Molecular responses to high-intensity interval exercise
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.
Available from: Heikki Kainulainen
- "A single bout of prolonged endurance exercise transiently increases PGC-1a mRNA content in human and rat skeletal muscle (Pilegaard et al. 2003; Gidlund et al. 2015; Baar et al. 2002; Chinsomboon et al. 2009). Furthermore , other types of physical activity (e.g., sprint and resistance exercise) can also result in an increase in the gene expression of PGC-1a (Gibala 2009; Ydfors et al. 2013). There are several intracellular signaling pathways that may contribute to eliciting the exercise-induced PGC-1a gene expression response including calcium signaling , AMPK and MAPK signaling, ROS-mediated regulation , and b-adrenergic signaling (Olesen et al. 2010). "
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ABSTRACT: The primary aim of the present study was to investigate the acute gene expression responses of PGC-1 isoforms and PGC-1α target genes related to mitochondrial biogenesis (cytochrome C), angiogenesis (VEGF-A), and muscle hypertrophy (myostatin), after a resistance or endurance exercise bout. In addition, the study aimed to elucidate whether the expression changes of studied transcripts were linked to phosphorylation of AMPK and MAPK p38. Nineteen physically active men were divided into resistance exercise (RE, n = 11) and endurance exercise (EE, n = 8) groups. RE group performed leg press exercise (10 × 10 RM, 50 min) and EE walked on a treadmill (~80% HRmax, 50 min). Muscle biopsies were obtained from the vastus lateralis muscle before, 30 min, and 180 min after exercise. EE and RE significantly increased the gene expression of alternative promoter originated PGC-1α exon 1b- and 1bxs'-derived isoforms, whereas the proximal promoter originated exon 1a-derived transcripts were less inducible and were upregulated only after EE. Truncated PGC-1α transcripts were upregulated both after EE and RE. Neither RE nor EE affected the expression of PGC-1β. EE upregulated the expression of cytochrome C and VEGF-A, whereas RE upregulated VEGF-A and downregulated myostatin. Both EE and RE increased the levels of p-AMPK and p-MAPK p38, but these changes were not linked to the gene expression responses of PGC-1 isoforms. The present study comprehensively assayed PGC-1 transcripts in human skeletal muscle and showed exercise mode-specific responses thus improving the understanding of early signaling events in exercise-induced muscle adaptations.
Available 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.
Available from: Jessica Norrbom
- "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. "
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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.
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