Bicarbonate + Beta-Alanine Supplementation, HIT Exercise Performance and Energy Substrates in 71 Trained Cyclists

If there's one take-home message from the study at hand, it is: While both SB& BA work, it depends on the sport/exercise test if the effects will be significant.

If you've been following my articles at the SuppVersity for some time, you will know that I have covered beta-alanine and sodium bicarbonate, two of the few ergogenic supplements for which we have enough evidence to assume that they actually work, extensively in the past.

You will yet also remember that the synergistic effects you'd expect to see when you combine intra- (beta alanine) and extra-cellular (sodium bicarbonate) H+ buffers didn't show in every pertinent study in the SuppVersity archive.

Danaher, et al. (2014), for example, found no effect of combining both during performance test with fixed intensity and volume, while Tobias et al. (2013), whose study tested upper body performance and didn't limit either intensity or volume, did - it almost doubled the total work the subjects performed. Why's that important? Well, if you look at the study design of the latest bicarb + beta-alanine (BB) study by scientists from the University of Sao Paulo (da Silva 2018) you will find that both the training intensity and the total volume were capped. Therefore, it is not totally surprising that the performance benefits didn't reach statistical significance (there were benefits, though).

If it works (no runs + high intensity+volume exercise) bicarbonate is the king of H+buffers:

Caffeine + Bicarb Make Champions

Bicarb + Asp = Muscle Magic!?

NaCHO3 & Leg Days're a Breeze

+100% Anaerobic Endurance

Bicarb Buffers Creatine

Instant 14% HIIT Boost

This doesn't mean, however, that the study wasn't worth looking at. After all, the scientists had their reasons to standardize the workload - without this standardization da Silva et al. wouldn't have been able to achieve their aim to conduct the first study that would investigate the energy metabolism during high-intensity exercise and cycling time-trial performance objectively - and that's only possible if you use work-matched tests that guarantee that one group won't exercise 10 minutes longer or at 10% higher work rates than the other. But let's (re-)address that later and take a closer look at the other key parameters of what I feel is a well-designed, interesting and eventually highly educative study - despite and/or because of the lack of significant performance differences:

• 

  If you develop digestive issues like "the runs" whenever you try to use sodium bicarbonate aka baking soda (NaHCO3), try to "serial load" it | learn here how that works.

  The subjects in da Silva 2018 were 72 trained cyclists (5 ± 4 years of experience in cycling, 9 ± 3 h of training/week, consisting of 235 ± 92 km/week) with a VO2max of 59-60 ml/kg/min that shows that they were real athletes (What's a high VO2max?). 
• Beta-alanine was preloaded for a month at a comparatively high dose (28 days at 6.4g/d; two capsules were ingested four times daily vs. maltodextrin (error in abstract) placebo).
• The 0.3g/kg body weight of sodium bicarbonate (or calcium carbonate placebo) was supplemented within max. 5 minutes 60 minutes before the performance test in 1-g gelatin capsules under supervision to ensure full compliance. Gastrointestinal discomfort was reported prior to and 60 min using a 10-point scale - serial loading protocol as I've described it in previous articles about the bicarb was not used.
• The food intake during the supplementation period was 'monitored' via 3-day food diaries the subjects had to fill on 2 non-consecutive weekdays and 1 weekend day. The analyses of these food logs showed that the subjects consumed ~2200kcal/d with approximately 52%, 18.5%, and 26.5% of the energy coming from carbs, protein, and fats, respectively - without inter-group differences.

The actual testing sessions that were conducted after pre-test and familiarization sessions consisted of a high-intensity intermittent cycling protocol (4x 60s at 110% of the subjects' individual maximal power-output with 60s rests between bouts) that was followed by a 30-kJ time-trial performance test. Both tests performed twice - once before and once after the 28 days of beta-alanine or placebo supplementation (compare the illustration of the study design and main trials in Figure 1).

Figure 1: Experimental design (upper panel) and overview of the main trials (lower panel). BA β-alanine, SB sodium bicarbonate, PL placebo, CaCO3 placebo for sodium bicarbonate, lac plasma lactate analysis, gas blood gas analysis, HICT-110% high-intensity cycling test performed at 110% of Wmax (da Silva 2018)

As it is necessary for any double-blind, parallel-group, placebo-controlled trial, the participants were randomly allocated to the BA (β-alanine + placebo; n = 20, 3 drop-outs), SB (placebo + sodium bicarbonate; n = 20, 3 drop-outs), BASB (β-alanine + sodium bicarbonate; n = 20, 1 drop-out), or PLA (placebo + placebo; n = 20, 2 drop-outs) groups and asked to identify their group allocation (i.e., BA or maltodextrin and SB or calcium carbonate) to verify the blinding process.

How can you effectively blind beta-alanine and sodium bicarbonate, when one gives you the tingles and the other one the runs? That's a valid question and you could argue that the fact that three volunteers reported paresthesia with BA (BASB group) and nine participants (SB: 5; BASB: 4) reported gastrointestinal discomfort after ingesting sodium bicarbonate confirms that blinding is not possible for the two agents. Even though seven volunteers in the BA, five individuals in SB, six in BASB, and five in the PLA group rightly identified the arm (BA/PLA) they had been randomized to, the Fischer’s exact test showed a p-value of p = 0.85 for BA and p = 0.82 for SB, respectively - hence suggesting efficient blinding in spite tingling and tummy aches ;-)

Maltodextrin (the abstract falsely claims it was dextrose, which would be a very bad placebo due to its characteristic taste) and calcium carbonate were the placebos for BA and SB. Moreover, the randomisation was performed in blocks of 4 with groups being matched for time to complete a 30-kJ test to avoid significant baseline performance differences between the groups. And finally, blood was sampled before and in-between exercise bouts and the time trial, respectively, and the VO2 consumption measured continuously before and during the HICT110% test.

Figure 2: Effects of β-alanine (BA) and sodium bicarbonate (SB) on the time to complete 30-kJ time-trial performance. The grey bar on c represents the 95% confidence interval of the coefficient of variation of the test. Positive and negative confidence intervals crossing zero on d were deemed nonsignificant (da Silva 2018).

Now, as previously announced, da Silva et al. did not find a significant effect of any of the three supplementation protocols on the subjects exercise performance. Both, Figure 2 (c) & (d) do yet suggest non-significant performance improvements - with the largest effect size being and a borderline significant effect being observed in the BA + SB group.

Measurable effects, but no significant performance increases - so what?

