Physiological adaptations to low-volume, high-intensity interval training in health and disease

Abstract

Exercise training is a clinically proven, cost-effective, primary intervention that delays and in many cases prevents the health burdens associated with many chronic diseases. However, the precise type and dose of exercise needed to accrue health benefits is a contentious issue with no clear consensus recommendations for the prevention of inactivity-related disorders and chronic diseases. A growing body of evidence demonstrates that high-intensity interval training (HIT) can serve as an effective alternate to traditional endurance-based training, inducing similar or even superior physiological adaptations in healthy individuals and diseased populations, at least when compared on a matched-work basis. While less well studied, low-volume HIT can also stimulate physiological remodelling comparable to moderate-intensity continuous training despite a substantially lower time commitment and reduced total exercise volume. Such findings are important given that 'lack of time' remains the most commonly cited barrier to regular exercise participation. Here we review some of the mechanisms responsible for improved skeletal muscle metabolic control and changes in cardiovascular function in response to low-volume HIT. We also consider the limited evidence regarding the potential application of HIT to people with, or at risk for, cardiometabolic disorders including type 2 diabetes. Finally, we provide insight on the utility of low-volume HIT for improving performance in athletes and highlight suggestions for future research.

Figure 1. Peak oxygen uptake (top panel) and the maximal activity of the mitochondrial enzyme citrate synthase measured in biopsy samples (bottom panel) obtained before (PRE) and after (POST) 6 weeks of Wingate-based high-intensity interval training (HIT) or traditional moderate-intensity endurance training (ET)

Total exercise volume was 90% lower in the HIT group. Redrawn from Burgomaster et al. (2008) with permission.* P < 0.05 vs Pre; main effect for time.

Figure 2. Potential intracellular signalling mechanisms involved in HIT-induced mitochondrial biogenesis

Low-volume HIT has been shown to activate 5′-AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (MAPK). Both of these exercise-responsive signalling kinases are implicated in direct phosphorylation and activation of PGC-1α. Increased nuclear abundance of PGC-1α following HIT is hypothesized to co-activate transcription factors (TF) to increase mitochondrial gene transcription, ultimately resulting in accumulation of more mitochondrial proteins to drive mitochondrial biogenesis.

Figure 3. The effect of varying the intensity of interval training on changes in 40 km time-trial performance

Well-trained male cyclists were randomly assigned to one of five different doses of high-intensity interval training (HIT): 12 × 30 s at 175% of peak sustained power output (PPO), 12 × 1 min s at 100% PPO, 12 × 2 min at 90% PPO, 8 × 4 min at 85% PPO, or 4 × 8 min at 80% PPO. Cyclists completed six HIT sessions over a 3 week period in addition to their habitual aerobic base training. Redrawn from Stepto et al. (1999) with permission.