Physiological adaptations to interval training and the role of exercise intensity

Abstract

Interval exercise typically involves repeated bouts of relatively intense exercise interspersed by short periods of recovery. A common classification scheme subdivides this method into high-intensity interval training (HIIT; 'near maximal' efforts) and sprint interval training (SIT; 'supramaximal' efforts). Both forms of interval training induce the classic physiological adaptations characteristic of moderate-intensity continuous training (MICT) such as increased aerobic capacity (V̇O2 max ) and mitochondrial content. This brief review considers the role of exercise intensity in mediating physiological adaptations to training, with a focus on the capacity for aerobic energy metabolism. With respect to skeletal muscle adaptations, cellular stress and the resultant metabolic signals for mitochondrial biogenesis depend largely on exercise intensity, with limited work suggesting that increases in mitochondrial content are superior after HIIT compared to MICT, at least when matched-work comparisons are made within the same individual. It is well established that SIT increases mitochondrial content to a similar extent to MICT despite a reduced exercise volume. At the whole-body level, V̇O2 max is generally increased more by HIIT than MICT for a given training volume, whereas SIT and MICT similarly improve V̇O2 max despite differences in training volume. There is less evidence available regarding the role of exercise intensity in mediating changes in skeletal muscle capillary density, maximum stroke volume and cardiac output, and blood volume. Furthermore, the interactions between intensity and duration and frequency have not been thoroughly explored. While interval training is clearly a potent stimulus for physiological remodelling in humans, the integrative response to this type of exercise warrants further attention, especially in comparison to traditional endurance training.

Keywords: aerobic capacity; cardiovascular; cycling; exercise duration; mitochondria; skeletal muscle; training frequency.

© 2016 The Authors. The Journal of Physiology © 2016 The Physiological Society.

Figures

Figure 1. A graphical depiction of the main types of aerobic exercise

A–C, representative examples of moderate intensity continuous training (MICT), high‐intensity interval training (HIIT), and low and high volumes of sprint interval training (SIT). The intensity is depicted as a percentage of the peak power output (PPO) obtained during a standard ramp V˙O2 peak test (e.g. MacInnis et al. 2016). Note that most recent studies of SIT used a low‐volume protocol (e.g. Burgomaster et al. 2006, 2008), whereas earlier studies of SIT used a high‐volume protocol (e.g. Saltin et al. 1976). D, the training volume associated with each protocol based on the durations and training frequencies provided. The MICT and HIIT protocols shown in A and B are work‐matched when performed for the same duration and at the same frequency. The low‐volume SIT protocol requires less total work to complete relative to HIIT and MICT, whereas performing three sessions of the high‐volume SIT protocol matches the training volume in the MICT and HIIT protocols.

Figure 2. A schematic diagram of the putative mechanisms through which high‐intensity exercise may elicit greater mitochondrial adaptations to aerobic training compared to lower intensities of exercise

Exercising at a higher intensity increases calcium release (A), requires greater ATP turnover (B), and leads to greater use of carbohydrates for fuel (C), compared to exercising at a lower intensity. As a result, there is a greater accumulation of metabolites, ions, and free radicals (D), which increase the activation of signalling proteins (E), including the kinases Ca2+/calmodulin‐dependent protein kinase II (CaMKII) and AMP‐activated protein kinase (AMPK). The increased activity of these protein kinases causes greater rates of gene expression for PGC‐1α (encoded by PPARGC1A), which in turn acts as a transcriptional co‐activator for nuclear genes encoding mitochondrial proteins (NUGEMPs; F). In turn, mitochondrial protein synthesis rates are greater for high‐intensity exercise (G), leading to a greater increase in mitochondrial content (H), relative to exercise at a lower intensity. Two additional ROS‐mediated mechanisms explaining the potency of low‐volume SIT have recently been reported. Firstly, through a ROS‐dependent mechanism, low‐volume SIT led to the fragmentation of the ryanodine receptor (RyR) of the sarcoplasmic reticulum and increased the intracellular calcium concentration (I), a signal for mitochondrial biogenesis. Similarly, two weeks of low‐volume SIT was associated with the inhibition of aconitase in the tricarboxylic acid cycle (TCA) and an increased intracellular citrate concentration, which was suggested to increase mitochondrial content via a reduction in mitophagy (J). For specific references, see ‘Exercise intensity mediates acute mitochondria‐related responses to exercise’ in text. ACN, aconitase; ATPase, adenosine triphosphatase; CK, creatine kinase; ETC, electron transport chain; PHOS, glycogen phosphorylase; HK, hexokinase; LDH, lactate dehydrogenase; MK, myosin kinase; PFK, phosphofructokinase; PDH, pyruvate dehydrogenase; TFAM, transcription factor A, mitochondria.

Figure 3. Changes in mitochondrial content in response to 2 weeks of high‐intensity interval training (HIIT) and moderate‐intensity continuous training (MICT), matched for total work

Subjects performed six sessions of single‐leg cycling with each leg, completing either a HIIT or MICT protocol. The greater increase in mitochondrial content elicited by HIIT as compared to MICT was evident from post‐training differences in maximal citrate synthase activity (A) and mitochondrial respiration (JO2), specifically oxidative phosphorylation capacity through complexes I and II (PCI&CII, B). Bars represent the mean responses for each group, whereas lines refer to the responses of individual subjects. Symbols indicate a significant difference from the within‐group, pre‐training mean (§), and significant differences between groups at the post‐training mean (†). Error bars represent 1 standard error of the mean. For A, n = 9 and for B, n = 8 subjects.