Acute and Chronic Effects of High-Intensity Interval Training (HIIT) on Postexercise Intramuscular Lipid Metabolism in Rats

Recovery from exercise refers to the period between the end of a bout of exercise and the subsequent return to a resting or recovered state. It is a dynamic period in which many physiological changes occur. A large amount of research has evaluated the effect of training on intramuscular lipid metabolism. However, data are limited regarding intramuscular lipid metabolism during the recovery period. In this study, lipid metabolism-related proteins were examined after a single bout of exercise in a time-dependent way to explore the mechanism of how exercise induces intramuscular lipid metabolism adaptation. Firstly, all rats in the exercise group underwent a five-week training protocol (HIIT, five times/week), and then performed a more intense HIIT session after 72 h of the last-time five-week training. After that, rats were sampled in a time-dependent way, including 0 h, 6 h, 12 h, 24 h, 48 h, 72 h, and 96 h following the acute training session. Our results discovered that five weeks of HIIT increased the content of intramuscular triglyceride (IMTG) and enhanced the lipolytic and lipogenesis-related proteins in skeletal muscle. Furthermore, IMTG content decreased immediately post HIIT and gradually increased to baseline levels 48 h postexercise, continuing to over-recover up to 96 h postexercise. Following acute exercise, lipolytic-related proteins showed an initial increase (6-12 h) before decreasing during recovery. Conversely, lipogenesis-related proteins decreased following exercise (6-12 h), then increased in the recovery period. Based on the changes, we speculate that skeletal muscle is predominated by lipid oxidative at the first 12 h postexercise. After this period, lipid synthesis-related proteins increased, which may be the result of body recovery. Together, these results may provide insight into how the lipid metabolism-related signaling changes after chronic and acute HIIT and how protein levels lipid metabolism correlates to IMTG recovery.

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Effects of epinephrine on lipid metabolism in resting skeletal muscle

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1998.275.2.e300 ◽

1998 ◽

Vol 275 (2) ◽

pp. E300-E309 ◽

Cited By ~ 27

Author(s):

Sandra J. Peters ◽

David J. Dyck ◽

Arend Bonen ◽

Lawrence L. Spriet

Keyword(s):

Skeletal Muscle ◽

Lipid Metabolism ◽

Lipid Synthesis ◽

Hormone Sensitive Lipase ◽

Simultaneous Estimation ◽

Lipid Hydrolysis ◽

Muscle Lipid ◽

Triacylglycerol Hydrolysis ◽

Skeletal Muscle Lipid ◽

Glycogen Breakdown

The effects of physiological (0, 0.1, 2.5, and 10 nM) and pharmacological (200 nM) epinephrine concentrations on resting skeletal muscle lipid metabolism were investigated with the use of incubated rat epitrochlearis (EPT), flexor digitorum brevis (FDB), and soleus (SOL) muscles. Muscles were chosen to reflect a range of oxidative capacities: SOL > EPT > FDB. The muscles were pulsed with [1-14C]palmitate and chased with [9,10-3H]palmitate. Incorporation and loss of the labeled palmitate from the triacylglycerol pool (as well as mono- and diacylglycerol, phospholipid, and fatty acid pools) permitted the simultaneous estimation of lipid hydrolysis and synthesis. Endogenous and exogenous fat oxidation was quantified by14CO2and3H2O production, respectively. Triacylglycerol breakdown was elevated above control at all epinephrine concentrations in the oxidative SOL muscle, at 2.5 and 200 nM (at 10 nM, P= 0.066) in the FDB, and only at 200 nM epinephrine in the EPT. Epinephrine stimulated glycogen breakdown in the EPT at all concentrations but only at 10 and 200 nM in the FDB and had no effect in the SOL. We further characterized muscle lipid hydrolysis potential and measured total hormone-sensitive lipase content by Western blotting (SOL > FDB > EPT). This study demonstrated that physiological levels of epinephrine cause measurable increases in triacylglycerol hydrolysis at rest in oxidative but not in glycolytic muscle, with no change in the rate of lipid synthesis or oxidation. Furthermore, epinephrine caused differential stimulation of carbohydrate and fat metabolism in glycolytic vs. oxidative muscle. Epinephrine preferentially stimulated glycogen breakdown over triacylglycerol hydrolysis in the glycolytic EPT muscle. Conversely, in the oxidative SOL muscle, epinephrine caused an increase in endogenous lipid hydrolysis over glycogen breakdown.

