Two weeks of high-intensity interval training increases skeletal muscle mitochondrial respiration via complex-specific remodeling in sedentary humans
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ABSTRACT:
PROVIDER: PRJNA916679 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22924700.fastq.gz | Fastqsanger.gz | |||
| SRR22924674.fastq.gz | Fastqsanger.gz | |||
| SRR22924675.fastq.gz | Fastqsanger.gz | |||
| SRR22924676.fastq.gz | Fastqsanger.gz | |||
| SRR22924677.fastq.gz | Fastqsanger.gz |
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Project description:Aerobic training remodels the quantity and quality (function per unit) of skeletal muscle mitochondria to promote substrate oxidation, however, there remain key gaps in understanding the underlying mechanisms during initial training adaptations. We used short-term high-intensity interval training (HIIT) to determine changes to mitochondrial respiration and regulatory pathways that occur early in remodeling. Fifteen normal-weight sedentary adults started seven sessions of HIIT over fourteen days and fourteen participants completed the intervention. We collected vastus lateralis biopsies before and 48-hours after HIIT to determine mitochondrial respiration, RNA sequencing, and western blotting for proteins of mitochondrial respiration and degradation via autophagy. HIIT increased respiration per mitochondrial protein for lipid (+23% P=0.020), complex I (+18%, P=0.0015), complex I+II (+14%, P<0.0001) and complex II (+24% P<0.0001). Transcripts that increased with HIIT identified several gene sets of mitochondrial respiration, particularly for complex I, while transcripts that decreased identified pathways of DNA and chromatin remodeling. HIIT lowered protein abundance of autophagy markers for p62 (-19%, P=0.012) and LC3 II/I (-20%, P=0.004) in whole-tissue lysates but not isolated mitochondria. Meal tolerance testing revealed HIIT increased the change in whole-body respiratory exchange ratio and lowered cumulative plasma insulin concentrations. Gene transcripts and respiratory function indicate remodeling of mitochondria within 2 weeks of HIIT. Overall changes are consistent with increased protein quality driving rapid improvements in substrate oxidation.
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Project description:High intensity exercise (HIE) has become a prominent training modality used to ameliorate cardiac disease conditions. The effects of HIE training on Hypertrophic Cardiomyopathy (HCM) have not been previously studied in animal models or in patients, largely due to concerns about triggering sudden arrhythmic events. Employing a transgenic cardiac troponin (cTnT-160E or TG) preclinical murine model that closely recapitulates human HCM, we evaluated the effects of a High Intensity Interval Training (HIIT) protocol on cardiorespiratory capacity (i.e., peak oxygen consumption or pVO2), which is a significant prognostic indicator of disease trajectory. 14 month old TG male mice had lower peak VO2 than non-transgenic (NTG) male mice of the same age at baseline, but there was no difference in pVO2 in female TG compared to nTG mice. HIIT significantly improved pVO2 in both nTG female (18%) , nTG male (18%), TG female (16%) and TG male (12%) mice compared to sedentary controls. There were no changes in structure, function or LV mass as measured by echocardiography or post mortem analyses in any of the groups, and no effect of HIIT on cardiac fibrosis. HIIT led to significant increases in lean muscle mass in both nTG and TG male mice, and nTG female mice but not TG female mice. The results of our study provide foundational evidence that HIE can improve pVO2 in HCM without adverse effects on disease phenotype.
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Project description:Twenty healthy subjects (25±5yrs) completed two high-intensity interval training interventions (training and retraining) lasting 8 weeks separated by 12 weeks of detraining. Measurements at baseline and after training, detraining and retraining included maximal oxygen consumption (V̇O2max), along with vastus lateralis biopsy for genome wide DNA methylation using Illumina Epic arrays in 5 of the participants for all conditions (baseline, training, detraining and retraining).
