Molecular responses to high-intensity interval exercise
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.
- SourceAvailable from: Antonino Bianco
- "This means that glucose and all gluconeogenic precursors will be spared from further oxidation and will be converted to glucose and glycogen, so lipids become the preferred oxidation substrate (Borsheim & Bahr, 2003); 2) the AMP kinases/acetyl CoA carboxylase (AMPK/ACC) pathway. It has been demonstrated that intense exercise increases AMPK (Gibala, 2009); thus, AMPK can phosphorylate ACC, decreasing its activity; the decreased ACC activity leads to a decrease in the rate of the synthesis of malonyl CoA, and consequently, there is a release of inhibition of carnitine palmitoyltransferase I (CPT1) activity leading to an increase in lipid oxidation (Winder, 2001); 3) an increase in atrial natriuretic peptide (ANP) stimulated by exercise could play a role in the increased rate of lipid oxidation ; production of ANP is related to the intensity of exercise (Moro et al., 2008; de Almeida et al., 2012), it has been demonstrated that ANP increases lipolysis (Souza et al., 2011), and this pathway appears to be more suitable than the increase in Figure 1 Changes in resting energy expenditure (REE) and respiratory exchange ratio (RER) at basal condition and 22 h after a session of traditional resistance training or high-intensity interval resistance training. ** P<0.005. "
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ABSTRACT: Although resistance training (RT) has long been accepted as a means for developing and maintaining muscular strength, endurance, power and muscle mass, its beneficial relationship with health factors and chronic disease has only recently been recognized in the scientific literature. Prior to 1990, resistance training was not a part of the recommended guidelines for exercise training and rehabilitation for either the American Heart Association or the American College of Sports Medicine (ACSM). In 1990, the ACSM recognized resistance training as a significant component of a comprehensive fitness programme for healthy adults of all ages, a position subsequently confirmed few years after. At present, even though interest in clinical applications of RT is increasing, there are still some concerns, among physicians, about the use of this exercise methodology in weight control programmes. This review aims to explore the metabolic effects of RT and its efficacy and feasibility in overweight subjects.Clinical Physiology and Functional Imaging 02/2014; 35(1). DOI:10.1111/cpf.12136 · 1.33 Impact Factor
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- "Via coactivation of transcription factors, for example, myocyte enhancer factor 2 and estrogen-related receptor, PGC-1a also plays an important role in other adaptive processes, such as vascular growth and induction of a " slower " muscle fiber phenotype (Lin et al. 2005; Arany et al. 2008). Such adaptations are typically associated with endurance-type exercise but other types of physical activity (e.g., sprint, and resistance exercise) also result in an increase in the levels of the PGC-1a transcript (Gibala 2009; Lundberg et al. 2013). Moreover, PGC-1a was recently shown to participate in the regulation of skeletal muscle hypertrophy (Ruas et al. 2012), which suggests a more complex regulation of exercise-induced transcription of PGC-1a in the control of adaptation. "
ABSTRACT: Recently, a truncated peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) splice variant, PGC-1α4, that originates from the alternative promoter was shown to be induced by resistance exercise and to elicit muscle hypertrophy without coactivation of "classical" PGC-1α targets involved in mitochondrial biogenesis and angiogenesis. In order to test if distinct physiological adaptations are characterized by divergent induction of PGC-1α splice variants, we investigated the expression of truncated and nontruncated PGC-1α splice variants and PGC-1α transcripts originating from the alternative and the proximal promoter, in human skeletal muscle in response to endurance and resistance exercise. Both total PGC-1α and truncated PGC-1α mRNA expression were increased 2 h after endurance (P < 0.01) and resistance exercise (P < 0.01), with greater increases after endurance exercise (P < 0.05). Expression of nontruncated PGC-1α increased significantly in both exercise groups (P < 0.01 for both groups) without any significant differences between the groups. Both endurance and resistance exercise induced truncated as well as nontruncated PGC-1α transcripts from both the alternative and the proximal promoter. Further challenging the hypothesis that induction of distinct PGC-1α splice variants controls exercise adaptation, both nontruncated and truncated PGC-1α transcripts were induced in AICAR-treated human myotubes (P < 0.05). Thus, contrary to our hypothesis, resistance exercise did not specifically induce the truncated forms of PGC-1α. Induction of truncated PGC-1α splice variants does not appear to underlie distinct adaptations to resistance versus endurance exercise. Further studies on the existence of numerous splice variants originating from different promoters are needed.11/2013; 1(6):e00140. DOI:10.1002/phy2.140
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- "Regular HIIT has also been shown to significantly increase both aerobic and anaerobic fitness, to decrease insulin resistance (Boutcher 2011) and to promote a number of skeletal muscle adaptations that result in enhanced fat oxidative capacity and improved glucose tolerance (Boutcher 2011). Indeed, HIIT increases maximal activity and protein content of mitochondrial enzymes such as citrate synthase, cytochrome oxidase, and enhances b hydroxyacyl coenzyme A dehydrogenase and phosphofructokinase activities (Gibala 2009; Talanian et al. 2007). The notion that HIIT can be performed by anybody (Metcalfe et al. 2011) needs to be proved, especially in obese subjects whose exercise capacity is reduced. "
ABSTRACT: We investigate the effects of 12-week interval training of moderate- or high-intensity exercise on blood lipids and plasma levels of adiponectin. Thirty-four obese adolescent females [age = 15.9 ± 0.3 years; BMI and BMI-Z-score = 30.8 ± 1.6 kg/m(2) and 3 ± 0.3, respectively], were randomized to high-intensity interval training (HIIT, n = 11), moderate-intensity interval training (MIIT, n = 11), or a control group (CG, n = 12). Maximal oxygen uptake ([Formula: see text]), maximal aerobic speed (MAS), plasma lipids and adiponectin levels were measured in all subjects before and after training. Following the training program, in both training groups, body mass, BMI-Z-score, and percentage body fat (% BF) decreased, while [Formula: see text] and MAS increased. Low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and adiponectin levels were positively altered (-12.6 and -7.4 %; 6.3 and 8.0 %; 35.8 and 16.2 %; high to moderate training program, respectively). Waist circumference, triglyceride and total cholesterol decreased only in HIIT group (-3.5; -5.3 and -7.0 %, respectively, in all P < 0.05). Significant decrease in the usual index of insulin resistance (HOMA-IR) occurred in HIIT and MIIT groups (-29.2 ± 5.3 and -18.4 ± 8.6 %, respectively; P < 0.01). The results show that HIIT positively changes blood lipids and adiponectin variables in obese adolescent girls, resulting in improved insulin sensitivity, as attested by a lower HOMA-IR, and achieving better results compared to moderate-intensity exercise.Arbeitsphysiologie 07/2013; 113(10). DOI:10.1007/s00421-013-2689-5 · 2.30 Impact Factor