Low-Volume Interval Training Improves Muscle Oxidative Capacity in Sedentary Adults
ABSTRACT High-intensity interval training (HIT) increases skeletal muscle oxidative capacity similar to traditional endurance training, despite a low total exercise volume. Much of this work has focused on young active individuals, and it is unclear whether the results are applicable to older less active populations. In addition, many studies have used "all-out" variable-load exercise interventions (e.g., repeated Wingate tests) that may not be practical for all individuals. We therefore examined the effect of a more practical low-volume submaximal constant-load HIT protocol on skeletal muscle oxidative capacity and insulin sensitivity in middle-aged adults, who may be at a higher risk for inactivity-related disorders.
Seven sedentary but otherwise healthy individuals (three women) with a mean ± SD age, body mass index, and peak oxygen uptake (VO(2peak)) of 45 ± 5 yr, 27 ± 5 kg·m(-2), and 30 ± 3 mL·kg(-1)·min(-1) performed six training sessions during 2 wk. Each session involved 10 × 1-min cycling at ∼60% of peak power achieved during a ramp VO(2peak) test (eliciting ∼80%-95% of HR reserve) with 1 min of recovery between intervals. Needle biopsy samples (vastus lateralis) were obtained before training and ∼72 h after the final training session.
Muscle oxidative capacity, as reflected by the protein content of citrate synthase and cytochrome c oxidase subunit IV, increased by ∼35% after training. The transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator 1α was increased by ∼56% after training, but the transcriptional corepressor receptor-interacting protein 140 remained unchanged. Glucose transporter protein content increased ∼260%, and insulin sensitivity, on the basis of the insulin sensitivity index homeostasis model assessment, improved by ∼35% after training.
Constant-load low-volume HIT may be a practical time-efficient strategy to induce metabolic adaptations that reduce the risk for inactivity-related disorders in previously sedentary middle-aged adults.
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- "PCG-1α, a key regulator of mitochondrial biogenesis and function that positively regulates the mitochondrial network (Wu et al., 1999; Finck and Kelly, 2006; Handschin and Spiegelman, 2006), is upregulated in human skeletal muscle following acute endurance exercise (Cartoni et al., 2005; Russell et al., 2005) and low-volume HIT (Gibala et al., 2009; Little et al., 2010). Short duration HIT has been shown to improve aerobic capacity (Burgomaster et al., 2005) and elevate mitochondrial enzyme activities (Gibala et al., 2006c; Hood et al., 2011; Little et al., 2011). Enzyme activity assays and mitochondrial-associated gene and protein expression provide static, surrogate measures of mitochondrial content and oxidative capacities. "
ABSTRACT: Purpose: High-intensity short-duration interval training (HIT) stimulates functional and metabolic adaptation in skeletal muscle, but the influence of HIT on mitochondrial function remains poorly studied in humans. Mitochondrial metabolism as well as mitochondrial-associated protein expression were tested in untrained participants performing HIT over a 2-week period. Methods: Eight males performed a single-leg cycling protocol (12×1min intervals at 120% peak power output, 90 s recovery, 4 days/week). Muscle biopsies (vastus lateralis) were taken pre- and post-HIT. Mitochondrial respiration in permeabilized fibers, citrate synthase (CS) activity and protein expression of peroxisome proliferator-activated receptor gamma coactivator (PGC-1α) and respiratory complex components were measured. Results: HIT training improved peak power and time to fatigue. Increases in absolute oxidative phosphorylation (OXPHOS) capacities and CS activity were observed, but not in the ratio of CCO to the electron transport system (CCO/ETS), the respiratory control ratios (RCR-1 and RCR-2) or mitochondrial-associated protein expression. Specific increases in OXPHOS flux were not apparent after normalization to CS, indicating that gross changes mainly resulted from increased mitochondrial mass. Conclusion: Over only 2 weeks HIT significantly increased mitochondrial function in skeletal muscle independently of detectable changes in mitochondrial-associated and mitogenic protein expression.Frontiers in Physiology 02/2015; 6(51):1-8. · 3.50 Impact Factor
