Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function

TLDR

The mechanisms underlying performance gains from high‑intensity interval training remain unclear. This study aimed to identify the physiological adaptations after six HIT sessions that explain improvements in exercise performance. Sixteen untrained adults completed six 60‑second high‑intensity cycling intervals at 100 % peak power with 75‑second low‑intensity recovery over two weeks, and researchers measured changes in muscle mitochondrial capacity, oxygenation, cardiac output, blood volumes, and fatigue resistance. Participants exhibited ~8 % higher VO₂peak and ~5 % longer cycling time, a ~20 % increase in muscle mitochondrial content and respiratory capacity, while cardiac output and blood volume were unchanged, suggesting mitochondrial expansion drives the performance improvements.

Abstract

Six sessions of high-intensity interval training (HIT) are sufficient to improve exercise capacity. The mechanisms explaining such improvements are unclear. Accordingly, the aim of this study was to perform a comprehensive evaluation of physiologically relevant adaptations occurring after six sessions of HIT to determine the mechanisms explaining improvements in exercise performance. Sixteen untrained (43 ± 6 ml·kg −1 ·min −1 ) subjects completed six sessions of repeated ( 8 – 12 ) 60 s intervals of high-intensity cycling (100% peak power output elicited during incremental maximal exercise test) intermixed with 75 s of recovery cycling at a low intensity (30 W) over a 2-wk period. Potential training-induced alterations in skeletal muscle respiratory capacity, mitochondrial content, skeletal muscle oxygenation, cardiac capacity, blood volumes, and peripheral fatigue resistance were all assessed prior to and again following training. Maximal measures of oxygen uptake (V̇o 2peak ; ∼8%; P = 0.026) and cycling time to complete a set amount of work (∼5%; P = 0.008) improved. Skeletal muscle respiratory capacities increased, most likely as a result of an expansion of skeletal muscle mitochondria (∼20%, P = 0.026), as assessed by cytochrome c oxidase activity. Skeletal muscle deoxygenation also increased while maximal cardiac output, total hemoglobin, plasma volume, total blood volume, and relative measures of peripheral fatigue resistance were all unaltered with training. These results suggest that increases in mitochondrial content following six HIT sessions may facilitate improvements in respiratory capacity and oxygen extraction, and ultimately are responsible for the improvements in maximal whole body exercise capacity and endurance performance in previously untrained individuals.