As previously hinted at, these results are not completely surprising, because the ergogenic effects of H+ buffers, in general, and bicarbonate in particular, critically depends on the build-up of sufficient amounts of H+ to be buffered. Within the very short (~60s) bouts of exercise that was aborted when the subjects hit the 30-kJ mark this requirement probably wasn't met - or, in view of the non-significant benefits, it was at least not met to a sufficient degree.

Figure 3: The amelioration of the decline in blood pH and bicarbonate shows that the SB treatment did what it was supposed to do - work as a buffer. However, as Figure 2 shows, the differences in pH and blood HCO3 were obviously too small to make a significant difference during the very short 30kJ performance test (da Silva 2018).

As Figure 3 shows, this doesn't mean that the buffers didn't work (SB successfully buffered the decrease in blood pH and we can assume that a muscle biopsy would have shown slightly reduced intra-cellular H+ levels due to BA). It just means that the biochemical differences to the control trial were too small and the inter-group variance too large to detect significant performance benefits.

My plot of the effect sizes for the impact of beta-alanine (BA), sodium bicarbonate (SB), the combination of both (BASB), and placebo on the glycolytic energy contribution illustrates quite nicely that it's bicarbonate, not beta-alanine that will keep you going towards the end of a team sport event or in the sprint before the finish line.

Why does SB increase the important glycolytic energy contribution during short bursts of high-intensity exercise, while BA fails? This is a relevant question because it's said increased ability to tap into your glycogen stores that will provide the 'second wind' you need to win the decisive sprints in team sports and track and field. If we assume that the SB-advantage is not a result of bicarbonate messing with the indirect measurement of the glycolytic energy contribution (remember no biopsies were performed), da Silva et al. suggest that absence of this benefit in BA may be due "to the total amount of H+ that can be neutralised by the working muscles" by sodium bicarbonate v. beta-alanine, respectively.

The scientists argue as follows: "Assuming the typical 6 mmol/l increase in blood bicarbonate following SB ingestion and 5 l of total blood volume, then SB ingestion would allow the neutralisation of ~ 30 mmoles of H+ above baseline (based on the 1:1 stoichiometry of HCO3− and H+ reaction). This is approximately two times more than the ~ 15 mmoles of H+ that a typical 80% increase in muscle carnosine (from 20 to 35 mmol/kg dry muscle after BA supplementation) can neutralise in both legs (assuming that legs correspond to 30% of BM, that 40% of leg mass is skeletal muscle, and that 70% of wet muscle is water—therefore, 3 kg of dry muscle times ~ 5 mmoles of H+ per kg of dry muscle that can be neutralised by a 15 mmol kg−1 dry muscle increase in muscle carnosine). Therefore, the effects of SB on the glycolytic activation could be more easily detectable than those of BA due [to] a possibly greater ability of SB to neutralise H+" (da Silva 2018).

With that being said, we could have been able to be more specific if it were not for two important limitations of the study the scientists willingly admit in the discussion of the results: The first limitation is the lack of direct muscle analyses that could have (a) told us if and to which degree the muscle carnosine actually changed in response to the BA supplementation and (b) confirmed that the indirect measurement of the effects on energy metabolism was indeed accurate. The second limitation, which is not related to the study design, is a temporary malfunctioning of laboratory equipment which made it impossible for da Silva et al. "to undertake the estimation of the energy systems in all participants" (da Silva 2018) - maybe, the analysis of a complete dataset would have shown measurable and significant increases in glycolytic energy contribution for BA, as well.

The same must be assumed of the lactate buffering effects of SB. In the scientists' multiple comparison analysis of the post-HICT-110% plasma lactate levels in the SB group, the latter approached significance (t = − 1.82, p = 0.074), and were significantly higher after the 30-kJ TT in both, the SB only (t = − 2.67, p = 0.01) and the BASB group (t = − 2.61, p = 0.011).

Figure 4: Effects of β-alanine (BA) and sodium bicarbonate (SB) supplementation on the absolute contribution of the energy systems during the HCT-110% test (da Silva 2018). The increase glycolytic flux and improved ability to tap into the readily available glucose sources can be ascribed to the pH buffering effect of SB (Sutton 1981).

Unfortunately, lactate still has an unwarrantedly bad rep (Cairns 2006). It is thus important to note that increased lactate levels are a necessary consequence of an increased use of glucose and by no means a reason to expect performance decrements. In fact, almost all SB studies which tested the level of lactate in the subjects' blood found it to be significantly increased in the presence of significant performance benefits! That's something people tend to forget in a day and age where even the superiority of glucose as the #1 substrate for high-intensity exercise is questioned (sorry keto fans, but that's simply what the contemporary evidence says - keto-adapted or not ;-).

"So, beta-alanine and sodium bicarbonate don't work, neither taken alone or in combination?" No, that's not what the study says. While significant effects on the performance markers measured in the study at hand were not observed, da Silva et al. found non-significant increases in exercise performance in both tests, especially, when the two H+ buffers were combined, and a potentially highly relevant 20% increase in the subjects ability to tap into their glycogen stores in the SB and BASB groups - in the "right" sport, this difference may well make the difference between winning an Olympic medal and ending up with a disappointing fourth rank (check out the infobox for more info why only sodium bicarbonate, but not beta-alanine, had this beneficial effect).

Bodybuilders have a sign. elevated muscle carnosine levels, it is yet not clear if that's an adaptational response to prolonged repetitive exposure to low muscle pH, the consumption of high carnosine foods like chicken, supplement use, or the use of anabolic steroids (Tallon 2005). Other studies show that men store more carnosine than women (Mannion 1992), omnivores more than vegetarians (Harris 2007), and that genetic factors which have hitherto only been confirmed in our omnivore 'cousins', the pigs (D'Astous-Pagé 2017), may figure as well. It is thus hardly surprising that the BA research as such yielded highly variable results which are, just as it's the case for the study at hand, difficult to interpret if the changes in muscle carnosine aren't measured.

Moreover, in view of the previously mentioned non-significant performance increases my provocative statement from the question at the beginning of this conclusion, i.e. that BA and SB "don't work" should rather read "exert mea-surable, yet highly variable performance benefits", which simply may not have reached statistical significance, because (1) the effiacy of both agents has a high inter-individual varia-bility, with BA potentially failing in subjects with diet- or training-related naturally high carnosine levels (cf. Figure 5) and SB countering its own ergogenic effects via gastrointestinal distress (which was reported by nine participants in the study at hand), or because (2) H+ buffers excel in exercise capacity tests, i.e. tests in which you exert yourselves to the point of volitional exhaustion, as opposed to performance tests with a fixed point like the 30 kJ test in the study at hand, or because (3) the results of the study at hand despite being one of the better-powered investigations, may still "lack of statistical significance [...] due to insufficient statistical power to detect small effects" (my emphasis in da Silva 2018) - it's also possible that all three contributed synergistically to the lack of statistical significance of the results.

