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.

6×1 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 22g 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!


  • 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.

HIIT Science Update 08/17: HIIT & the CNS, HIIT & Cortisol, HIIT, Diabetes, PWO Milk & Exercise (Non-)Responders syndicated from http://suppversity.blogspot.com


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