetics and the downstream effects and interactions of reduction of cytokines, such as the inteferon-induced proteins, which regulate immune functions, cell growth and apoptosis (Sen. 2000), increases in mitochondrial uncoupling protein 3 (UCP3) and UCP1, higher expressions of adiponectin and thyroid responsive protein and the steroyl-coenzyme A desaturase-1 enzyme, which converts saturated to mono unsaturated fatty acids and plays an important role in controlling inflammation, preventing atherosclerosis, steatohepatitis (fatty liver) and pancreatic beta cell dysfunction (Brown. 2010) resveratrol is a must have. As one of the most expensive currently available supplement with little to no actual human data from studies on healthy subjects, its usefulness for physical culturists is questionable and its cost-benefit ratio is abysmal, to say the least.

References:

1. Brown JM, Rudel LL. Stearoyl-coenzyme A desaturase 1 inhibition and the metabolic syndrome: considerations for future drug discovery. Curr Opin Lipidol. 2010 Jun;21(3):192-7. 
2. Burns J, Yokota T, Ashihara H, Lean ME, Crozier A. Plant foods and herbal sources of resveratrol. J Agric Food Chem. 2002 May 22;50(11):3337-40. 
3. Chan AY, Dolinsky VW, Soltys CL, Viollet B, Baksh S, Light PE, Dyck JR. Resveratrol inhibits cardiac hypertrophy via AMP-activated protein kinase and Akt. J Biol Chem. 2008 Aug 29;283(35):24194-201. Epub 2008 Jun 18.
4. Chen LL, Zhang HH, Zheng J, Hu X, Kong W, Hu D, Wang SX, Zhang P. Resveratrol  attenuates high-fat diet-induced insulin resistance by influencing skeletal muscle lipid transport and subsarcolemmal mitochondrial β-oxidation. Metabolism.  2011 Nov;60(11):1598-609. 
5. Dolinsky VW, Jones KE, Sidhu RS, Haykowsky M, Czubryt MP, Gordon T, Dyck JR. Improvements in Skeletal Muscle Strength and Cardiac Function Induced by Resveratrol Contribute to Enhanced Exercise Performance in Rats. J Physiol. 2012 Apr 2. [Epub ahead of print]  Epub 2011 May 31.
6. Fenning A, Harrison G, Dwyer D, Rose'Meyer R, Brown L. Cardiac adaptation to endurance exercise in rats. Mol Cell Biochem. 2003 Sep;251(1-2):51-9.
7. Momken I, Stevens L, Bergouignan A, Desplanches D, Rudwill F, Chery I, Zahariev A, Zahn S, Stein TP, Sebedio JL, Pujos-Guillot E, Falempin M, Simon C, Coxam V, Andrianjafiniony T, Gauquelin-Koch G, Picquet F, Blanc S. Resveratrol prevents the wasting disorders of mechanical unloading by acting as a physical exercise mimetic in the rat. FASEB J. 2011 Oct;25(10):3646-60.
8. Sen GC. Novel functions of interferon-induced proteins. Semin Cancer Biol. 2000 Apr;10(2):93-101.
9. Vitaglione P, Sforza S, Galaverna G, Ghidini C, Caporaso N, Vescovi PP, Fogliano V, Marchelli R. Bioavailability of trans-resveratrol from red wine in humans. Mol Nutr Food Res. 2005 May;49(5):495-504.
10. Wenzel E, Somoza V. Metabolism and bioavailability of trans-resveratrol. Mol Nutr Food Res. 2005 May;49(5):472-81.

SuppVersity World Cup Special: What Football Can Do For Your Health & Performance Now & As You Age - It's Better for Heart & Bones (!) Than Lifting

Soccer! For Young & Old, Heart & Bones, Blood Sugar & Body Fat Now & Beyond World Cup 2012

Ok, I have to admit, in spite of the fact that the World Cup starts today, I wouldn't have produced this article, if the editor(s) of the Scandinavian Journal of Medicine & Science in Sports didn't have a similar idea and I wouldn't have "early view" access to a bunch of soon-to-be-published on the beneficial and not so beneficial effects of what I call "football" and most of you call "soccer".

