title: Changes in mitochondrial function and mitochondria associated protein expression in response to 2-weeks of high intensity interval training.
abstract: OBJECTIVE
  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 × 1 min 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.
  
  
  CONCLUSIONS
  Over only 2 weeks HIT significantly increased mitochondrial function in skeletal muscle independently of detectable changes in mitochondrial-associated and mitogenic protein expression.
authors.affiliation: Centre for Physical Activity and Nutrition Research, School of Exercise and Nutrition Sciences, Deakin University Melbourne VIC, Australia ; Department of Sport and Exercise Science, The University of Auckland Auckland, New Zealand.
authors.forename: Grace
authors.initials: G
authors.lastname: Vincent
authors.affiliation: Centre for Physical Activity and Nutrition Research, School of Exercise and Nutrition Sciences, Deakin University Melbourne VIC, Australia.
authors.forename: Séverine
authors.initials: S
authors.lastname: Lamon
authors.affiliation: Department of Sport and Exercise Science, The University of Auckland Auckland, New Zealand.
authors.forename: Nicholas
authors.initials: N
authors.lastname: Gant
authors.affiliation: Department of General Practice and Primary Healthcare, Auckland School of Medicine, The University of Auckland Auckland, New Zealand.
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Vincent
authors.affiliation: Applied Surgery and Metabolism Laboratory, School of Biological Sciences, The University of Auckland Auckland, New Zealand.
authors.forename: Julia R
authors.initials: JR
authors.lastname: MacDonald
authors.affiliation: Liggins Institute, The University of Auckland Auckland, New Zealand.
authors.forename: James F
authors.initials: JF
authors.lastname: Markworth
authors.affiliation: Department of Sport and Exercise Science, The University of Auckland Auckland, New Zealand.
authors.forename: Johann A
authors.initials: JA
authors.lastname: Edge
authors.affiliation: Applied Surgery and Metabolism Laboratory, School of Biological Sciences, The University of Auckland Auckland, New Zealand.
authors.forename: Anthony J R
authors.initials: AJ
authors.lastname: Hickey
keywords: HIT; PGC-1α; mitochondria; oxidative phosphorylation; skeletal muscle