A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms

Abstract

High-intensity interval training (HIT) induces skeletal muscle metabolic and performance adaptations that resemble traditional endurance training despite a low total exercise volume. Most HIT studies have employed 'all out', variable-load exercise interventions (e.g. repeated Wingate tests) that may not be safe, practical and/or well tolerated by certain individuals. Our purpose was to determine the performance, metabolic and molecular adaptations to a more practical model of low-volume HIT. Seven men (21 ± 0.4 years,V O 2 peak = 46 ± 2 ml kg −1 min −1 ) performed six training sessions over 2 weeks. Each session consisted of 8-12 × 60 s intervals at ∼100% of peak power output elicited during a rampV O 2 peak test (355 ± 10 W) separated by 75 s of recovery. Training increased exercise capacity, as assessed by significant improvements on both 50 kJ and 750 kJ cycling time trials (P < 0.05 for both). Skeletal muscle (vastus lateralis) biopsy samples obtained before and after training revealed increased maximal activity of citrate synthase (CS) and cytochrome c oxidase (COX) as well as total protein content of CS, COX subunits II and IV, and the mitochondrial transcription factor A (Tfam) (P < 0.05 for all). Nuclear abundance of peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) was ∼25% higher after training (P < 0.05), but total PGC-1α protein content remained unchanged. Total SIRT1 content, a proposed activator of PGC-1α and mitochondrial biogenesis, was increased by ∼56% following training (P < 0.05). Training also increased resting muscle glycogen and total GLUT4 protein content (both P < 0.05). This study demonstrates that a practical model of low volume HIT is a potent stimulus for increasing skeletal muscle mitochondrial capacity and improving exercise performance. The results also suggest that increases in SIRT1, nuclear PGC-1α, and Tfam may be involved in coordinating mitochondrial adaptations in response to HIT in human skeletal muscle.

Physiological and molecular responses to an acute bout of reduced-exertion high-intensity interval training (REHIT)

“…This is supported by the recent findings that several markers of oxidative capacity in skeletal muscle, such as citrate synthase and COX IV, as well as protein levels of GLUT4 are increased following a 6-week REHIT intervention . Although such responses have commonly been observed following a variety of submaximal and supramaximal HIT protocols (Gibala et al 2009;Little et al 2011;Little et al 2010;Burgomaster et al 2005;Hood et al 2011;Gibala et al 2006), the current study and that by together suggest that these responses may be achieved with a much smaller volume of exercise than previously thought.…”

“…As 'lack of time' has been identified as one of the main barriers to becoming and remaining physically active (Korkiakangas et al 2009;Reichert et al 2007), over the past decade research has focused on high-intensity interval training (HIT) as a timeefficient alternative to aerobic exercise . Although initial studies have convincingly demonstrated equal or better health benefits with various HIT protocols compared to much larger volumes of aerobic exercise (Gibala et al 2006;Shepherd et al 2013;Cocks et al 2013;Burgomaster et al 2008;Trapp et al 2008;Gillen et al 2013;Little et al 2010), these HIT protocols tend to be very strenuous and as such are unlikely to be adhered to by sedentary populations. Furthermore, most HIT protocols are not as time-efficient as sometimes claimed, with the total time per exercise session generally exceeding 20-30 minutes (Gibala et al 2006;Rakobowchuk et al 2008;Shepherd et al 2013;Cocks et al 2013;Burgomaster et al 2008;Trapp et al 2008;Gillen et al 2013;Little et al 2010).…”

“…Although initial studies have convincingly demonstrated equal or better health benefits with various HIT protocols compared to much larger volumes of aerobic exercise (Gibala et al 2006;Shepherd et al 2013;Cocks et al 2013;Burgomaster et al 2008;Trapp et al 2008;Gillen et al 2013;Little et al 2010), these HIT protocols tend to be very strenuous and as such are unlikely to be adhered to by sedentary populations. Furthermore, most HIT protocols are not as time-efficient as sometimes claimed, with the total time per exercise session generally exceeding 20-30 minutes (Gibala et al 2006;Rakobowchuk et al 2008;Shepherd et al 2013;Cocks et al 2013;Burgomaster et al 2008;Trapp et al 2008;Gillen et al 2013;Little et al 2010). However, more recently we (Metcalfe et al 2012) and others Hazell et al 2010;Tjønna et al 2013) have demonstrated that performing HIT protocols consisting of fewer and/or shorter sprints does not appear to attenuate the associated training adaptations, as long as the exercise intensity remains high.…”

Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca 2+ leak after one session of high-intensity interval exercise

“…training (21)(22)(23)(24)(25). HIIT has been shown to effectively stimulate mitochondrial biogenesis in skeletal muscle and increase endurance in untrained and recreationally active healthy subjects (22,26), whereas positive effects in elite endurance athletes are less clear (21,27,28).…”

Respuestas metabólicas inducidas por ejercicio físico de alta intensidad en mujeres sedentarias con glicemia basal alterada e hipercolesterolemia

“…Esto concuerda con estudios anteriores realizados en mujeres pre diabéticas donde las mejoras en los niveles de glicemia se mantenían 72 h post intervención 12 . Adicionalmente, se puede señalar que las mejoras en los niveles de glicemia post-intervención podrían ser explicadas por estudios previos 18 que muestran los efectos del EF de alta intensidad sobre la activación de vías de señalización intracelularmediadas por la proteína 12 semanas de intervención (a 24 h y 48 h) en todos los grupos, excepto en el grupo normo-glicémico (N), en el cual sólo se observa una disminución significativa en la semana 12 (24 h) (Tabla 3). Los niveles de CT sólo disminuyeron significativamente en los grupos con hiper-colesterolemia (HH y NH) a las 12 semanas (24 h y 48 h).…”