Physiological and health-related adaptations to low-volume interval training: influences of nutrition and sex

Abstract

Interval training refers to the basic concept of alternating periods of relatively intense exercise with periods of lower-intensity effort or complete rest for recovery. Low-volume interval training refers to sessions that involve a relatively small total amount of exercise (i.e. ≤10 min of intense exercise), compared with traditional moderate-intensity continuous training (MICT) protocols that are generally reflected in public health guidelines. In an effort to standardize terminology, a classification scheme was recently proposed in which the term 'high-intensity interval training' (HIIT) be used to describe protocols in which the training stimulus is 'near maximal' or the target intensity is between 80 and 100 % of maximal heart rate, and 'sprint interval training' (SIT) be used for protocols that involve 'all out' or 'supramaximal' efforts, in which target intensities correspond to workloads greater than what is required to elicit 100 % of maximal oxygen uptake (VO2max). Both low-volume SIT and HIIT constitute relatively time-efficient training strategies to rapidly enhance the capacity for aerobic energy metabolism and elicit physiological remodeling that resembles changes normally associated with high-volume MICT. Short-term SIT and HIIT protocols have also been shown to improve health-related indices, including cardiorespiratory fitness and markers of glycemic control in both healthy individuals and those at risk for, or afflicted by, cardiometabolic diseases. Recent evidence from a limited number of studies has highlighted potential sex-based differences in the adaptive response to SIT in particular. It has also been suggested that specific nutritional interventions, in particular those that can augment muscle buffering capacity, such as sodium bicarbonate, may enhance the adaptive response to low-volume interval training.

Fig. 1

Examples of protocols employed in interval training studies, expressed relative to PPO that is required to elicit VO_2max or VO_{2 peak}. The figure shows typical MICT, e.g. 50 min at ~35 % of PPO, which elicits ~70 % of HR_max (hatched box); low-volume HIIT, e.g. 10 × 1 min at a constant workload corresponding to ~75 % of PPO, interspersed with 1 min of recovery, which elicits ~85–90 % of HR_max during the intervals (grey bars); and low-volume SIT, e.g. 4 × 30 s ‘all out’ effort at a variable power output corresponding to ~175 % of PPO (averaged over the course of the intervals), interspersed with 4 min of recovery, which elicits ~90–95 % of HR_max during the intervals (black bars). Power output and heart rate estimates are derived from Little et al. [31] and Skelly et al. [60]. PPO, peak power output, VO _2max, maximal oxygen uptake, VO ₂ peak, peak VO ₂, MICT, moderate-intensity continuous exercise, HR _max, maximum heart rate, HIIT, high-intensity interval training, SIT, sprint-interval training

Fig. 2

Hypothesized acute signaling mechanism underpinning enhanced training adaptations in response to chronic NaHCO₃ supplementation. a AMPK acts as an energy sensor that is activated by various signals generated during muscle contraction (e.g. increased AMP), which subsequently activates PGC-1α, leading to increased transcription of various genes involved in mitochondrial biogenesis. b Supplementation with NaHCO₃ may alter muscle metabolism, resulting in greater increases in AMP, which could enhance AMPK activation through interaction with the γ-subunit. Glycogen utilization during exercise is also increased after NaHCO₃ supplementation, and the AMPK β-subunit that is sequestered by glycogen may be liberated to a greater extent. Greater AMPK activation could result in greater downstream signaling, including activation of PGC-1α and increased gene expression. Red arrows depict potential mechanisms that are supported by experimental data, whereas question marks indicate areas that remain to be directly investigated. NaHCO ₃ sodium bicarbonate, AMPK adenosine monophosphate kinase, PGC-1α peroxisome proliferator-activated receptor γ co-activator