High-intensity interval training increases SIRT1 activity in human skeletal muscle

2010 ◽  
Vol 35 (3) ◽  
pp. 350-357 ◽  
Author(s):  
Brendon J. Gurd ◽  
Christopher G.R. Perry ◽  
George J.F. Heigenhauser ◽  
Lawrence L. Spriet ◽  
Arend Bonen
Keyword(s):  
Skeletal Muscle ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Citrate Synthase ◽  
Interval Training ◽  
Peak Oxygen Consumption ◽  
Peroxisome Proliferator ◽  
Mitochondrial Enzymes ◽  
High Intensity Interval Training ◽  
High Intensity Interval

The effects of training on silent mating-type information regulator 2 homolog 1 (SIRT1) activity and protein in relationship to peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and mitochondrial content were determined in human skeletal muscle. Six weeks of high-intensity interval training (∼1 h of 10 × 4 min intervals at 90% peak oxygen consumption separated by 2 min rest, 3 days per week) increased maximal activities of mitochondrial enzymes in skeletal muscle by 28% to 36% (citrate synthase, β-hydroxyacyl-coenzyme A dehydrogenase, and cytochrome c oxidase subunit IV) and PGC-1α protein (16%) when measured 4 days after training. Interestingly, total muscle SIRT1 activity (31%) and activity per SIRT1 protein (58%) increased despite decreased SIRT1 protein (20%). The present data demonstrate that exercise-induced mitochondrial biogenesis is accompanied by elevated SIRT1 activity in human skeletal muscle.

An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle

2011 ◽  
Vol 300 (6) ◽  
pp. R1303-R1310 ◽  
Author(s):  
Jonathan P. Little ◽  
Adeel Safdar ◽  
David Bishop ◽  
Mark A. Tarnopolsky ◽  
Martin J. Gibala
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
Acute Bout ◽  
Nuclear Abundance ◽  
Low Volume ◽  
High Intensity Interval

Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.

scholarly journals Forty high-intensity interval training sessions blunt exercise-induced changes in the nuclear protein content of PGC-1α and p53 in human skeletal muscle

2019 ◽  
Author(s):  
Cesare Granata ◽  
Rodrigo S.F. Oliveira ◽  
Jonathan P. Little ◽  
David J. Bishop
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Mitochondrial Biogenesis ◽  
Exercise Intensity ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
High Intensity Interval ◽  
Exercise Induced

ABSTRACTExercise-induced increases in peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and p53 protein content in the nucleus mediate the initial phase of exercise-induced mitochondrial biogenesis. Here we investigated if exercise-induced increases in these and other markers of mitochondrial biogenesis were altered after 40 sessions of twice-daily high-volume high-intensity interval training (HVT) in human skeletal muscle. Vastus lateralis muscle biopsies were collected from 10 healthy recreationally active participants before, immediately post, and 3h after a session of HIIE performed at the same absolute exercise intensity before and after HVT (Pre-HVT and Post-HVT, respectively). The protein content of common markers of exercise-induced mitochondrial biogenesis were assessed in nuclear- and cytosolic-enriched fractions by immunoblotting; mRNA contents of key transcription factors and mitochondrial genes were assessed by qPCR. Despite exercise-induced increases in PGC-1α, p53, and plant homeodomain finger-containing protein 20 (PHF20) protein content, the phosphorylation of p53 and acetyl-CoA carboxylase (p-p53Ser15 and p-ACCSer79, respectively), and PGC-1α mRNA Pre-HVT, no significant changes were observed Post-HVT. Forty sessions of twice-daily high-intensity interval training blunted all of the measured exercise-induced molecular events associated with mitochondrial biogenesis that were observed Pre-HVT. Future studies should determine if this loss relates to the decrease in relative exercise intensity, habituation to the same exercise stimulus, or a combination of both.

scholarly journals PO-030 Oxidative phosphorylation in response to high intensity interval training