Instead of trying to make a general statement about the two ergogenics, which have also made the ISSN's TOP5 list of OTC ergogenic supplements, only recently (Kerksick 2018), we should use the publication of the study at hand to remind ourselves that the benefits of any supplement are sports-, exercise- and as the pronounced benefits in Tobias et al. (2013) suggest (see data in and caption of Figure 6) potentially even muscle-specific (e.g. upper vs. lower body).

Figure 6: With an upper-body Wingate test, the study by Tobias et al. (2013) I covered 5 years ago used didn't just use an exercise capacity test that didn't limit the total work done, but also tested the effects on a different muscle group - et voila: Tobias et al. found significant increases in total work and mean power with the combination of BA +SB.

So, what should you do? Well, one thing should be obvious: you should not throw away your 5kg bag of sodium bicarbonate and your 1kg tub of beta-alanine. Even though the performance benefits in the study at hand were at best borderline significant, there's a reason that both agents have been around for years (beta-alanine) and decades (bicarbonate) in the absence of sufficient research to tell for sure who will and who won't benefit from using them | Comment!

References:

• Cairns, Simeon P. "Lactic acid and exercise performance." Sports Medicine 36.4 (2006): 279-291.
• Carr, Benjamin M., et al. "Sodium bicarbonate supplementation improves hypertrophy-type resistance exercise performance." European journal of applied physiology 113.3 (2013): 743-752.
• da Silva, Rafael Pires, et al. "Effects of β-alanine and sodium bicarbonate supplementation on the estimated energy system contribution during high-intensity intermittent exercise." Amino Acids (2018): 1-14.
• Danaher, Jessica et al. "The effect of β-alanine and NaHCO3co-ingestion on buffering capacity and exercise performance with high-intensity exercise in healthy males." Eur J Appl Physiol (2014) 114:1715–1724.
• Harris, Roger C., et al. "The carnosine content of V Lateralis in vegetarians and omnivores." (2007): A944-A944.
• Kerksick, Chad M., et al. "ISSN exercise & sports nutrition review update: research & recommendations." Journal of the International Society of Sports Nutrition 15.1 (2018): 38.
• Mannion, A. F., et al. "Carnosine and anserine concentrations in the quadriceps femoris muscle of healthy humans." European journal of applied physiology and occupational physiology 64.1 (1992): 47-50.
• D'Astous-Pagé, Joël, et al. "Identification of single nucleotide polymorphisms in carnosine-related genes and effects of genotypes on pork meat quality attributes." Meat science 134 (2017): 54-60.
• Sutton, J. R., N. L. Jones, and C. J. Toews. "Effect of pH on muscle glycolysis during exercise." Clinical science 61.3 (1981): 331-338.
• Tallon, Mark J., et al. "The carnosine content of vastus lateralis is elevated in resistance-trained bodybuilders." Journal of Strength and Conditioning Research 19.4 (2005): 725.
• Tobias, Gabriel, et al. "Additive effects of beta-alanine and sodium bicarbonate on upper-body intermittent performance." Amino acids 45.2 (2013): 309-317.

HIIT Science Update 08/17: HIIT & the CNS, HIIT & Cortisol, HIIT, Diabetes, PWO Milk & Exercise (Non-)Responders

You don't have to run/sprint or cycle, plyometrics, kettlebells, etc. there are dozens of ways to "HIIT it".

Taken on their own, the following studies would probably not have made the SuppVersity cut. They would have been in the Facebook News (I hope you have already subscribed), but they would not have gotten their own article. Together, however, I thought it may be a good idea to pack all of them into a "research update" on high-intensity interval training aka HIIT.  An update that yields insights into the effects of HIIT on the central nervous system, shows that classic "cardio", but not HIIT messes with cortisol to an extent that diminishes its health benefits, and highlights that and why HIIT is an anti-diabetes tool for almost everyone.

You can learn more about HIIT at the SuppVersity

The Optimal HIIT Program for Your Individual Goals

Tabata = 14.2kcal /min ≠ Fat Loss, Dietin' Necessary

30s Intervals + 2:1 Work/Rec. - Is That Optimal?

Making HIIT a Hit Part I/II - What Are the Options?

Making HIIT a Hit Part II/II - How to Program?

Triple Your HIIT Energy Expenditure

• HRV data suggests full central nervous system recovery within 24h -- You will remember from previous HIIT discussions as the SuppVersity that one of the potential issues with HIIT is that it is - just like strength training - taxing on the nervous system.
  
  And, indeed, a soon-to-be-published paper in the Journal of Strength and Conditioning Research confirms quite clearly: HIIT will attenuate parasympathetic function and thus offset the balance towards the sympathetic nervous system.
  

  

  Figure 1: Heart rate autonomic control at rest and at exercise. Parasympathetic role decreases when the intensity of exercise is increased, and the opposite happens with the sympathetic role (Almeida 2008).

  In said study, the authors compared the effects of two high-intensity interval exercises (HIIT) protocols on heart rate variability (HRV). Twelve young adult males (23.3 +/- 3.9 years, 177.8 +/- 7.4 cm, 76.9 +/- 12.9 kg) volunteered to participate. In a randomized cross-over design, subjects performed two HIIT protocols, one on a cycle ergometer (TBT; eight 20 s bouts at 170% Pmax interspersed by 10 s rest) and another with whole-body calisthenic exercises (MCR; eight 20 s all-out intervals interspersed by 10 s rest). HRV outcomes in the time, frequency, and nonlinear domains were assessed on three moments: (a) pre-session, (b) immediately post-session, and (c) 24h post-session.
  
  As previously pointed out, the authors' "main finding is that responses from HR autonomic control were similar in both protocols, despite different modes of exercise performed" (Schaun 2017). Specifically, exercises resulted in a high parasympathetic inhibition immediately after HIIT sessions with subsequent recovery within one day. As the scientists point out, "[t]hese results suggest that subjects were already recovered the day after and can help coaches to better program training sessions with such protocols" (Schaun 2017).