But enough of the prelude, let's take a look at what I have to report, here: Schmidt et al. present the amazing cardiovascular adaptations they observed in response to 4 and 12 months of football or strength training in 65- to 75-year-old untrained men.

If you want to get fit fast, try HIIT | learn more 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

Triple Your Energy Exp.

The study was conducted at the Copenhagen Centre for Team Sport and Health of the University of Copenhagen and involved, as you would have guessed, 26 untrained men (age: 68.2 ± 3.2 years). The guys were randomized to football training (FTG; n = 9), strength training (STG; n = 9), or control (CG; n = 8).

Football (soccer), older hearts will love it!

Maximum oxygen consumption (VO2max; L/min) and resting heart rate (RHR; bpm) in elderly healthy 65- to 75-yearold men at baseline, after 4 & 12 months of football training (FTG), strength training (STG), and control (CG) - Schmidt. 2014

Aside from the impressive improvements in VO2max (vs. no improvement in either the strength training or the control group; see Figure 1), the researchers observed the following beneficial structural changes of the heart:

• increases in left ventricular diastolic diameter +8%
• increases in end-diastolic volume +21%
• increases in ventricular mass index +18%

Unlike the improvements in ejection fraction (+8% in FTG vs. +5% in STG), these changes were "football"-exclusive.The systolic longitudinal two-dimensional strain increased by 8% (FTG) and 6% (STG), whereas the right ventricular systolic function improved (P < 0.05) by 22% in FTG, but not in STG and CG.

In conjunction with the football-exclusive increases in diastolic mitral inflow (E/A) ratio and peak early diastolic velocity (E') improved (25% and 12%, respectively), your 3x1h of training may thus be better spend on football than on resistance training if your main goal is to improve your VO2max and kick heart disease's ass.

If we look at the benefits the older guys in the Schmidt study derived from their soccer training it can hardly be surprising that Anderson et al. (2014a) report similarly "hearty" benefits in 31 untrained males with mild-to-moderate hypertension who were randomized 2:1 to a football training group (n = 20) and a control group receiving traditional recommendations on healthy lifestyle (n = 11).

While the football group exhibited significant (P < 0.05) changes in cardiac dimensions and function after just 3 months similar to those in the Schmidt study, as well as significant reduction in arterial blood pressure, the results in the "traditional take this *bs* advice" group were mediocre tat best. Consequently, the researchers conclude that even in the short term (3-6 months)...

"football training improves LV diastolic function in untrained men with mild-to-moderate arterial hypertension [and] improve longitudinal systolic function of both ventricles." (Anderson. 2014a)

 Now, SuppVersity readers are not generally hypertensive, and I am gathering that the few highly appreciated "best agers" in my readership are also in the minority. Against that background it's worth mentioning that the heart is not the only part of your body that will benefit from soccer practices - your bones will, too. Ok, I see you laughin' cause you're hittin' the weights, regularly, but what would you say if I told you that ...

"4 months of recreational football for elderly men had an osteogenic effect, which was further developed after 12 months, whereas resistance training had no effect."  (Helge. 2014)

I see, I've got your attention, now! Well, the authors, again researchers from the Copenhagen Centre for Team Sport and Health speculate that the anabolic response may be due to increased bone turnover, especially improved bone formation which was obviously promoted to a greater extent in those 9 of the initially 26 healthy sedentary men (age 68.2 ± 3.2 years) who had been randomized to the  football (F; n = 9) and not the resistance training (R; n = 9) group - and that despite the fact that both trained two to three times weekly for a total of 45–60 min training.