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Radosław Laskowski ◽  
Sylwester Kujach ◽  
Damian Flis ◽  
Maciej Chroboczek ◽  
Piotr Wąż ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
High Intensity ◽  
Citrate Synthase ◽  
Interval Training ◽  
Mitochondrial Respiratory Chain ◽  
Maximal Activity ◽  
Mitochondrial Enzymes ◽  
High Intensity Interval Training ◽  
Respiratory Chain Complexes ◽  
High Intensity Interval

Objective The aim of our study was to investigate  the adaptive effect of six sessions of high intensity interval training (HIIT) on changes in the amount and activity of mitochondrial enzymes. Methods Twenty seven students (age 21.2±0.9) were assigned to HIIT (n=10) and control (CON, n=17) group and performed six training sessions for 14 days:  6 × 90 s intervals at 80% maximal aerobic power (MAP) output separated by 180 s rest. Pre and post interventions anthropometric measurements, maximal activity of citrate synthase (CS) and 3-HydroxyacylCoA (HADH) was determined in muscle samples. The effect of HIIT on proteins involved in oxidative phosphorylation (OXPHOS) in the skeletal muscle was used via proteomic analysis’s. We took into consideration 89 identified subunits from the mitochondrial respiratory chain complexes and the ATP synthase complex. For these proteomic tests a muscle biopsy samples from the three representative participants HIIT and three CON before and after training were collected.  Results Training induced the moderate and large effects in maximal enzymes activities CS and HADH. The HIIT caused the increase of level proteins involved in oxidative phosphorylation. Conclusions HIIT can be an optimal strategy for the prevention of certain civilization diseases or for the rehabilitation of diseases, especially cardiovascular disease.

scholarly journals Exercise alters and β-alanine combined with exercise augments histidyl dipeptide levels and scavenges lipid peroxidation products in human skeletal muscle

2018 ◽  
Vol 125 (6) ◽  
pp. 1767-1778 ◽  
Author(s):  
David Hoetker ◽  
Weiliang Chung ◽  
Deqing Zhang ◽  
Jingjing Zhao ◽  
Virginia K. Schmidtke ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Exercise Training ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
Single Session ◽  
Lipid Peroxidation Products ◽  
High Intensity Interval

Carnosine and anserine are dipeptides synthesized from histidine and β-alanine by carnosine synthase (ATPGD1). These dipeptides, present in high concentration in the skeletal muscle, form conjugates with lipid peroxidation products such as 4-hydroxy trans-2-nonenal (HNE). Although skeletal muscle levels of these dipeptides could be elevated by feeding β-alanine, it is unclear how these dipeptides and their conjugates are affected by exercise training with or without β-alanine supplementation. We recruited 20 physically active men, who were allocated to either β-alanine or placebo-feeding group matched for peak oxygen consumption, lactate threshold, and maximal power. Participants completed 2 wk of a conditioning phase followed by 1 wk of exercise training, a single session of high-intensity interval training (HIIT), followed by 6 wk of HIIT. Analysis of muscle biopsies showed that the levels of carnosine and ATPGD1 expression were increased after CPET and decreased following a single session and 6 wk of HIIT. Expression of ATPGD1 and levels of carnosine were increased upon β-alanine-feeding after CPET, whereas ATPGD1 expression decreased following a single session of HIIT. The expression of fiber type markers myosin heavy chain I and IIa remained unchanged after CPET. Levels of carnosine, anserine, carnosine-HNE, carnosine-propanal, and carnosine-propanol were further increased after 9 wk of β-alanine supplementation and exercise training but remained unchanged in the placebo-fed group. These results suggest that carnosine levels and ATPGD1 expression fluctuates with different phases of training. Enhancing carnosine levels by β-alanine feeding could facilitate the detoxification of lipid peroxidation products in the human skeletal muscle.NEW & NOTEWORTHY Carnosine synthase expression and carnosine levels are altered in the human skeletal muscle during different phases of training. During high-intensity interval training, β-alanine feeding promotes detoxification of lipid peroxidation products and increases anserine levels in the skeletal muscle.

