Low-Volume Interval Training Improves Muscle Oxidative Capacity in Sedentary Adults

Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.
Medicine and science in sports and exercise (Impact Factor: 3.98). 03/2011; 43(10):1849-56. DOI: 10.1249/MSS.0b013e3182199834
Source: PubMed


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. "
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    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. · 3.53 Impact Factor
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    • "Body composition analysis to determine percentages of bone, fat, and lean muscle tissue were measured by dual x-ray absorptiometry (DXA) scanning (Lunar Prodigy Advance, Madison, WI). Maximal oxygen uptake (VO2max), maximal workload (Wmax), and average heart rate (HR) during exercise trials were determined for each participant using standardized protocols56. All of these parameters were measured prior to the start of the exercise training, as well as following the 6-week HIIT intervention for each subject in their naïve and trained states, respectively as previously described12. "
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    Scientific Reports 08/2014; 4:6166. DOI:10.1038/srep06166 · 5.58 Impact Factor
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    • "These benefits include increased cardiorespiratory fitness [3] [4] [5] [6] [7] [8] [9] and work capacity [10], increased muscle mitochondrial biogenesis and GLUT-4 levels [11], and improved insulin sensitivity [4] [6] [7]. 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 [12] [13] [14] [15] [16] [17], cardiovascular disease [18] [19] [20] [21], metabolic syndrome [17], and type 2 diabetes [22] [23] [24]. "
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