Playing soccer is good for your health, watching it... well, watching it can increase your risk of being hospitalized for acute myocardial infarction minimally (+1%; cf. Barone-Adesi. 2010), unless, of course, your team wins! During the 1998 World Cup, which was won by France, the myocardial infarction risk of French men was actually reduced by 35% (Berthier. 2003)

When it comes to improving the functional ability and physiological response to submaximal exercise, in older men, however, it's difficult to pinpoint a difference between three football and three resistance training sessions per week. Unsurprisingly, study #4 in today's review did yet report that only football trainign "additionally elevates maximal aerobic fitness and exhaustive exercise performance." (Anderson. 2014b).

What's left to discuss, oh yes! Anderson. 2014c and the effects on glucose management!

Yeah, with 21 middle-aged men (49.8 ± 1.7 years ± SEM) with T2DM as subjects, this study will certainly appeal to all the Average Joes out who unfortunately don't get their daily dose of SuppVersity wisdom, yet (Anderson. 2014c).

The said middle-aged subjects were divided into a football training group (FG; n = 12) and an inactive control group (CG; n = 9) - the absence of a strength training "control" is a pity... but alas, after the 24-week intervention period, in the course of which the sick guys covered only During 4.7 ± 0.2 km at a mean heart reate of 83 ± 2% of HRmax per 1h soccer training, they experienced a 11% increase in VO2peak and lost 1.7 kg and 12.8% of their total fat and android fat, respectively.

Against that background it's not that surprising that Anderson et al. report concomitant improvements in plasma glucose and an increased expression of the glucose transporters (GLUT-4). Most importantly, however, the Danish researchers did also observe an overall time effect for glycosylated hemoglobin (HbA1) and thus significant and continuous improvements in glucose management in the soccer group.

Bottom line: "There you have it" ... that's actually something my good friend Carl Lanore from www.superhumanradio.com like to say. There you have the benefits of playing soccer. Improved heart health, fat loss and reductions in blood glucose in type II diabetes are probably nothing, you wouldn't have expected, anyways, right?

 "The 100 Squats A Day Challenge: Body Weight Squats Get You in Shape in Less Than 3 Minutes." | read more

Well, what about the benefits on bone health, then? I personally was surprised that the impact of soccer training was more pronounced than the one of strength training. In the end, I would yet expect equal results if the latter, i.e. the strength training had included free-weight squats and/or deadlifts. Those and not sissy curls and lat pulldowns are true bone builders, but honestly - when I see some of the 60+ agers at my gym do them I think to myself: You better leave that to true physical culturists, like my previously mentioned friend Carl Lanore (www.superhumanradio.com) and head over to the soccer training, folks ;-)

References:

• Andersen, L. J., Randers, M. B., Hansen, P. R., Hornstrup, T., Schmidt, J. F., Dvorak, J., Søgaard, P., Krustrup, P. and Bangsbo, J. (2014a), Structural and functional cardiac adaptations to 6 months of football training in untrained hypertensive men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12237 
• Andersen, T. R., Schmidt, J. F., Nielsen, J. J., Randers, M. B., Sundstrup, E., Jakobsen, M. D., Andersen, L. L., Suetta, C., Aagaard, P., Bangsbo, J. and Krustrup, P. (2014b), Effect of football or strength training on functional ability and physical performance in untrained old men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12245
• Andersen, T. R., Schmidt, J. F., Thomassen, M., Hornstrup, T., Frandsen, U., Randers, M. B., Hansen, P. R., Krustrup, P. and Bangsbo, J. (2014b), A preliminary study: Effects of football training on glucose control, body composition, and performance in men with type 2 diabetes. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12259
• Barene, Svein, et al. "Soccer and Zumba as health-promoting activities among female hospital employees: a 40-weeks cluster randomised intervention study." Journal of sports sciences ahead-of-print (2014): 1-11. 
• Barone-Adesi, Francesco, et al. "It is just a game: lack of association between watching football matches and the risk of acute cardiovascular events." International journal of epidemiology 39.4 (2010): 1006-1013.
• Berthier, Fabrice, and Frédéric Boulay. "Lower myocardial infarction mortality in French men the day France won the 1998 World Cup of football." Heart 89.5 (2003): 555-556.
• Helge, E. W., Andersen, T. R., Schmidt, J. F., Jørgensen, N. R., Hornstrup, T., Krustrup, P. and Bangsbo, J. (2014), Recreational football improves bone mineral density and bone turnover marker profile in elderly men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12239.
• Ramírez-Campillo, Rodrigo, et al. "Effects of In-Season Low-Volume High-Intensity Plyometric Training on Explosive Actions and Endurance of Young Soccer Players." The Journal of Strength & Conditioning Research 28.5 (2014): 1335-1342.
• Schmidt, J. F., Hansen, P. R., Andersen, T. R., Andersen, L. J., Hornstrup, T., Krustrup, P. and Bangsbo, J. (2014), Cardiovascular adaptations to 4 and 12 months of football or strength training in 65- to 75-year-old untrained men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12217

