Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women

2007 ◽  
Vol 102 (4) ◽  
pp. 1439-1447 ◽  
Author(s):  
Jason L. Talanian ◽  
Stuart D. R. Galloway ◽  
George J. F. Heigenhauser ◽  
Arend Bonen ◽  
Lawrence L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Protein Content ◽  
High Intensity ◽  
Interval Training ◽  
Cardiovascular Responses ◽  
Fat Oxidation ◽  
Whole Body ◽  
Aerobic Interval Training ◽  
Before And After

Our aim was to examine the effects of seven high-intensity aerobic interval training (HIIT) sessions over 2 wk on skeletal muscle fuel content, mitochondrial enzyme activities, fatty acid transport proteins, peak O2 consumption (V̇o2 peak), and whole body metabolic, hormonal, and cardiovascular responses to exercise. Eight women (22.1 ± 0.2 yr old, 65.0 ± 2.2 kg body wt, 2.36 ± 0.24 l/min V̇o2 peak) performed a V̇o2 peak test and a 60-min cycling trial at ∼60% V̇o2 peak before and after training. Each session consisted of ten 4-min bouts at ∼90% V̇o2 peak with 2 min of rest between intervals. Training increased V̇o2 peak by 13%. After HIIT, plasma epinephrine and heart rate were lower during the final 30 min of the 60-min cycling trial at ∼60% pretraining V̇o2 peak. Exercise whole body fat oxidation increased by 36% (from 15.0 ± 2.4 to 20.4 ± 2.5 g) after HIIT. Resting muscle glycogen and triacylglycerol contents were unaffected by HIIT, but net glycogen use was reduced during the posttraining 60-min cycling trial. HIIT significantly increased muscle mitochondrial β-hydroxyacyl-CoA dehydrogenase (15.44 ± 1.57 and 20.35 ± 1.40 mmol·min−1·kg wet mass−1 before and after training, respectively) and citrate synthase (24.45 ± 1.89 and 29.31 ± 1.64 mmol·min−1·kg wet mass−1 before and after training, respectively) maximal activities by 32% and 20%, while cytoplasmic hormone-sensitive lipase protein content was not significantly increased. Total muscle plasma membrane fatty acid-binding protein content increased significantly (25%), whereas fatty acid translocase/CD36 content was unaffected after HIIT. In summary, seven sessions of HIIT over 2 wk induced marked increases in whole body and skeletal muscle capacity for fatty acid oxidation during exercise in moderately active women.

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.

Reduced plasma FFA availability increases net triacylglycerol degradation, but not GPAT or HSL activity, in human skeletal muscle

2004 ◽  
Vol 287 (1) ◽  
pp. E120-E127 ◽  
Author(s):  
Matthew J. Watt ◽  
Anna G. Holmes ◽  
Gregory R. Steinberg ◽  
Jose L. Mesa ◽  
Bruce E. Kemp ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Body Fat ◽  
Plasma Free Fatty Acid ◽  
Fat Oxidation ◽  
Dry Mass ◽  
Hormone Sensitive Lipase ◽  
Whole Body ◽  
Plasma Ffa

Intramuscular triacylglycerols (IMTG) are proposed to be an important metabolic substrate for contracting muscle, although this remains controversial. To test the hypothesis that reduced plasma free fatty acid (FFA) availability would increase IMTG degradation during exercise, seven active men cycled for 180 min at 60% peak pulmonary O2 uptake either without (CON) or with (NA) prior ingestion of nicotinic acid to suppress adipose tissue lipolysis. Skeletal muscle and adipose tissue biopsy samples were obtained before and at 90 and 180 min of exercise. NA ingestion decreased ( P < 0.05) plasma FFA at rest and completely suppressed the exercise-induced increase in plasma FFA (180 min: CON, 1.42 ± 0.07; NA, 0.10 ± 0.01 mM). The decreased plasma FFA during NA was associated with decreased ( P < 0.05) adipose tissue hormone-sensitive lipase (HSL) activity (CON: 13.9 ± 2.5, NA: 9.1 ± 3.0 nmol·min−1·mg protein−1). NA ingestion resulted in decreased whole body fat oxidation and increased carbohydrate oxidation. Despite the decreased whole body fat oxidation, net IMTG degradation was greater in NA compared with CON (net change: CON, 2.3 ± 0.8; NA, 6.3 ± 1.2 mmol/kg dry mass). The increased IMTG degradation did not appear to be due to reduced fatty acid esterification, because glycerol 3-phosphate activity was not different between trials and was unaffected by exercise (rest: 0.21 ± 0.07; 180 min: 0.17 ± 0.04 nmol·min−1·mg protein−1). HSL activity was not increased from resting rates during exercise in either trial despite elevated plasma epinephrine, decreased plasma insulin, and increased ERK1/2 phosphorylation. AMP-activated protein kinase (AMPK)α1 activity was not affected by exercise or NA, whereas AMPKα2 activity was increased ( P < 0.05) from rest during exercise in NA and was greater ( P < 0.05) than in CON at 180 min. These data suggest that plasma FFA availability is an important mediator of net IMTG degradation, and in the absence of plasma FFA, IMTG degradation cannot maintain total fat oxidation. These changes in IMTG degradation appear to disassociate, however, from the activity of the key enzymes responsible for synthesis and degradation of this substrate.