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- "These benefits include increased cardiorespiratory fitness        and work capacity , increased muscle mitochondrial biogenesis and GLUT-4 levels , and improved insulin sensitivity   . Relative to the effect of continuous aerobic exercise, HIIT has also been shown to induce comparable improvements in fitness and insulin sensitivity in clinical populations, including those with overweight/obesity      , cardiovascular disease    , metabolic syndrome , and type 2 diabetes   . "
ABSTRACT: Objective. The purpose of this study was to assess the effect of high intensity interval training (HIIT) versus continuous aerobic exercise training (CONT) or placebo (PLA) on body composition by randomized controlled design. Methods. Work capacity and body composition (dual-energy X-ray absorptiometry) were measured before and after 12 weeks of intervention in 38 previously inactive overweight adults. Results. There was a significant group × time interaction for change in work capacity (), which increased significantly in CONT (%) and HIIT (%) but not PLA (%). There was a near-significant main effect for percentage trunk fat, with trunk fat reducing in CONT by % and in PLA by %, but not in HIIT (increase of %) (). There was a significant reduction in android fat percentage in CONT (%) and PLA (%) but not HIIT (increase of %) (). Conclusion. These data suggest that HIIT may be advocated as a time-efficient strategy for eliciting comparable fitness benefits to traditional continuous exercise in inactive, overweight adults. However, in this population HIIT does not confer the same benefit to body fat levels as continuous exercise training.Journal of obesity 01/2014; 2014.
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- "Specifically, HIt has been shown to improve insulin sensitivity and glycaemic control (Burgomaster et al. 2006, 2008; gibala et al. 2006; Wisløff et al. 2007; tjønna et al. 2008; Babraj et al. 2009; Haram et al. 2009; nybo et al. 2010; richards et al. 2010; Whyte et al. 2010; gaesser and Angadi. 2011; Hood et al. 2011; little et al. 2011; Shepherd et al. 2013) as well as other cardiovascular health factors (Fletcher et al. 1996) after just 2 weeks of training (typically six training sessions). An intriguing body of research has also emerged documenting beneficial changes in body composition and/ or mass in response to HIt (Boutcher 2010) with studies reporting favourable changes within short time-frames. "
ABSTRACT: High-intensity intermittent exercise training (HIT) may favourably alter body composition despite low training volumes and predicted energy expenditure (EE). To characterise the acute impact of two common HIT protocols on EE and post-exercise oxygen consumption (11 h EPOC). Oxygen consumption (l min(-1)), respiratory exchange ratio (RER) and EE were measured in nine healthy, lean males over 12 h under three conditions: control (CON), HIT1 (10 × 1 min high-intensity cycling bouts followed by 1 min rest) and HIT2 (10 × 4 min high-intensity cycling bouts followed by 2 min rest). Total exercise period EE during HIT1 (1,151 ± 205 kJ) (mean ± SD) was significantly lower than HIT2 (2,788 ± 322 kJ; p < 0.001). EE within the 60 min after exercise was significantly albeit marginally higher after HIT1 (388 ± 44 kJ; p = 0.02) and HIT2 (389 ± 39 kJ; p = 0.01) compared with CON (329 ± 39 kJ), with no difference between exercise conditions (p = 0.778). RER during this period was significantly lower in HIT1 (0.78 ± 0.06; p = 0.011) and HIT2 (0.76 ± 0.04; p = 0.004) compared with CON (0.87 ± 0.06). During the 'slow phase' of EPOC (1.25-9.75 h), there were no significant differences in EE (p = 0.07) or RER (p = 0.173) between trials. Single HIT sessions notably increases EE during exertion; however, the influence on metabolic rate post-exercise is transient and relatively minor.Arbeitsphysiologie 10/2013; 113(12). DOI:10.1007/s00421-013-2741-5 · 2.30 Impact Factor