Beet Root Juice Supplementation Improves Exercise Performance. Nitrate Content of the Beets Decreases ATP Turnover in High Intensity Exercise.

Nitrates have long been decried as toxic and dangerous and I bet, before their latest appearance to the supplement market, none of you would even have remotely considered to consciously increase his/her dietary nitrate supply. Yet, recent scientific studies confirm that nitrate (in moderate doses) is not only safe, but also has, its effects on vasodilation aside, quantifiable effects on exercise performance.

A group of scientists from the UK tried to find out the underlying mechanisms of the ergodicity of supplemental nitrate (Baily. 2011). Following a six day supplementation period in the course of which seven males (aged 19-38 yr) consumed 500 mL per day of either nitrate-rich beetroot juice (~300mg nitrate content) or placebo (PL, with negligible nitrate content). What they observed is best described as a "tuning effect" that was observable both, in the course of high, as well as in the course of low intensity exercise training.

During low intensity exercise, the pulmonary VO2 amplitude and thus the oxygen need during this kind of aerobic exercise decreased by -7%. An even more profound effect of nitrate supplementation was observed during high intensity activity (knee extensor exercises) where the ATP turnover decreased by -25%. These results stand in line with an overall increase in exercise tolerance of +25% in the nitrate supplemented group over placebo.

Other than a some other researchers had speculated, Baily et al. did not find any indications of a changed phosphate vs. oxygen (P/O) ratio in the muscle. The changes in ATP turnover a 6-day loading phase with dietary nitrate from beet root juice triggers, must thus be considered the underlying mechanism of the ergogenic effect of nitrates, which, as you may have notices, appear in various forms (amino acid nitrates, creatine nitrates, etc.) in recently released supplements - not without reason, as it turns out.

Resistance Training Causes Fat Accumulation in Muscle - A Reason to Stay Away From Weights? Quite The Contrary!

Weights works for ladies, too! Really!

I am not sure if you remember it, but you've read about what I would like to refer to as the "proximity hypothesis" before, here at the SuppVersity.

The basic idea behind is eventually similar to the notion of "localized fat loss", yet on the micro- not the macro-scale. In other words, instead of "do sit-ups to burn abdominal fat" the no-bro-science-variety of the "proximity hypothesis" says: "Train your legs to empty the huge intra-muscular fat stores and have them refilled from the abdominal fat."

Probably you will already have realized that this is "proximity" as in "right next to the skeletal muscle mitochondria" and not "proximity" as "a fat depot next to the muscle your train".

SuppVersity Suggested Read: If you are less interested in ramping up your intramusclar fat stores than in increasing and replenishing your muscular glycogen stores, I suggest you take a look at my previous article " Post-Workout Glycogen Repletion - The Role of Protein, Leucine, Phenylalanine and Insulin. Plus: Protein & Carbs How Much do You Actually Need After a Workout?" | go for it!