scholarly journals Forty high-intensity interval training sessions blunt exercise-induced changes in the nuclear protein content of PGC-1α and p53 in human skeletal muscle

2020 ◽  
Vol 318 (2) ◽  
pp. E224-E236 ◽  
Author(s):  
Cesare Granata ◽  
Rodrigo S. F. Oliveira ◽  
Jonathan P. Little ◽  
David J. Bishop
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Mitochondrial Biogenesis ◽  
Exercise Intensity ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
High Intensity Interval ◽  
Exercise Induced

Exercise-induced increases in peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and p53 protein content in the nucleus mediate the initial phase of exercise-induced mitochondrial biogenesis. Here, we investigated whether exercise-induced increases in these and other markers of mitochondrial biogenesis were altered after 40 sessions of twice-daily high-volume, high-intensity interval training (HVT) in human skeletal muscle. Vastus lateralis muscle biopsies were collected from 10 healthy recreationally active participants before, immediately postexercise, and 3 h after a session of high-intensity interval exercise (HIIE) performed at the same absolute exercise intensity before and after HVT (pre-HVT and post-HVT, respectively). The protein content of common markers of exercise-induced mitochondrial biogenesis was assessed in nuclear- and cytosolic-enriched fractions by immunoblotting; mRNA contents of key transcription factors and mitochondrial genes were assessed by qPCR. Despite exercise-induced increases in PGC-1α, p53, and plant homeodomain finger-containing protein 20 (PHF20) protein content, the phosphorylation of p53 and acetyl-CoA carboxylase (p-p53 Ser15 and p-ACC Ser79, respectively), and PGC-1α mRNA Pre-HVT, no significant changes were observed post-HVT. Forty sessions of twice-daily high-intensity interval training blunted all of the measured exercise-induced molecular events associated with mitochondrial biogenesis that were observed pre-HVT. Future studies should determine whether this loss relates to the decrease in relative exercise intensity, habituation to the same exercise stimulus, or a combination of both.

High-intensity aerobic interval training increases fat and carbohydrate metabolic capacities in human skeletal muscle

2008 ◽  
Vol 33 (6) ◽  
pp. 1112-1123 ◽  
Author(s):  
Christopher G.R. Perry ◽  
George J.F. Heigenhauser ◽  
Arend Bonen ◽  
Lawrence L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
High Intensity ◽  
Citrate Synthase ◽  
Interval Training ◽  
Carbohydrate Oxidation ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Moderate Intensity ◽  
Mitochondrial Enzymes ◽  
Aerobic Interval Training

High-intensity aerobic interval training (HIIT) is a compromise between time-consuming moderate-intensity training and sprint-interval training requiring all-out efforts. However, there are few data regarding the ability of HIIT to increase the capacities of fat and carbohydrate oxidation in skeletal muscle. Using untrained recreationally active individuals, we investigated skeletal muscle and whole-body metabolic adaptations that occurred following 6 weeks of HIIT (~1 h of 10 × 4 min intervals at ~90% of peak oxygen consumption (VO2 peak), separated by 2 min rest, 3 d·week–1). A VO2 peak test, a test to exhaustion (TE) at 90% of pre-training VO2 peak, and a 1 h cycle at 60% of pre-training VO2 peak were performed pre- and post-HIIT. Muscle biopsies were sampled during the TE at rest, after 5 min, and at exhaustion. Training power output increased by 21%, and VO2 peak increased by 9% following HIIT. Muscle adaptations at rest included the following: (i) increased cytochrome c oxidase IV content (18%) and maximal activities of the mitochondrial enzymes citrate synthase (26%), β-hydroxyacyl-CoA dehydrogenase (29%), aspartate-amino transferase (26%), and pyruvate dehydrogenase (PDH; 21%); (ii) increased FAT/CD36, FABPpm, GLUT 4, and MCT 1 and 4 transport proteins (14%–30%); and (iii) increased glycogen content (59%). Major adaptations during exercise included the following: (i) reduced glycogenolysis, lactate accumulation, and substrate phosphorylation (0–5 min of TE); (ii) unchanged PDH activation (carbohydrate oxidation; 0–5 min of TE); (iii) ~2-fold greater time during the TE; and (iv) increased fat oxidation at 60% of pre-training VO2 peak. This study demonstrated that 18 h of repeated high-intensity exercise sessions over 6 weeks (3 d·week–1) is a powerful method to increase whole-body and skeletal muscle capacities to oxidize fat and carbohydrate in previously untrained individuals.

