Skeletal Muscle Metabolic Adaptations in Response to 6 Weeks of High-Intensity Interval Training

2006 ◽  
Vol 38 (Suppl 1) ◽  
pp. S25
Author(s):  
Christopher G.R. Perry ◽  
Jason L. Talanian ◽  
George J.F. Heigenhauser ◽  
Lawrence L. Spriet
2020 ◽  
Vol 105 (8) ◽  
pp. e2941-e2959 ◽  
Author(s):  
Benjamin J Ryan ◽  
Michael W Schleh ◽  
Cheehoon Ahn ◽  
Alison C Ludzki ◽  
Jenna B Gillen ◽  
...  

Abstract Objective We compared the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on insulin sensitivity and other important metabolic adaptations in adults with obesity. Methods Thirty-one inactive adults with obesity (age: 31 ± 6 years; body mass index: 33 ± 3 kg/m2) completed 12 weeks (4 sessions/week) of either HIIT (10 × 1-minute at 90%HRmax, 1-minute active recovery; n = 16) or MICT (45 minutes at 70%HRmax; n = 15). To assess the direct effects of exercise independent of weight/fat loss, participants were required to maintain body mass. Results Training increased peak oxygen uptake by ~10% in both HIIT and MICT (P < 0.0001), and body weight/fat mass were unchanged. Peripheral insulin sensitivity (hyperinsulinemic-euglycemic clamp) was ~20% greater the day after the final exercise session compared to pretraining (P < 0.01), with no difference between HIIT and MICT. When trained participants abstained from exercise for 4 days, insulin sensitivity returned to pretraining levels in both groups. HIIT and MICT also induced similar increases in abundance of many skeletal muscle proteins involved in mitochondrial respiration and lipid and carbohydrate metabolism. Training-induced alterations in muscle lipid profile were also similar between groups. Conclusion Despite large differences in training intensity and exercise time, 12 weeks of HIIT and MICT induce similar acute improvements in peripheral insulin sensitivity the day after exercise, and similar longer term metabolic adaptations in skeletal muscle in adults with obesity. These findings support the notion that the insulin-sensitizing effects of both HIIT and MICT are mediated by factors stemming from the most recent exercise session(s) rather than adaptations that accrue with training.


2018 ◽  
Vol 9 ◽  
Author(s):  
Mariana Aguiar de Matos ◽  
Dênia Vargas Vieira ◽  
Kaio Cesar Pinhal ◽  
Jennifer Freitas Lopes ◽  
Marco Fabrício Dias-Peixoto ◽  
...  

2019 ◽  
Vol 226 (2) ◽  
pp. e13245 ◽  
Author(s):  
Flemming Dela ◽  
Arthur Ingersen ◽  
Nynne B. Andersen ◽  
Maria B. Nielsen ◽  
Helga H. H. Petersen ◽  
...  

2019 ◽  
Vol 1 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Ferenc Torma ◽  
Zoltan Gombos ◽  
Matyas Jokai ◽  
Masaki Takeda ◽  
Tatsuya Mimura ◽  
...  

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

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.


2011 ◽  
Vol 300 (6) ◽  
pp. R1303-R1310 ◽  
Author(s):  
Jonathan P. Little ◽  
Adeel Safdar ◽  
David Bishop ◽  
Mark A. Tarnopolsky ◽  
Martin J. Gibala

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.


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