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.

High-intensity interval training increases intrinsic rates of mitochondrial fatty acid oxidation in rat red and white skeletal muscle

2013 ◽  
Vol 38 (3) ◽  
pp. 326-333 ◽  
Author(s):  
Daisuke Hoshino ◽  
Yuko Yoshida ◽  
Yu Kitaoka ◽  
Hideo Hatta ◽  
Arend Bonen
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
High Intensity ◽  
Interval Training ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Mitochondrial Fatty Acid ◽  
Mitochondrial Volume ◽  
High Intensity Interval

High-intensity interval training (HIIT) can increase mitochondrial volume in skeletal muscle. However, it is unclear whether HIIT alters the intrinsic capacity of mitochondrial fatty acid oxidation, or whether such changes are associated with changes in mitochondrial FAT/CD36, a regulator of fatty acid oxidation, or with reciprocal changes in the nuclear receptor coactivator (peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1α)) and the corepressor (receptor-interacting protein 140 (RIP140)). We examined whether HIIT alters fatty acid oxidation rates in the isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria of red and white skeletal muscle and (or) induces changes in muscle PGC-1α and RIP140 proteins and mitochondrial FAT/CD36 protein content. Rats were divided into untrained or HIIT-trained groups. HIIT animals performed 10 bouts of 1-min high-intensity treadmill running (30–55 m·min–1), separated by 2 min of rest, for 5 days a week for 4 weeks. As expected, after the training period, HIIT increased mitochondrial enzymes (citrate synthase, COXIV, and β-hydroxyacyl CoA dehydrogenase) in red and white muscle, indicating that muscle mitochondrial volume had increased. HIIT also increased the rates of palmitate oxidation in mitochondria of red (37% for SS and 19% for IMF) and white (36% for SS and 12% for IMF) muscle. No changes occurred in SS and IMF mitochondrial FAT/CD36 proteins, despite increasing FAT/CD36 at the whole-muscle level (27% for red and 22% for white). Concurrently, muscle PGC-1α protein was increased in red (22%) and white (16%) muscle, but RIP140 was not altered. These results indicate that increases in SS and IMF mitochondrial fatty acid oxidation induced by HIIT are accompanied by an increase in PGC-1α, but not RIP140 or FAT/CD36.

Divergent response of metabolite transport proteins in human skeletal muscle after sprint interval training and detraining

2007 ◽  
Vol 292 (5) ◽  
pp. R1970-R1976 ◽  
Author(s):  
Kirsten A. Burgomaster ◽  
Naomi M. Cermak ◽  
Stuart M. Phillips ◽  
Carley R. Benton ◽  
Arend Bonen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
High Intensity ◽  
Interval Training ◽  
Oxidative Capacity ◽  
Transport Proteins ◽  
High Intensity Exercise ◽  
Fatty Acid Transport ◽  
Sprint Interval Training ◽  
Muscle Oxidative Capacity

Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22 ± 1 yr; peak oxygen uptake = 50 ± 2 ml·kg−1·min−1) performed 4–6 × 30 s all-out cycling efforts with 4-min recovery, 3 days/wk for 6 wk. Needle muscle biopsy samples (vastus lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT, and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by ∼35% after 1 wk of SIT and remained higher compared with Pre, even after 6 wk of detraining ( P < 0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained ∼20% higher compared with baseline during detraining ( P < 0.05). The monocarboxylate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared with Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining ( P < 0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) ( P > 0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate, and fatty acid transport.

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.

Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration

2006 ◽  
Vol 290 (2) ◽  
pp. E380-E388 ◽  
Author(s):  
Trent Stellingwerff ◽  
Lawrence L. Spriet ◽  
Matthew J. Watt ◽  
Nicholas E. Kimber ◽  
Mark Hargreaves ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Total Energy ◽  
Random Order ◽  
Fat Oxidation ◽  
Whole Body ◽  
Peak Power Output ◽  
High Fat ◽  
Regulatory Enzymes ◽  
Before And After ◽  
Experimental Trials

Five days of a high-fat diet while training, followed by 1 day of carbohydrate (CHO) restoration, increases rates of whole body fat oxidation and decreases CHO oxidation during aerobic cycling. The mechanisms responsible for these shifts in fuel oxidation are unknown but involve up- and downregulation of key regulatory enzymes in the pathways of skeletal muscle fat and CHO metabolism, respectively. This study measured muscle PDH and HSL activities before and after 20 min of cycling at 70% V̇o2 peak and 1 min of sprinting at 150% peak power output (PPO). Estimations of muscle glycogenolysis were made during the initial minute of exercise at 70% V̇o2 peak and during the 1-min sprint. Seven male cyclists undertook this exercise protocol on two occasions. For 5 days, subjects consumed in random order either a high-CHO (HCHO) diet (10.3 g·kg−1·day−1 CHO, or ∼70% of total energy intake) or an isoenergetic high-fat (FAT-adapt) diet (4.6 g·kg−1·day−1 FAT, or 67% of total energy) while undertaking supervised aerobic endurance training. On day 6 for both treatments, subjects ingested an HCHO diet and rested before their experimental trials on day 7. This CHO restoration resulted in similar resting glycogen contents (FAT-adapt 873 ± 121 vs. HCHO 868 ± 120 μmol glucosyl units/g dry wt). However, the respiratory exchange ratio was lower during cycling at 70% V̇o2 peak in the FAT-adapt trial, which resulted in an ∼45% increase and an ∼30% decrease in fat and CHO oxidation, respectively. PDH activity was lower at rest and throughout exercise at 70% V̇o2 peak (1.69 ± 0.25 vs. 2.39 ± 0.19 mmol·kg wet wt−1·min−1) and the 1-min sprint in the FAT-adapt vs. the HCHO trial. Estimates of glycogenolysis during the 1st min of exercise at 70% V̇o2 peak and the 1-min sprint were also lower after FAT-adapt (9.1 ± 1.1 vs. 13.4 ± 2.1 and 37.3 ± 5.1 vs. 50.5 ± 2.7 glucosyl units·kg dry wt−1·min−1). HSL activity was ∼20% higher ( P = 0.12) during exercise at 70% V̇o2 peak after FAT-adapt. Results indicate that previously reported decreases in whole body CHO oxidation and increases in fat oxidation after the FAT-adapt protocol are a function of metabolic changes within skeletal muscle. The metabolic signals responsible for the shift in muscle substrate use during cycling at 70% V̇o2 peak remain unclear, but lower accumulation of free ADP and AMP after the FAT-adapt trial may be responsible for the decreased glycogenolysis and PDH activation during sprinting.

scholarly journals Mice with Whole-Body Disruption of AMPK-Glycogen Binding Have Increased Adiposity, Reduced Fat Oxidation and Altered Tissue Glycogen Dynamics

2021 ◽  
Vol 22 (17) ◽  
pp. 9616
Author(s):  
Natalie R. Janzen ◽  
Jamie Whitfield ◽  
Lisa Murray-Segal ◽  
Bruce E. Kemp ◽  
John A. Hawley ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Fat Oxidation ◽  
Liver Glycogen ◽  
Whole Body ◽  
Fed State ◽  
Reduced Fat ◽  
Insulin Tolerance ◽  
Serum Hormone ◽  
Whole Body Metabolism

The AMP-activated protein kinase (AMPK), a central regulator of cellular energy balance and metabolism, binds glycogen via its β subunit. However, the physiological effects of disrupting AMPK-glycogen interactions remain incompletely understood. To chronically disrupt AMPK-glycogen binding, AMPK β double knock-in (DKI) mice were generated with mutations in residues critical for glycogen binding in both the β1 (W100A) and β2 (W98A) subunit isoforms. We examined the effects of this DKI mutation on whole-body substrate utilization, glucose homeostasis, and tissue glycogen dynamics. Body composition, metabolic caging, glucose and insulin tolerance, serum hormone and lipid profiles, and tissue glycogen and protein content were analyzed in chow-fed male DKI and age-matched wild-type (WT) mice. DKI mice displayed increased whole-body fat mass and glucose intolerance associated with reduced fat oxidation relative to WT. DKI mice had reduced liver glycogen content in the fed state concomitant with increased utilization and no repletion of skeletal muscle glycogen in response to fasting and refeeding, respectively, despite similar glycogen-associated protein content relative to WT. DKI liver and skeletal muscle displayed reductions in AMPK protein content versus WT. These findings identify phenotypic effects of the AMPK DKI mutation on whole-body metabolism and tissue AMPK content and glycogen dynamics.

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