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Acute Exercise Induced Mitochondrial H2O2Production in Mouse Skeletal Muscle: Association with p66Shcand FOXO3a Signaling and Antioxidant Enzymes

Oxidative Medicine and Cellular Longevity ◽

10.1155/2015/536456 ◽

2015 ◽

Vol 2015 ◽

pp. 1-10 ◽

Cited By ~ 11

Author(s):

Ping Wang ◽

Chun Guang Li ◽

Zhengtang Qi ◽

Di Cui ◽

Shuzhe Ding

Keyword(s):

Skeletal Muscle ◽

Antioxidant Enzymes ◽

Acute Exercise ◽

Exercise Group ◽

Time Dependent ◽

Dependent Manner ◽

Complex Interplay ◽

Muscle Tissues ◽

Exercise Muscle ◽

Exercise Induced

Exercise induced skeletal muscle phenotype change involves a complex interplay between signaling pathways and downstream regulators. This study aims to investigate the effect of acute exercise on mitochondrial H2O2production and its association withp66Shc, FOXO3a, and antioxidant enzymes. Male ICR/CD-1 mice were subjected to an acute exercise. Muscle tissues (gastrocnemius and quadriceps femoris) were taken after exercise to measure mitochondrial H2O2content, expression ofp66Shcand FOXO3a, and the activity of antioxidant enzymes. The results showed that acute exercise significantly increased mitochondrial H2O2content and expressions ofp66Shcand FOXO3a in a time-dependent manner, with a linear correlation between the increase in H2O2content andp66Shcor FOXO3a expression. The activity of mitochondrial catalase was slightly reduced in the 90 min exercise group, but it was significantly higher in groups with 120 and 150 min exercise compared to that of 90 min exercise group. The activity of SOD was not significantly affected. The results indicate that acute exercise increases mitochondrial H2O2production in the skeletal muscle, which is associated with the upregulation ofp66Shcand FOXO3a. The association ofp66Shcand FOXO3a signaling with exercise induced H2O2generation may play a role in regulating cellular oxidative stress during acute exercise.

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Rat skeletal muscle hexokinase II mRNA and activity are increased by a single bout of acute exercise

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1994.266.2.e171 ◽

1994 ◽

Vol 266 (2) ◽

pp. E171-E178 ◽

Cited By ~ 24

Author(s):

R. M. O'Doherty ◽

D. P. Bracy ◽

H. Osawa ◽

D. H. Wasserman ◽

D. K. Granner

Keyword(s):

Skeletal Muscle ◽

Acute Exercise ◽

Recovery Period ◽

Exhaustive Exercise ◽

Male Rats ◽

Hexokinase Ii ◽

Glut 4 ◽

Heat Stable ◽

Single Bout

This study addresses the potential role of skeletal muscle hexokinase (HK) II in the regulation of glucose uptake and metabolism in vivo. Male rats undertook a single bout of treadmill exercise and were then killed immediately or after a predetermined recovery period. Three muscles [soleus (Sol), gastrocnemius/plantaris (Gc), and white vastus] were excised, and HK II mRNA, GLUT-4 mRNA, total HK (HK I and HK II) and heat-stable HK (predominantly HK I) activities were assessed. Three hours after the cessation of a single bout of exhaustive exercise, HK II mRNA was significantly increased in all three muscles. Ninety or thirty minutes of exercise, with a 3-h recovery, increased Gc HK II mRNA to the same extent as exhaustive exercise, but 15 min of exercise had no effect. Gc HK II mRNA continued to increase up to 8 h after the cessation of 90 min of exercise but returned to basal by 24 h postexercise. In contrast to HK II mRNA, Gc GLUT-4 mRNA was unchanged at 0, 3, 8, and 24 h after the cessation of 90 min of exercise. Total HK activity was significantly increased in Sol and Gc, 8 and 24 h after the cessation of 90 min of exercise. Heat-stable HK activity was unchanged in all three muscles. The increase in total HK activity, inferred to be an increase of HK II, may be important in the persistence of the postexercise increase in insulin action.