SuppVersity Suggested Read: " Spot Reduce Abdominal Fat With Green Tea, Green Clay & Magnesium Sulfate Soaked "Plaster Body Wrap"... Really!?" | read more

As S.O. Shepherd and his colleagues from the Liverpool John Moores University, the University of Birmingham and the University of Stirling point out, it has long been speculated that part of the improvements in insulin sensitivity following endurance training

"[...] are mechanistically linked to increases in muscle oxidative capacity, intramuscular triglyceride (IMTG) utilization during endurance exercise and increases in the content of the lipid droplet-associated perilipin-2 (PLIN2) and PLIN5." (Shepherd. 2014)

These lipid droplet-associated proteins (or short PLINs) coat the lipid droplets in fat and other cells and protect them from lipases of which you, as a SuppVersity reader know that they are enzymes our body uses to break down and "free" stored body fat - a process scientists usually refer to as "lipolysis".

An increase in perilipin in the musculature will thus necessarily increase the storage of lipid droplets in the muscle; and since it does not affect fat storage in the adipose organ and in view of the fact that the fat must come from somewhere (nutrition, endogenous fatty acid production from glucose, or stored body fat) this is not a bad thing.

More fat in the muscle? That's bad, right?

It's thus not shocking to have a "high" amount of fat in the muscle, as long as it is deposited there as a fat reserves for the mitochondria and serves as an alternative, additional or auxiliary, astonishingly readily available energy source for the muscle. A "range extender" with profound beneficial effects on muscular endurance.

Figure 1: Changes in heart rate VO2max, carbohydrate + fat oxidation, and respiratory exchange ratio (left); blood glucose + insulin levels after an oral glucose tolerance test before and after RT intervention (Shepherd. 2014)

Any marathon runner, ironman or -woman and even pharmaceutically enhanced Tour de France drivers would thus be happy if they experienced a similar increase in intramuscular triglyceride stores (IMGT) as the thirteen sedentary males (20±1 years, 24.8±0.8 kg/m²) in the study at hand.

The guys had perfoemed a 6-weeks whole-body resistance training program (3 sessione per week) in the course of which Shepherd et al. observed not just the previously mentioned increases in IMTG, and PLIN2 and PLIN5 protein content, but also highly significant increases in intramuscular fat breakdown during "light" cardio training (65% VO2max; +43% in slow-twitch type I and +37% in fast-twitch type II fibers).

Don't forget: As long as you are solely working out to burn calories you are doomed to stay fat forever. Want to learn why? Read more about the  The Fallacy of Working Out To "Burn Calories" | here

Beneficial effects for everyone: All in all, the increased intramuscular triglycerides, the accompanying increase in fatty acid oxidation and the ensuing beneficial effects on the endurance capacity suggest that doing a simple whole body workout (chest press, leg press, latissimus dorsi pull down, leg curl, leg extension, shoulder press, bicep curl, tricep extension and abdominal crunches; 80% 1RM) thrice a week is the ideal "non-cardio" training for the sedentary slob and could be the ideal adjunct to the endless hours, of running, cycling or swimming in endurance athletes...

What? Oh, yes of course, for the average gymgoer, the results are a welcome confirmation of his regular training practice: Helps with endurance, helps with fat loss and makes you strong; and don't forget - just as Carl says: "Muscle is metabolic currency" (and, as recent studies show, the best quality of life ensurance you can invest in; cf. Silva. 2011; Geirsdottir. 2012; Rizzoli. 2013)

References:

• Geirsdottir, Olof Gudny, et al. "Physical function predicts improvement in quality of life in elderly Icelanders after 12 weeks of resistance exercise." The journal of nutrition, health & aging 16.1 (2012): 62-66.
• O'Connell, Matthew DL, et al. "Do the effects of testosterone on muscle strength, physical function, body composition, and quality of life persist six months after treatment in intermediate-frail and frail elderly men?." Clinical Endocrinology and Metabolism 96.2 (2010): 454-458.
• Rizzoli, René, et al. "Quality of life in sarcopenia and frailty." Calcified tissue international 93.2 (2013): 101-120. 
• Shepherd, Sam O., et al. "Resistance training increases skeletal muscle oxidative capacity and net intramuscular triglyceride breakdown in type I and II fibres of sedentary males." Experimental Physiology (2014).
• Silva, Neto LS, et al. "Association between sarcopenia, sarcopenic obesity, muscle strength and quality of life variables in elderly women." Revista brasileira de fisioterapia (Sao Carlos (Sao Paulo, Brazil)) 16.5 (2011): 360-367.