scholarly journals High-Intensity Interval Training Remodels the Proteome and Acetylome of Human Skeletal Muscle

2021 ◽  
Author(s):  
Morten Hostrup ◽  
Anders Krogh Lemminger ◽  
Ben Nicholas Stocks ◽  
Alba Gonzalez-Franquesa ◽  
Jeppe Kjærgaard Larsen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
High Intensity Interval

scholarly journals Treating fructose-induced metabolic changes in mice with high-intensity interval training: insights in the liver, white adipose tissue, and skeletal muscle

2017 ◽  
Vol 123 (4) ◽  
pp. 699-709 ◽  
Author(s):  
Victor F. Motta ◽  
Thereza L. Bargut ◽  
Marcia B. Aguila ◽  
Carlos A. Mandarim-de-Lacerda
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Intensity ◽  
Interval Training ◽  
Peroxisome Proliferator ◽  
High Intensity Interval Training ◽  
Gene Expressions ◽  
Peroxisome Proliferator Activated Receptor ◽  
High Intensity Interval

Fructose-rich caloric sweeteners induce adverse changes in the metabolism of humans. The study evaluated the effects of high-intensity interval training (HIIT) on a fructose feeding model, focusing on the liver, white adipose tissue (WAT), skeletal muscle, and their interplay. Male C57BL/6 mice were fed for 18 wk one of the following diets: control (C; 5% of total energy from fructose) or fructose (F; 55% of total energy from fructose). In the 10th week, for an additional 8-wk period, the groups were divided into nontrained (NT) or HIIT groups, totaling four groups: C-NT, C-HIIT, F-NT, and F-HIIT. At the end of the experiment, fructose consumption in the F-NT group led to a high systolic blood pressure, high plasma triglycerides, insulin resistance with glucose intolerance, and lower insulin sensitivity. We also observed liver steatosis, adipocyte hypertrophy, and diminished gene expressions of peroxisome proliferator-activated receptor-γ coactivator 1-α and fibronectin type III domain containing 5 (FNDC5; irisin) in this F-NT group. These results were accompanied by decreased gene expressions of nuclear respiratory factor 1 and mitochondrial transcription factor A (markers of mitochondrial biogenesis), and peroxisome proliferator-activated receptor-α and carnitine palmitoyltransferase 1 (markers of β-oxidation). HIIT improved all of these data in the C-HIIT and F-HIIT groups. In conclusion, in mice fed a fructose diet, HIIT improved body mass, blood pressure, glucose metabolism, and plasma triglycerides. Liver, WAT, and skeletal muscle were positively modulated by HIIT, indicating HIIT as a coadjutant treatment for diseases affecting these tissues. NEW & NOTEWORTHY We investigated the effects of high-intensity interval training (HIIT) in mice fed a fructose-rich diet and the resulting severe negative effect on the liver, white adipose tissue (WAT), and skeletal muscle, which reduced the expression of fibronectin type III domain containing 5 (FNDC5, irisin) and PGC1α and, consequently, affected markers of mitochondrial biogenesis and β-oxidation. Because HIIT may block these adverse effects in all of these three tissues, it might be suggested that it functions as a coadjutant treatment in combatting the alterations caused by high-fructose intake.

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