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Improved skeletal muscle Ca2+ regulation in vivo following contractions in mice overexpressing PGC-1α

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00032.2017 ◽

2017 ◽

Vol 312 (6) ◽

pp. R1017-R1028 ◽

Cited By ~ 11

Author(s):

Hiroaki Eshima ◽

Shinji Miura ◽

Nanami Senoo ◽

Koji Hatakeyama ◽

David C. Poole ◽

...

Keyword(s):

Skeletal Muscle ◽

Tibialis Anterior Muscle ◽

Recovery Period ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Protein Levels ◽

S 100 ◽

Intracellular Ca ◽

Related Proteins

In skeletal muscle, resting intracellular Ca2+ concentration ([Ca2+]i) homeostasis is exquisitely regulated by Ca2+ transport across the sarcolemmal, mitochondrial, and sarcoplasmic reticulum (SR) membranes. Of these three systems, the relative importance of the mitochondria in [Ca2+]i regulation remains poorly understood in in vivo skeletal muscle. We tested the hypothesis that the capacity for Ca2+ uptake by mitochondria is a primary factor in determining [Ca2+]i regulation in muscle at rest and following contractions. Tibialis anterior muscle of anesthetized peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α)-overexpressing (OE, increased mitochondria model) and wild-type (WT) littermate mice was exteriorized in vivo and loaded with the fluorescent probe fura 2-AM, and Rhod 2-AM Ca2+ buffering and mitochondrial [Ca2+] were evaluated at rest and during recovery from fatiguing tetanic contractions induced by electrical stimulation (120 s, 100 Hz). In addition, the effects of pharmacological inhibition of SR (thapsigargin) and mitochondrial [carbonyl cyanide- 4-(trifluoromethoxy) phenylhydrazone (FCCP)] function were examined at rest. [Ca2+]i in WT remained elevated for the entire postcontraction recovery period (+6 ± 1% at 450 s), but in PGC-1α OE [Ca2+]i returned to resting baseline within 150 s. Thapsigargin immediately and substantially increased resting [Ca2+]i in WT, whereas in PGC-1α OE this effect was delayed and markedly diminished (WT, +12 ± 3; PGC-1α OE, +1 ± 2% at 600 s after thapsigargin treatment, P < 0.05). FCCP abolished this improvement of [Ca2+]i regulation in PGC-1α OE. Mitochondrial [Ca2+] accumulation was observed in PGC-1α OE following contractions and thapsigargin treatment. In the SR, PGC-1α OE downregulated SR Ca2+-ATPase 1 (Ca2+ uptake) and parvalbumin (Ca2+ buffering) protein levels, whereas mitochondrial Ca2+ uptake-related proteins (Mfn1, Mfn2, and mitochondrial Ca2+ uniporter) were upregulated. These data demonstrate a heretofore unappreciated role for skeletal muscle mitochondria in [Ca2+]i regulation in vivo following fatiguing tetanic contractions and at rest.