True or False? Adding Fat to A Carby Meal Lowers Insulin Response. Muscle Hypertrophy Impairs Oxygen Diffusion. Reducing Carb Intake Improve Muscular Insulin Sensitivity

Will the additional butter on top of the potatoes reduce the insulin response? You can find the answer to this and the other questions in today's episode of "True or False?"

If you are a regular here at the SuppVersity you should by now recognize the "True or False" part of the headline of today's SuppVersity article. Therefore it's probably unnecessary to say this explicitly, but this is a new series, where I could use a little help from your side. Well, ... I should say, I believe it would become even more fun, if you lend me a hand and send me short pieces of wisdom or idiocy like "Adding fat to a carby meal reduces the insulin response"  you deem worthy of being addressed in the True or False series. I cannot, or rather will not promise that I will address each and every of your suggestions, but if it interests me and can be tackled in a 2-3 paragraph text, your chances ain't bad to get your suggestions dealt with - if you got any ideas, just post them in the comment section of one of the previous installments (including today's, obviously).

Adding Fat to A Meal Will Ameliorate the Insulin Response

False. When you are browsing the Internet it is easy to get the impression that what is wrong or right is not determined by scientific evidence, but by the number of people who repeat it in their blogs, on their facebook walls and in their bulletin board contributions. The common "wisdom" that it would be a good idea to add some fat to a meal to reduce the insulin spike it will give you is one of those paradigms that remain intrinsically flawed no matter how often they are repeated.

Figure 1: Althoug the glucose AUC drops after the addition of fat (slowed absorption of glucose from the intestine), the amount of insulin (2ndary axis) that is needed to stash the glucose away is 8.5x higher (on a per unit base; cf. violet bar) and the absolute insulin response does not decrease at all in lean healthy men and women (Collier. 1983)

If you do take a look at what actually happens, when you add fat to a meal, it is yet not difficult to understand how that myth came about. Just like people don't understand that the GI of a certain carbohydrate source doesn't tell you much about it's effect on insulin, the fact that the addition of fat ameliorates the postprandial spike in glucose gets misinterpreted as "fatty meals are less insulinogenic than low fat meals". In fact, the addition of 50g of butter on top of the 50g of carbohydrates the 8 lean, weight stable men and women (N=4, each) consumed in form of potatoes, did not have any effect on the post-prandial insulin release at all.

GIP Or Not GIP - That is the Question: "Fat intake, in addition to ingestion of carbohydrate, stimulates GIP release. Therefore, during a mixed meal GIP might act to promote the storage of both triglyceride and glucose indirectly via the release of insulin." (Kieffer. 2003)

The amount of the fat storage peptide GIP (learn more), on the . Therefore, Collier and O'Dea are 100% right, when they state in the conclusion of their 1983 paper that...

"despite the apparent improvement in glucose tolerance when carbohydrate is ingested together with fat, the accompanying potentiation of insulin secretion could form the basis of long-term changes in insulin sensitivity which accompany alterations in dietary fat intake." (Collier. 1983)

You may want to remember that, whenever you feel inclined to add a ton of bacon on top of your sweet potatoes in the false believe that this would "mitigate" the effects of the carb-laden tubers the insulin response.

This obviously does not change the fact that having some fat in a meal does have the added benefit of increasing GLP-1 and PYY levels and thus contributing to a longer satiety effect (eg. Knut. 2008)

 Skeletal Muscle Hypertrophy Impairs Oxygen Diffusion

"Some HIIT For Life & Less LISS For More!" As the study at hand shows, this mantra is all the more important for the more muscular SuppVersity readers - that does not change that exercising longer to burn more fat won't work for anyone, muscular or not (learn why).