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Project description:Skeletal muscle tissue is a highly adaptable tissue, responding to the specific demands it is subjected to. High-intensity interval training (HIIT) has been shown to generate similar, or even greater, molecular changes in skeletal muscle as that of constant load longer-lasting endurance-type training at moderate intensities. Despite shorter exposure times, the higher intensity provided by HIIT training leads to greater metabolic perturbations and thereby larger improvements in mitochondrial content and maximal oxygen uptake. During a period of regular exercise training, the performance improvements follow a non-linear pattern with a relatively faster pace initially and a gradual ‘plateauing-off’ after weeks and months. It is believed that this ‘plateau effect’ is due to a blunting of the molecular responses to acute exercise with exercise training. In the present study we utilised an explorative global transcriptomic approach to investigate the phenomenon of transcriptional-level blunting of the acute exercise response in human skeletal muscle over the course of a three-week HIIT intervention. We hypothesize that the blunting of transcription at this time-point is specific to certain pathways, including metabolic regulation and that these genes have communal transcriptional regulation.
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Project description:Human skeletal muscle transcriptome in response to high-intensity interval training
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Project description:Human skeletal muscle possesses an epigenetic memory of high intensity interval training
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Project description:Exercise 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 novel protein adaptations to exercise training involved in metabolism and excitation-contraction coupling. Furthermore, HIIT increased the acetylation of mitochondrial proteins, particularly those of complex V, likely via non-enzymatic mechanisms. We also highlight the regulation of novel 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.
2022-06-09 | PXD023084 | Pride
Project description:Beneficial Effects of High Intensity Interval Training in a Mouse Model of Hypertrophic Cardiomyopathy
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Project description:Ten healthy male participants were recruited and successfully completed all preliminary testing and the two exercise bouts (Figure 1A). This randomized crossover design permitted signaling responses to workload- and duration-matched HIIT and MICT exercise to be mapped and interrogated within the same participant. Baseline whole-body anthropometric and blood glucose and lipid measurements confirmed these participants (age 25.4 ± 3.2 y; BMI 23.5 ± 1.6 kg/m2) were metabolically healthy, and maximal exercise capacity testing confirmed they were recreationally active but relatively untrained (relative V̇O2 peak 37.9 ± 5.2) in line with our recruitment strategy to maximize detection of skeletal muscle signaling responses to exercise (Figure 1B). Peak power output (Wpeak; 207.5 ± 40.3 W) was used to prescribe the relative work-matched intensities for HIIT and MICT. Lean mass from the DXA scan and resting metabolic rate (Figure 1B) were used to prescribe a standardized meal for each participant to consume prior to each exercise trial day. Following consumption of a standardized dinner meal the night before the HIIT or MICT exercise trial, blood and skeletal muscle biopsy samples were collected in the fasted state at baseline and at 5 min and 10 min of each respective exercise intensity. Participants completing the acute bout of HIIT, which consisted of 10 min total of 1-min ‘on’ intervals at 85 ± 0.1% of individual Wpeak (176 ± 34 W) and 1-min ‘off’ intervals at 50 W, displayed increased plasma lactate concentrations at 5 and 10 min of exercise relative to pre-exercise baseline (Figure 1C; P < 0.0001 and P < 0.001, respectively; main effect of time P < 0.0001) and no changes in plasma glucose (Figure 1D). In response to total work- and duration-matched acute bout of MICT at 55 ± 2% individual Wpeak (113 ± 17 W), participants displayed increased plasma lactate concentrations at 5 and 10 min of exercise versus baseline (Figure 1C; P < 0.001; main effect of time P < 0.0001) and no changes in plasma glucose (Figure 1D), with a main effect of higher plasma lactate levels in response to HIIT (Figure 1C; P < 0.05). To map the signaling networks regulated by HIIT and MICT, proteins from each skeletal muscle biopsy sample were extracted, digested to peptides with trypsin, isobarically labelled prior to phosphopeptide enrichment, fractionation and LC-MS/MS phosphoproteomic analysis (Figure 2A).
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