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Salvia hispanica L. (chia) seed improves skeletal muscle lipotoxicity and insulin sensitivity in rats fed a sucrose-rich diet by modulating intramuscular lipid metabolism

Journal of Functional Foods ◽

10.1016/j.jff.2019.103775 ◽

2020 ◽

Vol 66 ◽

pp. 103775 ◽

Cited By ~ 1

Author(s):

María del Rosario Ferreira ◽

María Eugenia Oliva ◽

Victoria Aiassa ◽

María Eugenia D'Alessandro

Keyword(s):

Skeletal Muscle ◽

Lipid Metabolism ◽

Insulin Sensitivity ◽

Salvia Hispanica ◽

Chia Seed ◽

Intramuscular Lipid ◽

Salvia Hispanica L

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Effect of contractile activity on PGC-1α transcription in young and aged skeletal muscle

Journal of Applied Physiology ◽

10.1152/japplphysiol.01110.2017 ◽

2018 ◽

Vol 124 (6) ◽

pp. 1605-1615 ◽

Cited By ~ 10

Author(s):

Heather N. Carter ◽

Marion Pauly ◽

Liam D. Tryon ◽

David A. Hood

Keyword(s):

Skeletal Muscle ◽

Dna Methylation ◽

Transcription Factor ◽

Mitochondrial Biogenesis ◽

Acute Exercise ◽

Contractile Activity ◽

Expression Patterns ◽

Recovery Period ◽

Peroxisome Proliferator ◽

Altered Expression

Mitochondrial impairments are often noted in aged skeletal muscle. The transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is integral to maintaining mitochondria, and its expression declines in aged muscle. It remains unknown whether this is due to a transcriptional deficit during aging. Our study examined PGC-1α transcription in muscle from young and old F344BN rats. Using a rat PGC-1α promoter-reporter construct, we found that PGC-1α transcription was reduced by ∼65% in aged TA muscle, accompanied by decreases in PGC-1α mRNA and transcript stability. Altered expression patterns in PGC-1α transcription regulatory factors, including nuclear respiratory factor 2, upstream transcription factor 1, activating transcription factor 2, and yin yang 1, were noted in aged muscle. Acute contractile activity (CA) followed by recovery was employed to examine whether PGC-1α transcription could be activated in aged muscle similar to that observed in young muscle. AMPK and p38 signaling was attenuated in aged muscle. CA evoked an upregulation of PGC-1α transcription in both young and aged groups, whereas mRNAs encoding PGC-1α and cytochrome oxidase subunit IV were induced during the recovery period. Global DNA methylation, an inhibitory event for transcription, was enhanced in aged muscle, likely a result of elevated methyltransferase enzyme Dnmt3b in aged muscle. Successive bouts of CA for 7 days to evaluate longer-term consequences resulted in a rescue of PGC-1α and downstream mRNAs in aged muscle. Our data indicate that diminished mitochondria in aged muscle is due partly to a deficit in PGC-1α transcription, a result of attenuated upstream signaling. Contractile activity is an appropriate countermeasure to restore PGC-1α expression and mitochondrial content in aged muscle. NEW & NOTEWORTHY PGC-1α is a regulator of mitochondrial biogenesis in muscle. We demonstrate that PGC-1α expression is reduced in aging muscle due to decreases in transcriptional and posttranscriptional mechanisms. The transcriptional deficit is due to alterations in transcription factor expression, reduced signaling, and DNA methylation. Acute exercise can initiate signaling to reverse the transcriptional defect, restoring PGC-1α expression toward young values, suggesting a mechanism whereby aged muscle can respond to exercise for the promotion of mitochondrial biogenesis.

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Increased intramuscular lipid synthesis and low saturation relate to insulin sensitivity in endurance-trained athletes

Journal of Applied Physiology ◽

10.1152/japplphysiol.00684.2009 ◽

2010 ◽

Vol 108 (5) ◽

pp. 1134-1141 ◽

Cited By ~ 65

Author(s):

Bryan C. Bergman ◽

Leigh Perreault ◽

Devon M. Hunerdosse ◽

Mary C. Koehler ◽

Ali M. Samek ◽

...

