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For years, exercise scientists have been convinced that the only way to increase mitochondrial density is with aerobic endurance training, but recent studies have proved otherwise. Not only is an increase in the size and number of mitochondria a proven adaptation to HIIT, but the mitochondrial benefit of HIIT goes way beyond size and number. For example, all your mitochondria contain oxidative enzymes, such as citrate synthase, malate dehydrogenase, and succinate dehydrogenase. These oxidative enzymes lead to improved metabolic function of your skeletal muscles—particularly by causing more effective fat and carbohydrate breakdown for fuel and also by accelerating energy formation from ATP. So more oxidative enzymes means that you have a higher capacity for going longer and harder. And it turns out that, according to an initial study on the effect of HIIT on oxidative enzymes, there were enormous increases in skeletal muscle oxidative enzymes in seven weeks in subjects who did four to ten thirty-second maximal cycling sprints followed by four minutes of recovery just three days a week. But what about HIIT as opposed to aerobic cardio? Another six-week training study compared the increase in oxidative enzymes that resulted from either: 1. Four to six thirty-second maximal-effort cycling sprints, each followed by four-and-a-half minutes of recovery, performed three days a week (classic HIIT training) or 2. Forty to sixty minutes of steady cycling at 65 percent VO2 max (an easy aerobic intensity) five days a week The levels of oxidative enzymes in the mitochondria in subjects who performed the HIIT program were significantly higher—even though they were training at a fraction of the volume of the aerobic group. How could this favorable endurance adaptation happen with such short periods of exercise? It turns out that the increased mitochondrial density and oxidative-enzyme activity from HIIT are caused by completely different message-signaling pathways than those created by traditional endurance training.
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