Smartphone Based Morning HRV Analyses Adequately Reflect Training Loads in Recent Overload + Taper Study (Dissertation) -- You may have asked yourselves whether any of the smartphone apps you may have seen that claim to accurately measure the HRV even work. Well, a recent dissertation would suggest they do... assuming you input data is reliable, though.

• When done within the limits of your individual ability to recovery from exercise, HIIT will elevate testosterone and muscle power, a study in master athletes shows -- High-intensity interval training (HIIT) improves peak power output (PPO) in sedentary aging men but has not been examined in masters endurance athletes.
  
  Therefore, scientists investigated whether a six-week program of low-volume HIIT would (i) improve PPO in masters athletes and (ii) whether any change in PPO would be associated with steroid hormone perturbations.
  

  

  Figure 2: Effects of 9x HIIT/6wk on peak power and free testosterone of master endurance athletes (Herbert 2017)

  Seventeen male masters athletes (60 ± 5 years) completed the intervention, which comprised nine HIIT sessions over six weeks. HIIT sessions involved six 30-s sprints at 40% PPO, interspersed with 3 min active recovery. Absolute PPO (799 ± 205 W and 865 ± 211 W) and relative PPO (10.2 ± 2.0 W/kg and 11.0 ± 2.2 W/kg) increased from pre- to post-HIIT respectively (P < 0.001, Cohen's d = 0.32-0.38). No significant change was observed for total testosterone (15.2 ± 4.2 nmol/L to 16.4 ± 3.3 nmol/L (P = 0.061, Cohen's d = 0.32)), while a small increase in free testosterone occurred following HIIT (7.0 ± 1.2 ng/dL to 7.5 ± 1.1 ng/dL pre- to post-HIIT (P = 0.050, Cohen's d = 0.40)).
  
  "Six weeks' HIIT improves PPO in masters athletes and increases free testosterone. Taken together, these data indicate there is a place for carefully timed HIIT epochs in regimes of masters athletes," the authors conclude.
• HIIT is just as enjoyable for the obese as steady-state-exercise -- A commonly heard-of problem with HIIT is that obese clients don't stick to it because they don't like the intense nature of HIIT. A group of American and Russian scientists, however, conducted a study that refutes this notion.
  
  They compared adherence, enjoyment, and cardiometabolic outcomes after 8 weeks of HIIT or moderate-intensity continuous training (MICT), matched for energy expenditure, in overweight and obese young adults. To this ends, 17 adults were randomized to HIIT or MICT. After completing 12 sessions of supervised training over 3 weeks, participants were asked to independently perform HIIT or MICT for 30 min, 4 times/week for 5 weeks. Cardiometabolic outcomes included cardiorespiratory fitness (VO2 peak), lipids, and inflammatory markers. Exercise enjoyment was measured by the validated Physical Activity Enjoyment Scale.
  
  

  

  Figure 3: Physical Activity Enjoyment Scale during the intervention (mean ± SD). Closed circles MICT, open circles HIIT, p < .05 (Vella 2017).

  Exercise adherence (93.4 ± 3.1% vs. 93.1 ± 3.7%, respectively) and mean enjoyment across the intervention (100.1 ± 4.3 vs. 100.3 ± 4.4, respectively) were high, with no differences between HIIT and MICT (p > .05). Similarly, enjoyment levels did not change over time in either group (p > .05). After training, HIIT exhibited a greater decrease in low-density lipoprotein cholesterol than MICT (-0.66 mmol L-1 vs. -0.03 mmol L-1, respectively) and a greater increase in VO2 peak than MICT (p < .05, +2.6 mL kg min-1 vs. +0.4 mL kg min-1, respectively).
  
  Interleukin-6 and C-reactive protein increased in HIIT (+0.5 pg mL-1 and + 31.4 nmol L-1, respectively) and decreased in MICT (-0.6 pg mL-1 and -6.7 nmol L-1, respectively, p < .05).
  
  Whether the said increase in markers of inflammation is a problem, not a hormetic advantage, will have to be elucidated in specific trials. With the available evidence suggesting that HIIT improves cardiometabolic health during supervised lab-based studies (which is also in line with the augmented reduction in LDL in the study at hand), though, it's very unlikely that this is going to be a major problem.
• Study sheds a new corticosteroid (cortisol) light on the never-ending HIIT vs. steady-intensity training (SIT) debate -- In fact, if the results from a recent rodent study by Chinese scientists translates to human beings, they would suggest that HIIT, not SIT is the way to go.
  
  In the corresponding experiment, Shen et al. compared the effects of high-intensity interval training (HI) to mild-intensity endurance training (ME), combined with a high-fat diet (HFD) or control diet (CD) on metabolic phenotype and corticosterone levels in rats. Now that's interesting as it models - as well as you can expect that from the average rodent study - patterns you will observe in large parts of the human population: eat like crap, exercise to mitigate the damage.
  
  Fifty-three rats were randomized to 6 groups according to diet and training regimen as follows: CD and sedentary (CS, n = 11), CD and ME (CME, n = 8), CD and HI (CHI, n = 8), HFD and sedentary (HS, n = 10), HFD and ME (HME, n = 8), and HFD and HI (HHI, n = 8). All exercise groups were trained for 10 weeks and had matched running distances. Dietary intake, body composition, blood metabolites, and corticosterone levels were measured. Histological lipid droplets were observed in the livers.
  
  As you'd expect, the HFD, of which I'd like to remind you that it is both, high in carbohydrates and fat and should thus rather be called a "hypercaloric diet", led to hyperglycemia, hyperlipidemia and higher body fat (all, P < 0.01, η2 > 0.06), as well as higher corticosterone levels (P < 0.01, η2 = 0.09) compared with the CD groups.
  
  Just as the aforementioned "junk-food-eaters + compensatory-exercisers" hope for, though, the exercise training improved fat weight, glucose, and lipid profiles, and reduced corticosterone levels (P < 0.01, η2 = 0.123). In that, it is yet important to note that body and fat weight, serum glucose and triglycerides, lipid content in the liver, and corticosterone levels (P < 0.05) were lower with HI training compared to ME training.
  

  

  Figure 4: Correlations between serum corticosterone and several variables (Shen 2017).

  A similar response was observed for the reductions in HFD-induced body weight gain, blood glucose, and lipid profiles, and corticosterone levels, as well as improvements in QUICKI were better with HHI compared to HME.
  
