Since Tabata et al’s 1996 study demonstrating that high intensity interval training improved both anaerobic and aerobic capacity, intervals have come back into vogue. Many athletes are running sprints and lactate threshold training is becoming more commonplace. While Dr. Tabata’s team measured the effects the different exercise programs (cycling at 70% of VO2max for 60min vs. cycling at 170% of VO2max for 20 seconds with 10 secs at near rest for 7-8 intervals) had on VO2max and maximal oxygen debt, no investigation at the time was done on what mechanism occurred that stimulated these changes at the cellular or systemic levels.
Laursen and Jenkins 2002 point out that no evidence of oxidative or glycolytic enzyme activity have been observed in endurance trained athletes put on these programs. Study after study is cited showing p < 0.05 improvement in VO2max and anaerobic capacity yet the exact mechanism of action remains unknown. It is hypothesized that the buffering capacity of the muscle may be involved. They say that the next steps for investigation would be plasma volume, stroke volume, muscle cation pumps, myoglobin, capillary density and fibre type have yet to be investigated.
By 2010, enough research had been conducted. Psilander et al 2010 and Little et al 2011 demonstrate that mitochondrial gene expression is altered by this form of training. The mRNA markers which regulate mitochondrial gene transcription (PGC-1a, PRC and PPARo) are activated after a single session of 7 intervals of 30 secs all out with 30 secs rest. These factors increased to 6, 1.5 and 1.5 times normal levels post exercise, peaked 3h after exercise and remained elevated for 24 hours. PGC-1a is considered the master regulator for mitochondrial biogenesis. So here we have the mechanism! The body upregulates the mRNA and new mitochondria in the stressed muscle are created. New mitochondria mean the cell can burn more energy, more efficiently, faster and with fewer waste products- thus resulting in improved aerobic and anaerobic capacities!