True! Contrary to the previous myth about the beneficial effects of adding fat to a high carb meal, which was not just totally messed up, but also pretty well-known the physical necessity that marked skeletal muscle hypertrophy will have a negative effect on he O2 diffusion of the "balooned up" musculature is something I would guess few of you have ever heard about before.

I have to admit that the 15-20% reduction in maximal oxygen consumption per kg of quadriceps mass a group of researchers from the University of Udine observed in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (body mass ~103kg), when they compared their them to 11 normal controls (body mass ~77kg) looks scary at first.

If you do yet also take into consideration that this decrease in oxygenation was accompanying improvements in ADP-stimulated mitochondrial respiration (+59%; takes place, when the ATP stores are used up) and a tighter coupling of oxidative phosphorylation, it becomes evident that the training induced enhancements in mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O₂ diffusion.

"The net results are an enhanced whole body oxidative function at peak exercise, and unchanged efficiency and O₂ cost at submaximal exercise, despite a much greater body mass." (Salvadego. 2013)

In other words, despite "suboptimal" oxygenation of the musculature a bigger metabolic engine will still burn more fat... but only when it's working at peak intensity. It won't do so at submaximal intensities, where the O2 costs are "identical" (statistically). So, what does that tell us about the usefulness of training in the non-existent fat burning zone for advanced, heavily muscled trainees? Yep, it's even smaller than for the average sedentary housewife.

Low Carb High Fat Diets Lead to Acute Improvements in Muscular Insulin Sensitivity

False. Although the slowly abating low-carb craze does still make it appear as if "just eating less carbs" was the solution to everything, it is only logical that low carb dieting leads to changes in skeletal muscle insulin signaling, i.e. decreases in insulin-stimulated tyrosine phosphorylation of IRS-1 and PI3-kinase activity, which reduce, not increase the ability / willingness of the musculature to suck up glucose from the blood stream within no more than 5 days (cf. Pessin. 2000; Reusch. 2002).

Figure 2: Changes (before vs. after 5-day intervention) in fasting glycemia and lipidemia and glucose rate of appearance and disposal during euglycemic clamp conditions (Wang. 2013)

So even in the absence of significant effects on the body composition or signs of full-blown whole body  insulin resistance, the changes Cecilia C.L. Wang and colleagues observed in muscle samples that were taken from their insulin tolerant, but overweight subjects are identical to those you would observe in the early stages of diabetes, and do thus predate "changes in whole body insulin sensitivity" (Wang. 2013).

"But that ain't low carb!" Certainly a valid critism w/30% carbs and 20% protein in the diet it is practically impossible to reach ketosis, but - believe it or not - this is representative of the "low carb" diets you will usually see in the pertinent literature.

Wang et al. base their conclusion on the results of a recently conducted weight loss intervention that involved 18 obese individuals without diabetes who underwent euglycemic-hyperinsulinemic clamp and skeletal muscle biopsy after:

• 5 days of eucaloric diet (30% fat, 50% carbohydrate), and 

• 5 days of a 30% calorie-restricted diet, containing either...

• LF/HC: 20% fat, 60% carbs
• HF/LC: 50% fat, 30% carbs.

As mentioned in the introduction it's only logical and not necessary a bad thing that the skeletal muscle of the LF/HC group reacted with favorable changes in inulin receptor phosphorylation and lead to improvements in the IRS-1-associated PI3-kinase activity, which also figures in the exercise and nutrient induced increase in skeletal muscle protein synthesis (its among others the main target of IGF-1, of which keto dieters are known to have significantly reduced levels, anyway; cf. Fraser. 2000; Glass. 2003).