  What is worth noting about the data in Figure 4, is that the authors' correlation analyses revealed that corticosterone levels were significantly associated with phenotype variables (P < 0.01). Corticosterone level was inversely correlated with QUICKI (r = −0.38, P < 0.01). Accordingly, it's valid to assume that the modification of the diet-induced exacerbation of basal serum corticosterone level may be at the heart of the metabolic imbalance; an imbalance, of which the study at hand shows that it is attenuated to a greater degree with high intensity vs. moderate intensity exercise.
• Metabolic benefits of HIIT in T2DM are not affected by post-workout milk supplementation -- In view of the fact that one may believe that the benefits of HIIT depend on an (over-)expression of AMPK after the highly glycolytic training sessions, you may be (mis-)lead to believe that the same post-workout protein shake, of which I wrote in 2012, already, that it will boost your protein synthesis by 43-222% (re-read the article), could mess with the often-confirmed health benefits of HIIT.
  
  

  

  Figure 5: Change from pre intervention (week 0 vs. post week 12) for (A) % body fat, (B) lean body mass, (C) cardiorespiratory fitness (V˙O2peak) and (D) glycosylated hemoglobin (HbA1c) in the milk, protein, and water groups (all main effect of time p < 0.05, no group interaction p > 0.05 | Francois 2017)

  Benefits of which a recent study in 53 adults with uncomplicated type 2 diabetes that was conducted at the University of British Columbia shows that they include significant reductions in 24-h mean glucose (-0.5 ± 1.1 mmol/L), HbA1c (-0.2 ± 0.4%), percent body fat (-0.8 ± 1.6%), and lean mass (+1.1 ± 2.8 kg), regardless of whether the subjects consumed milk, an isonutrient control or flavored water placebo after 12 weeks with three weekly HIIT workouts, which involved 10 X 1-min high-intensity intervals of 2x cardio and 1x resistance training separated by 1-min low-intensity recovery periods. 
• HIIT's performance does not depend on how insulin resistance you are -- Non-responders are a hitherto not understood problem in all three, resistance, classic cardio and HIIT training. One potential determinant of an individuals response to training is his/her insulin tolerance. In fact, previous studies seemed to suggest that there's a relevant difference between populations with higher or lower levels of insulin resistance.
  
  With their latest study, scientists from the Universidad de Los LagosOsorno tried to assess the effects of high-intensity interval training (HIIT) and the prevalence of non-responders (NRs) in adult women with higher (H-IR) and lower (L-IR) levels of insulin resistance.
  
  

  

  Figure 6: The worse you are off, the greater your improvements in HOMA-IR are going to be - good news for HIIT as a T2DM treatment in sedentary adult women (Álvarez 2017).

  To this ends, forty adult women were assigned to a HIIT program, and after training were analyzed in two groups; a group with higher insulin resistance (H-IR, 40 ± 6 years; BMI: 29.5 ± 3.7 kg/m2; n = 20) and a group with lower insulin resistance (L-IR, 35 ± 9 years; 27.8 ± 2.8 kg/m2; n = 20). Anthropometric, cardiovascular, metabolic, and performance variables were measured at baseline and after 10 weeks of training.
  
  There were significant training-induced changes [delta percent (Δ%)] in fasting glucose, fasting insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) scores in the H-IR group (-8.8, -26.5, -32.1%, p < 0.0001), whereas no significant changes were observed in the L-IR. Both groups showed significant pre-post changes in other anthropometric variables [waist circ. (-5.2, p < 0.010, and -3.8%, p = 0.046) and tricipital (-13.3, p < 0.010, and -13.6%, p < 0.0001), supra-iliac (-19.4, p < 0.0001, and -13.6%, p < 0.0001), and abdominal (-18.2, p < 0.0001, and -15.6%, p < 0.010) skinfold measurements]. Both groups showed sign. increases in 1RMLE (+12.9, p < 0.010, and +14.7%, p = 0.045).
  
  What did differ, however, is the change in systolic blood pressure, which decreased sign. only in the L-IR group (-3.2%, p < 0.010).  There were also sign. differences in the prevalence of NRs between the H-IR and L-IR groups for fasting glucose (25 vs. 95%, p < 0.0001) and fasting insulin (p = 0.025) but not for HOMA-IR (25 vs. 45%, p = 0.185), but that's not surprising: If you have elevated blood pressure, fasting glucose and insulin, it is obvious that exercise will produce greater reductions ... in fact, it's good news, because it shows that - at least in sedentary adult women - those who need it the most will also benefit the most from HIIT as a means of cardiometabolic disease progression in a sedentary population.

6x1 Min HIIT Before Lifting Shed Extra Fat, Don't Impair 'ur Gainz | Daily AM/PM Training = ZERO Gainz | Alcohol W/Out Acute Effect on Workout Recovery of Trained Women | more

What else is worth mentioning? Well, maybe the recent demonstration that both, HIIT and MICT, will significantly increase the 22h (that's all that was measured 24h-2h) post-exercise resting energy expenditure (REE) by 64±119 kcal 103±137 kcal in MICT and HIIT, respectively - obviously, with the previously established HIIT advantage, of which the latest study shows that it is not a result of increased muscle damage, which was estimated base on increases in CK (9.6±25.5 units/liter in HIIT and 22.2±22.8 units/liter in MICT), but potentially related to the increased sympathetic tone (urine norepinephrine) in response to HIIT (1.1±10.6 ng/mg) that was not observed in response to MICT.

This is, by the way, in line with the initially surprising realization that adolescents will increase, not compensate for school-based HIIT training by reducing their non-HIIT physical activity on days when they HIIT it (Costigan 2017) - a result that seems to clearly refute the "activitystat hypothesis" that posits that an individual maintains a steady level of physical activity (or energy expenditure); and therefore if physical activity increases/decreases in one domain (e.g., school day, leisure time, organized activity, etc.) or time of day, compensatory changes will occur to sustain a "set point" (Rowland 1998) | Comment!

