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

2010 ◽  
Vol 588 (6) ◽  
pp. 1011-1022 ◽  
Author(s):  
Jonathan P. Little ◽  
Adeel Safdar ◽  
Geoffrey P. Wilkin ◽  
Mark A. Tarnopolsky ◽  
Martin J. Gibala
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
Practical Model ◽  
Low Volume ◽  
High Intensity Interval ◽  
Muscle Potential

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 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 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.

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

2021 ◽  
Author(s):  
M Hostrup ◽  
AK Lemminger ◽  
B Stocks ◽  
A Gonzalez-Franquesa ◽  
JK Larsen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Metabolic Diseases ◽  
Interval Training ◽  
Calcium Sensitivity ◽  
High Intensity Interval Training ◽  
Post Translational Modifications ◽  
Muscle Proteome ◽  
High Intensity Interval

AbstractExercise is an effective strategy in the prevention and treatment of metabolic diseases. Alterations in the skeletal muscle proteome, including post-translational modifications, regulate its metabolic adaptations to exercise. Here, we examined the effect of high-intensity interval training (HIIT) on the proteome and acetylome of human skeletal muscle, revealing the response of 3168 proteins and 1263 lysine acetyl-sites on 464 acetylated proteins. We identified global protein adaptations to exercise training involved in metabolism, excitation-contraction coupling, and myofibrillar calcium sensitivity. Furthermore, HIIT increased the acetylation of mitochondrial proteins, particularly those of complex V, likely via non-enzymatic mechanisms. We also highlight the regulation of exercise-responsive histone acetyl-sites. These data demonstrate the plasticity of the skeletal muscle proteome and acetylome, providing insight into the regulation of contractile, metabolic and transcriptional processes within skeletal muscle. Herein, we provide a substantial hypothesis-generating resource to stimulate further mechanistic research investigating how exercise improves metabolic health.

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