Saturday, May 3, 2014

HIIT Not as Effective in Building Mitochondria as Previously Thought? Study Puts Question Mark Behind Low Volume HIT & Minimalist Short Interval + Long Rest HIIT Regimen

Have you been running for nothin'?
It has gotten a somewhat quiet around HIIT, as of late and while I suspect the abating hype is mostly due to the fact that it is f***ly intense, a recent human study from the McMaster University in Hamilton, Ontario, Canada, would suggest that a the previously reported long-term effects may in fact have been overblown. At least with a "minimal" volume, in this case 6x30s wingate sprints with 4 min rest in-between, the expected increases in mitochondrial firepower was not see in their study and if those don't occur this could mean that you are working your ass off for nothing.
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.
I do yet have a good reason to use the conditional, here. In view of the estrogen-related sexual differences in the adaptational response to exercise the fact that the Canadian researchers had 8 guys in their HIIT group and 5 men and 4 women in their work-matched steady group could be a serous design-flaw - a flaw which renders the comparison of 4x30s wingate all out cycling tests w/ 4 min break or a workmatched (see Figure 1) 4 min steady state exercise trial.
Figure 1: Comparison of total workload, peak power output, mean power output, work duration and ratings of perceived exerction between the intermittent and steady state acute trials (Cochran. 2014)
Moreover, and for this I have to credit the researchers, themselves, there is a huge difference between the reported absence of mitochondrial adaptations and the general beneficial effects on the fitness level of the recreatinally trained subjects, which increased to a similar extend in both the intermittent (HIIT) 6 week exercise study (three short training sessions per week) as it did in a second classic steady-state exercise trial in the course of which the subjects had to perform their traning in a classic high intensity steady-state fashion.

Acute vs. long-term effects - a question of total volume?

It is this comparison of the long-term effects which eventually yielded different results for the work-matched intermittent and steady-state regimen. For the acute training, on the other hand, there were no significant differences in any of the measured parameters (see Figure 2)
Figure 2: When it's done at high intensities and with identical workloads intermittent and continuous exercise produce identical acute effects (Cochran. 2014)
Aside from the expression of Acetyl-CoA carboxylase and the lactate levels after the exercise session, there was an identical use of muscle glycogen (-25% within only 2min! for the HIIT trial!) and even the phosphorylation of p38 MAPK and PGC-1α expression were identical (4x increased, 3h after the workout).

In the "long run", in this case 6 weeks, Cochran et al. did yet observe differences not between their HIIT and steady state protocols, but between their current and previous results by Burgomaster et al. (2008), where a similar protocol did yield the changes in mitochondrial enzyme markers that were absent in the study at hand.

As Cochran et al. correctly point out, a 1:1 comparison of their data to the findings of Burgomaster is not exactly scientifically valid. There was after all no direct direct comparison between the CONT and INT protocols in the study at hand. Still, a recent review by Bishop et al. (2013) suggested that training volume is more important for increasing mitochondrial content than training intensity and the volume in the previously cited study by Burgomaster was higher - 50% higher (6 vs. 4 wingates).

The volume difference alone may thus explain the missing changes in citric acid synthase activity and the disappointing absence of increases in GLUT4, MCT1 and MCT4, which would signal an increased propensity to use both glucose and fat as a substrate.
Calm down, but don't be too lazy. In view of the many previous studies in which HIIT triggered the highly desirable increases in mitochondrial firepower and given the fact that both the HIIT and steady state (HIT) trial lead to significant improvements in VO2max, I would not discount high intensity interval training as a feasible means to increase your mitochondrial firepower.

To build mitochondria, shorter rest times and more intervals appear to be more effective | learn more
What we should maybe keep in mind, though, is that not all HIIT regimen are created equal (learn more). In fact, we've seen just that before with an advantage of higher volume and longer intervals in a previous article I've written about interval training. And in case you want it quick your HIIT protocol should probably have shorter rest times (10s) and more intervals 8x20s - similar to the one in the study by Ma et al. I wrote about in "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" | read more.
  • Burgomaster, Kirsten A., et al. "Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans." The Journal of physiology 586.1 (2008): 151-160.
  • Cochran, Andrew JR, et al. "Intermittent and continuous high‐intensity exercise training induce similar acute but different chronic muscle adaptations." Experimental physiology (2014).
  • 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.