References:

• Almeida, Marcos B., and Claudio Gil S. Araújo. "Effects of aerobic training on heart rate." Revista Brasileira de Medicina do Esporte 9.2 (2003): 113-120.
• Álvarez, Cristian, et al. "Prevalence of Non-responders for Glucose Control Markers after 10 Weeks of High-Intensity Interval Training in Adult Women with Higher and Lower Insulin Resistance." Frontiers in Physiology 8 (2017).
• Costigan, et al. "Exploring the impact of high intensity interval training on adolescents' objectively measured physical activity: Findings from a randomized controlled trial." J Sports Sci. 2017 Jul 20:1-8. doi: 10.1080/02640414.2017.1356026. [Epub ahead of print]
• Francois, et al. "Combined Interval Training and Post-exercise Nutrition in Type 2 Diabetes: A Randomized Control Trial." Front Physiol. 2017 Jul 25;8:528. doi: 10.3389/fphys.2017.00528. eCollection 2017.
• Hertbert et al. "HIIT produces increases in muscle power and free testosterone in male masters athletes." Endocr Connect. 2017 Oct;6(7):430-436. doi: 10.1530/EC-17-0159.
• Hunter, et al. "Potential Causes of Elevated REE following High-Intensity Exercise." Med Sci Sports Exerc. 2017 Jul 21. doi: 10.1249/MSS.0000000000001386. [Epub ahead of print]
• Rowland, Thomas W. "The biological basis of physical activity." Medicine and science in sports and exercise 30.3 (1998): 392-399.
• Schaun & Del Vecchio. "High-Intensity Interval Exercises' Acute Impact on Heart Rate Variability: Comparison Between Whole-Body and Cycle Ergometer Protocols." Journal of Strength & Conditioning Research: Post Acceptance: August 04, 2017. doi: 10.1519/JSC.0000000000002180
• Shen, Youqing, et al. "Effects of high-intensity interval versus mild-intensity endurance training on metabolic phenotype and corticosterone response in rats fed a high-fat or control diet." PloS one 12.7 (2017): e0181684.

26% Body Fat, Zero Lean Mass Loss W/ HIIT + 3x500mg Green Tea Supp in 10Wks | Is EGCG Liver-Toxic?

Lean, not skinny: In the long run HIIT + GTE could take you there, but there's one caveat... at least w/ the green tea.

The social networks are full of women complaining that they are not losing fat. If you ask them what they have tried to ignite body fat loss, the answer usually is: reduced energy, fat/carb intakes and, if any sport at all, endless cardio sessions... now, while studies show that this approach to fat loss works, it's (a) mostly the caloric deficit that determines the loss of body weight and (b) is often accompanied by significant lean mass losses.

An attractive alternative would be (i) not having to diet, (ii) not having to do endless cardio sessions and (iii) having a fat loss supplement that actually works.

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Well, guess what, Afzalpour et al. have an ahead-of-print paper they tagged with the keywords "HIIT;
Catechins; SRIT1; PGC-1 "(Afzalpour. 2017) that appears to suggest that this 'attractive alternative' does actually exist - at least for those women who have the most body fat to complain about for whom the scientists speculated that it could be the combination of "green tea consumption along with HIIT training" that "would improve body composition in overweight individuals and would show significantly greater improvements compared green tea consumption or HIIT training alone" (Afzalpour. 2017) - without dieting (or I should say: without prescribed dieting, the scientists did not access the women's food intake over the 10-week period; there was just a baseline reading)!

Table: Anthropometric characteristics of the subjects in the three groups (Afzalpou. 2017); note: there were no significant baseline differences in body composition and fitness between the three groups of young women.

To assess the validity of this hypothesis, the researchers from the University of Birnjad, in Iran, recruited thirty overweight young women (21.07 ± 1.2 years, BMI: 27.5 ± 1.3 kg/m²2 and body fat percentage: 34.1 ± 1.5%) and randomly assigned them to 3 groups (cf. Table 1):

• HIIT plus 1.5g/day green tea in 3x500mg servings with meals (HIIT+G),
• HIIT plus placebo (HIIT), and
• no training and supplementation control group (CON).

Said HIIT training program included 3 sessions of high-intensity interval training (HIIT) performed per week for 10 weeks with the intensity of 85—95% HR max. More specifically, ...

Figure 1: Overview of the HIIT parcours and the periodization scheme (Afzalpour. 2017).

"[t]he protocol of HIIT required the participants to finish a determined path (20 meters) with their maximum speed within 30 seconds. The starting point of the test was exactly in the middle of the obstacles, i.e., 10 meters from each obstacle. 

The training included running from the middle line to the first obstacle and then returning a 20-meter path to the second obstacle. After each run, there was an active rest for 30 seconds (Figure 1). 

In the first and second weeks, the training was performed with 4 repeats, in the third and fourth weeks with 5 repeats, in the fifth and sixth weeks with 6 repeats, in the seventh and eight weeks with 7 repeats, and in the ninth and tenth weeks with 8 repeats (Figure 1). In each session before the training protocol, the participants had [to] warm up for 5—10 minutes, and they cooled down for 5—10 minutes at the end of each session." (Afzalpour. 2017).

The intensity of training within the activity was controlled by measuring the heart rate during
the activity by pulse meter and using maximum heart rate formula (220-age). Besides, the Borg scale (6—20) was used to ensure greater control over the intensity of training.

Rodent studies clearly confirm the hepatoxicity of high doses of green tea; with the often-hailed EGCG having the most significant impact on the liver health of mice - with death being a consequence of the injection of a human-equivalent-dose of "only" 12mg/kg, or 850mg - luckily, the oral bioavailability of EGCG is low (Galati. 2006).

Weren't there recent studies showing ill-health effects of green tea? Well, "recent" is relative. I guess it all started w/ the testosterone-reducing effects of green tea I discussed back in 2011, already.

More recently, however, there have 24 case-reports of liver problems in response to the consumption of green tea supplements in man from 1999 to 2009, only (Mazzanti. 2009) - a response of which scientists say that it is due to (-)-epigallocatechin gallate (EGCG) or its metabolites "which, under particular conditions related to the patient’s metabolism, can induce oxidative stress in the liver" (Mazzanti. 2009).

Whether that's actually the case in the human case studies is particularly difficult to tell (Molinari. 2006), because it is well possible that "[i]n a few cases, toxicity related to concomitant medications could also be involved" (Mazzanti. 2009) - especially because EGCG messes significantly with the cytochrome P450 cascade, inhibiting, CYP1A2, CYP2D6, CYP2C9, and CYP3A4, which metabolizes not just all sorts of anti-depressive drugs, but also estrogen and could potentially explain the T-reductions in the previously mentioned 2011 study. In addition to that, a more recent series of studies (James. 2016) suggests that

"EGCG treatment induced hepatotoxicity [is dose dependent] and it induced oxidative stress by inhibiting antioxidant response. Mitochondrial function was impaired based on reduced biogenesis and inhibition of complexes following EGCG treatment." (James. 2016)

As bad as it may sound, this can (a) explain why it worked in the study at hand - practically speaking it did the opposite of what the anti-oxidants which hampered the gains in Bjornson et al. (2015 | discussed in detail, here), did it added to the pressure to adapt - and (b) and must be reconciled with the already low and chronically decreasing bioavailability of EGCG with chronic administration.

