Molecular responses to high-intensity interval exerciseThis paper is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process.

Abstract

From a cell-signaling perspective, short-duration intense muscular work is typically associated with resistance training and linked to pathways that stimulate growth. However, brief repeated sessions of high-intensity interval exercise training (HIT) induce rapid phenotypic changes that resemble traditional endurance training. Given the oxidative phenotype that is rapidly upregulated by HIT, it is plausible that metabolic adaptations to this type of exercise could be mediated in part through signaling pathways normally associated with endurance training. A key controller of oxidative enzyme expression in skeletal muscle is peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), a transcriptional coactivator that serves to coordinate mitochondrial biogenesis. Most studies of acute PGC-1alpha regulation in humans have used very prolonged exercise interventions; however, it was recently shown that a surprisingly small dose of very intense interval exercise, equivalent to only 2 min of all-out cycling, was sufficient to increase PGC-1alpha mRNA during recovery. Intense interval exercise has also been shown to acutely increase the activity of signaling pathways linked to PGC-1alpha and mitochondrial biogenesis, including AMP-activated protein kinase (alpha1 and alpha2 subunits) and the p38 mitogen-activated protein kinase. In contrast, signaling pathways linked to muscle growth, including protein kinase B/Akt and downstream targets p70 ribosomal S6 kinase and 4E binding protein 1, are generally unchanged after acute interval exercise. Signaling through AMP-activated protein kinase and p38 mitogen-activated protein kinase to PGC-1alpha may therefore explain, in part, the metabolic remodeling induced by HIT, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.

Decreasing sprint duration from 20 to 10 s during reduced-exertion high-intensity interval training (REHIT) attenuates the increase in maximal aerobic capacity but has no effect on affective and perceptual responses

“…The mechanisms which underpin the increases in VȮ2max with HIIT and SIT remain unclear , but have been proposed to rely on activation of skeletal muscle signalling pathways involving 5' adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferatoractivated receptor gamma coactivator 1-alpha (PGC-1α) (Gibala, 2009), and potentially other signalling molecules such as p38 mitogen-activated protein kinase (p38 MAPK) (Little et al, 2011), sirtuin 1 (SIRT1) (Guerra et al, 2010) and sirtuin 3 (SIRT3) (Edgett et al, 2016). It has been proposed that the activation of relevant signalling pathways with supramaximal exercise may be reliant on achieving peak power output (Hazell et al, 2010), but we have proposed an alternative theory suggesting that activation of signalling pathways could plausibly be related to rapid glycogenolysis associated with supramaximal exercise (Metcalfe et al, 2015).…”

Postprandial lipoprotein profile in two modes of high-intensity intermittent exercise

“…Recently, low-volume, high-intensity exercise has drawn attention, since it can result similar physiological and morphological effects, such as improvement of anaerobic and aerobic fitness, and body composition that those adaptations from moderate intensity exercise (Gibala, 2009; Gibala et al, 2009; Gibala et al, 2012; Gist et al, 2014; Hazell et al, 2014; Little et al, 2010). Moreover, a single session of high-intensity exercise was able to reduce total cholesterol and its fraction LDL-c (Lira et al, 2009).…”

“…Investigations have demonstrated benefits of high-intensity exercise performed in all-out manner (Gibala, 2009; Gibala et al, 2012), but this kind of exercise have particularities that make difficult its practical execution given that is necessary a specialized equipment as a mechanical cycle ergometer, treadmill or to be performed outside. Moreover, according to Gillen and Gibala (2014) such form of exercise may not be safe, tolerable or practical for many individuals.…”

p38 MAPK activation and H3K4 trimethylation is decreased by lactate in vitro and high intensity resistance training in human skeletal muscle

“…As high intensity exercise is generally associated with beneficial results of skeletal muscle adaptation [26, 50], it has to be particularly determined whether acute metabolically demanding exercise offers detrimental or advantageous effects for myoblast differentiation and skeletal muscle adaptation under conditions of recurring metabolic stress. This will be of importance for the evaluation of high exercise intensity in training regimen under time efficient guidelines for competing athletes and in clinical settings.…”