Have you been running for nothin'? |
You can learn more about HIIT at the SuppVersity
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) |
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) |
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.
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.
Reference:To build mitochondria, shorter rest times and more intervals appear to be more effective | learn 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.