One important advice I want to give you at this point is still: do not fall for the notion that 'more helps more' (toxicity of really high doses of GTE in rodents has been proven multiple times), do not buy a pure EGCG product and stop using your green tea supplements if you notice the first symptoms of liver problems (usually otherwise inexplicable fatigue).

An intensity that yielded impressive effects, not only, but especially in terms of the subjects' body at loss that was not unreliably assessed with BIA, but - assuming the authors of the study knew what they did - with body fat calipers (I calculated the more meaningful absolute body fat and lean mass values based on the body fat % from the study). A 26% body fat loss and a 7% improvement in body fat percentage - without dieting - that's quite huge... isn't it?

Figure 2: Total changes (kg) in body fat and total lean mass and corresponding relative changes (in %) above the bars.

Yes, it is, but the way these beneficial effects on the women's body composition relates to their SIRT-1 and PGC-1alpha level is a putative one. Yes, the levels increased significantly in both the HIIT and the HIIT+G group, but the study design does not allow for statements about a causal link between the two: body fat and SIRT-1 and PGC-1a expression. In the end, I guess most women will say that it doesn't really matter, the fact that the PGC-1A expression was another 31% higher in the green tea group (HIIT+G) and went hand in hand with an exclusively significant increase in VO2-max (for the other treatments, the changes were non-significant) would yet argue in favor of an independent or interactive effect of green tea on the expression of these regulatory proteins that could have triggered the additional benefits.

Figure 3: Relative changes in SIRT1, PGC-1A activity and physical fitness as measured by the women's VO2-max.

What does matter, however, is the potential hepatoxicity (see red box), especially green tea products with a high EGCG content appear to have for some, but not all individuals. Against that background it is very unfortunate that (a) the product in the study at hand was either not standardized or the standardization was not reported, and that (b) any effect would have gone unobserved, in the study at hand, simply because no relevant parameters were measured... reason enough to re-address the issue in (a) the red box (general discussion) and the bottom line (weight loss adjuvant specific discussion).

Don't get me wrong: There are a lot of studies showing beneficial effects of green tea extracts, including the recently discussed study showing that "Green Tea Extract Reduces the Amount of Insulin You Need to Store Your PWO Carbs by ~20%". Unfor-tunately, its probably individual liver-damaging effects are being observed in more and more studies, too. 

What do I have to know: The concomitant use of 3x500 mg green tea supplements ingested with all three main meals accelerates the already impressive body fat loss a 10-week HIIT (3x per week) regimen produces in otherwise healthy overweight young women.

Now, the question remains: Is it worth taking the (probably small, but existing) risk of putting your liver health in jeopardy? You got to answer this question for yourself, but if you're having liver problems already, high dose EGCG supplements should IMHO be a no-go... the good news is: since the authors didn't report any EGCG standardization for their supplement, it is very likely that they are also not necessary and drinking green tea, which is a way of preparing your own hot water extract from tea, alone, with every meal could boost your fat loss and is associated w/ a reduced risk of liver cancer (Ni. 2017) |  Comment!

References:

• Afzalpour, M. E., E. Ghasemi, and A. Zarban. "Effects of 10 weeks of high intensity interval training and green tea supplementation on serum levels of Sirtuin-1 and peroxisome proliferator-activated receptor gamma co-activator 1-alpha in overweight women." Science & Sports (2017).
• Galati, Giuseppe, et al. "Cellular and in vivo hepatotoxicity caused by green tea phenolic acids and catechins." Free Radical Biology and Medicine 40.4 (2006): 570-580.
• James, Karma. Effect of dietary pretreatment and obesity on (-)-epigallocatechin-3-gallate (EGCG) mediated hepatotoxicity and the underlying mechanism. Diss. The Pennsylvania State University, 2016.
• Mazzanti, Gabriela, et al. "Hepatotoxicity from green tea: a review of the literature and two unpublished cases." European journal of clinical pharmacology 65.4 (2009): 331-341.
• Molinari, Michele, et al. "Acute liver failure induced by green tea extracts: case report and review of the literature." Liver transplantation 12.12 (2006): 1892-1895.
• Ni, Chen-Xu, et al. "Green Tea Consumption and the Risk of Liver Cancer: A Meta-Analysis." Nutrition and Cancer (2017): 1-10.

Hitting it After Weights - Nothing but Benefits? Not Exactly, but Systemically Impaired Strength & Size Gains are a Myth

Has your cardio-addiction held you back in the past? That does not mean that a short HIIT training after an RT workout will do the same, does it?

Right from the University of Athens comes new paper by Tsitkanou et al. (2016). In their study the Greek scientists investigated whether high-intensity interval cycling performed immediately after resistance training would inhibit muscle hypertrophy and strength improvements induced by resistance training per se.

Based upon previous studies utilizing low-intensity cycling as well as acute studies investigating molecular pathways it was hypothesized that high-intensity interval cycling performed immediately after resistance training would not hinder muscle strength and hypertrophy but would negatively affect the rate of force development. So, no effect on muscle but on strength gains.

You can learn more about the optimal exercise order at the SuppVersity

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Study: Over-training Exists

Recovering from the Athlete's Triad

The subjects, twenty-two male university students (age 21.8 0.6 years, body height 177.4 1.5 cm, body mass 74.2 2.1 kg, estimated VO2peak on a cycle ergometer 38.2 0.9 ml/kg/min) who had not been involved in systematic training (resistance or endurance) for at least 6 months before the initiation of the study but participated in recreational activities such as basketball, soccer, and jogging, 2–3 h per week, were assigned into two experimental groups according to their initial 1-RM leg press strength:

"One group of participants (RE, n = 11) performed resistance training only and the other group (REC, n = 11) performed the same resistance training but each session was followed by high-intensity interval cycling. [...] Training was performed two times per week for 8 weeks. Warm-up was the same for both training groups and included 5-min cycling at 50–75 W, lower body muscle stretching and 2 sets 9 - 10 repetitions of three exercises for the trunk (abdominal crunches, lateral crunches, dorsal raises) aiming to strengthen the lumbar spine area for injury prevention. The inclined leg press (45° angle) and the half-squat (knee angle 90°) Smith machine were used for the strength training of the lower extremities. The RE group performed four sets of 6-RM for each exercise (Zaras et al., 2014; approximately 85% of 1-RM: 220 14 kg and 127 +/- 7 kg in leg press and in halfsquat, respectively). In the first week, the training load was set at 80% of 6-RM (176 +/- 11 kg and 102 +/- 6 kg in leg press and half-squat, respectively). Thereafter, the resistance training load was set at 6-RM and it was increased by 2.0–2.5% in every training session so as to maintain at 6-RM until the last week of training intervention" (Tsitkanou. 2016).

