title: Physiological and molecular responses to an acute bout of reduced-exertion high-intensity interval training (REHIT).
abstract: OBJECTIVE
  We have previously shown that 6 weeks of reduced-exertion high-intensity interval training (REHIT) improves VO2max in sedentary men and women and insulin sensitivity in men. Here, we present two studies examining the acute physiological and molecular responses to REHIT.
  
  
  METHODS
  In Study 1, five men and six women (age: 26 ± 7 year, BMI: 23 ± 3 kg m(-2), VO2max: 51 ± 11 ml kg(-1) min(-1)) performed a single 10-min REHIT cycling session (60 W and two 20-s 'all-out' sprints), with vastus lateralis biopsies taken before and 0, 30, and 180 min post-exercise for analysis of glycogen content, phosphorylation of AMPK, p38 MAPK and ACC, and gene expression of PGC1α and GLUT4. In Study 2, eight men (21 ± 2 year; 25 ± 4 kg·m(-2); 39 ± 10 ml kg(-1) min(-1)) performed three trials (REHIT, 30-min cycling at 50 % of VO2max, and a resting control condition) in a randomised cross-over design. Expired air, venous blood samples, and subjective measures of appetite and fatigue were collected before and 0, 15, 30, and 90 min post-exercise.
  
  
  RESULTS
  Acutely, REHIT was associated with a decrease in muscle glycogen, increased ACC phosphorylation, and activation of PGC1α. When compared to aerobic exercise, changes in VO2, RER, plasma volume, and plasma lactate and ghrelin were significantly more pronounced with REHIT, whereas plasma glucose, NEFAs, PYY, and measures of appetite were unaffected.
  
  
  CONCLUSIONS
  Collectively, these data demonstrate that REHIT is associated with a pronounced disturbance of physiological homeostasis and associated activation of signalling pathways, which together may help explain previously observed adaptations once considered exclusive to aerobic exercise.
authors.affiliation: Department for Health, University of Bath, Bath, BA2 7AY, UK.|Sport and Exercise Sciences Research Institute, School of Sport, University of Ulster, Derry, UK.
authors.forename: R S
authors.initials: RS
authors.lastname: Metcalfe
authors.affiliation: Department of Biology and Biochemistry, University of Bath, Bath, UK.
authors.forename: F
authors.initials: F
authors.lastname: Koumanov
authors.affiliation: Department for Health, University of Bath, Bath, BA2 7AY, UK.
authors.forename: J S
authors.initials: JS
authors.lastname: Ruffino
authors.affiliation: Department for Health, University of Bath, Bath, BA2 7AY, UK.
authors.forename: K A
authors.initials: KA
authors.lastname: Stokes
authors.affiliation: Department of Biology and Biochemistry, University of Bath, Bath, UK.
authors.forename: G D
authors.initials: GD
authors.lastname: Holman
authors.affiliation: Department for Health, University of Bath, Bath, BA2 7AY, UK.
authors.forename: D
authors.initials: D
authors.lastname: Thompson
authors.affiliation: Department for Health, University of Bath, Bath, BA2 7AY, UK. n.vollaard@bath.ac.uk.
authors.forename: N B J
authors.initials: NB
authors.lastname: Vollaard
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000263:Adenylate Kinase / Q000378:metabolism; D000328:Adult; D005260:Female; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology*; D010766:Phosphorylation; D064797:Physical Conditioning, Human / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D055815:Young Adult; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D019344:Lactic Acid; D006003:Glycogen; D048051:p38 Mitogen-Activated Protein Kinases; D000263:Adenylate Kinase
keywords: AMPK; Energy balance; Exercise metabolism; Glycogen; HIT; Signalling pathways