scholarly journals High-Intensity Interval Training Improves Markers of Oxidative Metabolism in Skeletal Muscle of Individuals With Obesity and Insulin Resistance

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 ◽  
...  

Author(s):  
Sajad Ahmadizad ◽  
Alireza Salimi Avansar ◽  
Khosrow Ebrahim ◽  
Mohsen Avandi ◽  
Mansour Ghasemikaram

AbstractExercise training is an effective method of weight management, and knowing about its influence on the hormones involved in the regulation of food intake and inflammation could be useful for body weight management. Therefore, the purpose of this study was to compare the effects of 6 weeks of high-intensity interval training (HIIT) and moderate-intensity continuous exercise training (MCT) on nesfatin-1, interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α).Thirty sedentary overweight men (Mean±SD; age, 25±1 years) were divided into three (n=10) body mass index-matched groups. The participants in the training groups performed either HIIT or MCT protocols 3 days per week for 6 weeks followed by a week of detraining.Plasma IL-6 and TNF-α did not significantly change after training, but nesfatin increased significantly only with HIIT compared with the control group (p<0.05). In addition, fasting glucose, insulin, and homeostasis model estimated insulin resistance (HOMA-IR), decreased significantly following both HIIT and MCT training (p<0.05). After a detraining period, the plasma nesfatin-1 did not return to pre-training levels in the HIIT group.Both the HIIT and MCT groups had similar effects on inflammatory markers and insulin resistance in men who are overweight, but the HIIT seems to have better anorectic effects (as indicated by nesfatin) compared with MCT.


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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