Keyword(s):

Insulin Resistance ◽

Skeletal Muscle ◽

Insulin Action ◽

Lipid Synthesis ◽

Tolerance Test ◽

Intravenous Glucose Tolerance Test ◽

Synthesis Rate ◽

Dietary Control ◽

Intravenous Glucose ◽

Intramuscular Lipid

Intramuscular triglyceride (IMTG) has received considerable attention as a potential mechanism promoting insulin resistance. Endurance-trained athletes have high amounts of IMTG but are insulin sensitive, suggesting IMTG content alone does not change insulin action. Recent data suggest increased muscle lipid synthesis protects against fat-induced insulin resistance. We hypothesized that rates of IMTG synthesis at rest would be increased in athletes compared with controls. Eleven sedentary men and 11 endurance-trained male cyclists participated in this study. An intravenous glucose tolerance test was performed to assess insulin action. After 3 days of dietary control and an overnight fast, [13C16]palmitate was infused at 0.0174 μmol·kg−1·min−1 for 4 h, followed by a muscle biopsy to measure isotope incorporation into IMTG and diacylglycerol. Compared with controls, athletes were twice as insulin sensitive ( P = 0.004) and had a significantly greater resting IMTG concentration (athletes: 20.4 ± 1.6 μg IMTG/mg dry wt, controls: 14.5 ± 1.8 μg IMTG/mg dry wt, P = 0.04) and IMTG fractional synthesis rate (athletes: 1.56 ± 0.37%/h, controls: 0.61 ± 0.15%/h, P = 0.03). Stearoyl-CoA desaturase 1 mRNA expression ( P = 0.02) and protein content ( P = 0.03) were also significantly greater in athletes. Diacylglycerol, but not IMTG, saturation was significantly less in athletes compared with controls ( P = 0.002). These data indicate endurance-trained athletes have increased synthesis rates of skeletal muscle IMTG and decreased saturation of skeletal muscle diacylglycerol. Increased synthesis rates are not due to recovery from exercise and are likely adaptations to chronic endurance exercise training.

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Exercise induces a transient increase in transcription of the GLUT-4 gene in skeletal muscle

AJP Cell Physiology ◽

10.1152/ajpcell.1993.265.6.c1597 ◽

1993 ◽

Vol 265 (6) ◽

pp. C1597-C1603 ◽

Cited By ~ 128

Author(s):

P. D. Neufer ◽

G. L. Dohm

Keyword(s):

Skeletal Muscle ◽

Exercise Training ◽

Protein Content ◽

Gene Transcription ◽

Training Session ◽

Transient Increase ◽

Initial Increase ◽

Control Mechanisms ◽

Glut 4 ◽

Response To Exercise

Endurance exercise training elicits an increase in mitochondrial density as well as GLUT-4 glucose transporter protein content in skeletal muscle. Corresponding increases in mRNA for respiratory enzymes and GLUT-4 indicate that pretranslational control mechanisms are involved in this adaptive process. To directly test whether transcription of the GLUT-4 gene is activated in response to exercise training, nuclei were isolated from red hindlimb skeletal muscle of rats after 1 wk of exercise training (8% grade, 32 m/min, 40 min, twice/day). Rats were killed either 30 min, 3 h, or 24 h after the last training session. GLUT-4 transcription, determined by nuclear run-on analysis, was unaltered after 30 min, increased by 1.8-fold after 3 h, but was no longer different from controls 24 h after exercise. A similar transient increase in GLUT-4 transcription was evident, but less pronounced (1.4-fold), in untrained rats after a single bout of exercise, suggesting that the postexercise induction in GLUT-4 gene transcription is enhanced by exercise training. GLUT-4 protein content was increased 1.7-fold after 1 wk of training in the absence of any corresponding change in GLUT-4 mRNA, providing evidence that the initial increase in GLUT-4 expression involves translational and/or posttranslational control mechanisms. These findings demonstrate that muscle GLUT-4 expression in response to exercise training is subject to both transcriptional and posttranscriptional regulation. We propose that the increase in GLUT-4 mRNA evident with extended periods of training may result from a shift to pretranslational control and is the cumulative effect of repeated postexercise transient increases in GLUT-4 gene transcription.

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