Unlike the previously described resistance training protocol with rest periods of 3 minutes and between sets and 5 minutes between exercises, HIIT cycling was performed only by the subjects in the REC group. 10 minutes after the completion of the resistance exercises, the participants performed 10 sets of 60-s duration on a stationary bicycle with 100% of maximal aerobic power and 55–60 revolutions/min. The cycling workload was being increased (~2%) in every training session. The passive recovery between sets was static and amounted to 60 s.

Figure 1:  Δ Physical performance (%) before and after the training period; *: p < 0.05, §: p < 0.001 (Tsitkanou. 2016).

The authors of the study estimate the extra energy cost of performing high-intensity cycling in REC was less than 50 Kcal per day, for the whole training period. "Therefore, the participants of the REC group did not receive any extra nutritional direction in order to compensate for this extra energy loss
compared to RE," the authors argue and are probably right: it is very unlikely that those 50kcal would have a sign. effect on the lean mass and/or strength gains.

What the data in Figure 1 does tell you, however, is that there was a non-significant effect of the training type; albeit with a practically hardly relevant "advantage" for either of the workout protocols. If anything you may argue that the increase in maximal aerobic power of the subjects in the REC group, though it's likewise not statistically significant compared to the RE group, provides evidence of potentially relevant training benefits that would be confirmed by the significant improvements in heart rate at four submaximal workloads you can see in Figure 2.

Figure 2: Heart Rate at four submaximal workloads before and after 8 weeks of resistance training only (RE, a), and resistance plus aerobic training (REC, b). *P < 0.05, difference before and after 8-week training period (Tsitkanou. 2016).

For resistance trainees that may not be the most important benefit, but in view of the fact that the main muscle size increase, i.e. in the quads, did not differ and considering the fact that the vastus lateralis (VL) and rectus femoris (RF) size gains virtually cancel each other out, a significant systemic impairment of muscle hypertrophy as it is often cited as potential side effect of concomitant training.

Figure 3: Cross-sectional area of the right quadriceps and its’ four heads, and architectural characteristics of vastus lateralis before and after 8 weeks of resistance training per se and resistance plus high-intensity aerobic cycling | †P < 0.05 difference in percentage changes between two groups (RE > REC). ‡P < 0.05 difference in percentage changes between two groups (RE < REC). VL = vastus lateralis; RF = rectus femoris; VI = vastus intermedius; VM = vastus medialis; CSA = cross-sectional area; Quad = whole quadriceps (Tsitkanou. 2016).

Rather than that, the data in Figure 3 suggests an activity-dependent selective hypertrophy of the rectus femoris; whether the vastus lateralis simply gets too much exercise (previous studies show a steep inline in VL activity as the intensity of cycling increases / in running, the EMG activity is many times lower | Bijker. 2002) or if there's another reason for the lack of CSA increases, will have to be investigated in future studies
Since the type of training didn't affect the fiber composition of the subjects, either (both groups seeing similar increases in Type IIA and IIX - without sign. inter-group differences), the study at does indeed confirmed the authors' research hypothesis: "[H]igh-intensity interval cycling performed immediately after lower body resistance training did not inhibit muscle hypertrophy induced by chronic resistance training, in moderately trained individuals" (Tsitkanou. 2016). In fact, the additional increase in muscle capillarization and previously discussed beneficial effects on conditioning would even argue in favor of doing HIIT after every workout if...

A study by Kazior, et al. found sign. increases in muscle anabolism with "cardio" before resistance training.,For both studies it may be an important that we are dealing with cycling, not sprinting in the study at hand. After all, a recent review suggests cycling is the least likely to affect your gains (Murach. 2016).

... this study would suggest that doing HIIT after resistance training is a hit, but there are things we shouldn't forget. There's the potential difference between trained and more-or-less untrained individuals as they were recruited for the study at hand. Especially in individuals with a higher training volume and frequency, for example, adding a HIIT session towards the end of every resistance training workout may simply be too taxing.

Furthermore, the existing non-significant inter-group differences may accumulate over time with both the small decrements in strength and size gains having the potential to achieve statistical significance after another 8 weeks - previous studies, such as Häkkinen, et al. 2003, appear to confirm just that.

In their 21-week, study the scientists came close to a sign. difference with larger increases in the CSA of all muscle fiber types in response to strength training per se (I: 46%, IIA: 26%, IIX: 39%) compared with concurrent training (I: 13%, IIA: 23%, IIX: 31%). On the other hand, there are studies like Kazior et al (2016) that seem to provide reliable evidence of an increased muscle anabolic response - albeit with "pre-lifting" cardio training which, in turn, could make a significant difference to the "post-lifting" cardio applied in the study at hand. And then, there's the lack of data on upper body muscles and different types of cardio... ah, so many things we still don't know

Eventually, the best advice I can give you is thus still: try it, judge if it appears to impair your performance and recovery, evaluate your training logs every two weeks and - if possible - do your "cardio" on separate days, anyway | Comment on Facebook!

References:

• Bijker, K., G. De Groot, and A. Hollander. "Differences in leg muscle activity during running and cycling in humans." European journal of applied physiology 87.6 (2002): 556-561.
• Häkkinen, K., et al. "Neuromuscular adaptations during concurrent strength and endurance training versus strength training." European journal of applied physiology 89.1 (2003): 42-52.
• Kazior, Zuzanna, et al. "Endurance Exercise Enhances the Effect of Strength Training on Muscle Fiber Size and Protein Expression of Akt and mTOR." PloS one 11.2 (2016): e0149082.
• Murach, Kevin A., and James R. Bagley. "Skeletal Muscle Hypertrophy with Concurrent Exercise Training: Contrary Evidence for an Interference Effect." Sports Medicine (2016): 1-11.
• Tsitkanou, S., et al. "Effects of high‐intensity interval cycling performed after resistance training on muscle strength and hypertrophy." Scandinavian Journal of Medicine & Science in Sports (2016).
• Zaras, Nikolaos D., et al. "Rate of force development, muscle architecture, and performance in young competitive track and field throwers." The Journal of Strength & Conditioning Research 30.1 (2016): 81-92.