In other words, "No, 'just eat no carbs' is not the solution to everything", but will lead to certain metabolic adaptations which are not exactly conducive to returning to a normal carb diet afterwards. Plus, if you are a lean gymrat striving to to maximize your lean mass gains the full-blown hepatic growth hormone resistance and corresponding -50% drop in hepatic IGF-1 mRNA expression Bielohuby et al. observed in a rodent model of ketogenic dieting in 2011 probably won't come handy in the long run (on a side note: The "keto rodents", with their 92.8% fat diet also had a 5% reduction in lean mass and 46%, 56% and 223% higher relative amounts of visceral fat in the inguinal, epididymal and perirenal fat pads; cf. Bielohub. 2011)

Keep in mind this is a physiological form of insulin resistance

Learn how Adelfo lost his carbophobia and saw nothing but benefits from it (read more). That someone in the >30kg/m² BMI region with type II diabetes should keep a close eye on carb intake is a whole different story.

That being said, it is at least in part due to this mechanism that this type of diet works so well for highly insulin resistant individuals. It does not require the body to become insulin sensitive to work, but provides your body with a substrate that would - in and out of itself - require a certain degree of insulin resistance to make sure your muscle don't suck away the little glucose that's floating around and make you feel miserable and hypoglycemic. That you cannot observe those changes with a glucometer at home should be obvious. After all you are not eating carbs, are you?

Would the effect have been different with a true keto diet? The weight loss? Maybe. The transient insulin resistance? More pronounced, if anything. If you are already obese and freakin' insulin resistant to begin with, this does yet hardly matter. Low fat, high fat, keto - I don't care! The weight loss, the ensuing reduction in chronic inflammation and the new room to actually stash away superfluous energy alone will sooner or later also help you to reduce your insulin resistance.

Suggested read on physiological (=adaptation to diet / exercise) insulin resistance: "The Marathon Paradox - How Temporary Exercise-Induced Insulin Resistance Paves the Way for Fat Burning Machines" (complete article)


References:

• Berk ES, Kovera AJ, Boozer CN, Pi-Sunyer FX, Johnson JA, Albu JB. Adiponectin levels during low- and high-fat eucaloric diets in lean and obese women. Obes Res. 2005 Sep;13(9):1566-71.
• Bielohuby M, Sawitzky M, Stoehr BJ, Stock P, Menhofer D, Ebensing S, Bjerre M, Frystyk J, Binder G, Strasburger C, Wu Z, Christ B, Hoeflich A, Bidlingmaier M. Lack of dietary carbohydrates induces hepatic growth hormone (GH) resistance in rats. Endocrinology. 2011 May;152(5):1948-60.
• Collier G, O'Dea K. The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr. 1983 Jun;37(6):941-4.
• Fraser DA, Thoen J, Bondhus S, Haugen M, Reseland JE, Djøseland O, Førre O, Kjeldsen-Kragh J. Reduction in serum leptin and IGF-1 but preserved T-lymphocyte numbers and activation after a ketogenic diet in rheumatoid arthritis patients. Clin Exp Rheumatol. 2000 Mar-Apr;18(2):209-14.
• Glass DJ. Molecular mechanisms modulating muscle mass. Trends Mol Med. 2003 Aug;9(8):344-50. Review.
• Kieffer TJ. GIP or not GIP? That is the question. Trends Pharmacol Sci. 2003 Mar;24(3):110-2.
• Knuth ND, Shrivastava CR, Horowitz JF. Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration. J Appl Physiol. 2009 Jan;106(1):122-9. doi: 10.1152/japplphysiol.90404.2008. Epub 2008 Nov 13. 
• Pessin JE, Saltiel AR. Signaling pathways in insulin action:molecular targets of insulin resistance. J Clin Invest. 2000;106(2):165–9.
• Salvadego D, Domenis R, Lazzer S, Porcelli S, Rittweger J, Rizzo G, Mavelli I, Simunic B, Pisot R, Grassi B. Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training. J Appl Physiol. 2013 Mar 21.
• Reusch JE. Current concepts in insulin resistance, type 2 diabetes mellitus, and the metabolic syndrome. Am J Cardiol. 2002;90(5A):19G–26G.
• Wang CC, Adochio RL, Leitner JW, Abeyta IM, Draznin B, Cornier MA. Acute effects of different diet compositions on skeletal muscle insulin signalling in obese individuals during caloric restriction. Metabolism. 2013; 62:595–603