title: Aerobic interval training improves oxygen uptake efficiency by enhancing cerebral and muscular hemodynamics in patients with heart failure.
abstract: BACKGROUND
  Abnormal ventilatory/hemodynamic responses to exercise contribute to functional impairment in patients with heart failure (HF). This study investigates how interval and continuous exercise regimens influence functional capacity by modulating ventilatory efficiency and hemodynamic function in HF patients.
  
  
  METHODS
  Forty-five HF patients were randomized to perform either aerobic interval training (AIT; 3-minute intervals at 40% and 80% VO(2peak)) or moderate continuous training (MCT; sustained 60% VO()for 30 min/day, 3 days/week for 12 weeks, or to a control group that received general healthcare (GHC). A noninvasive bio-reactance device was adopted to measure cardiac hemodynamics, whereas a near-infrared spectroscopy was employed to assess perfusion/O2 extraction in frontal cerebral lobe (∆[THb]FC/∆[HHb]FC) and vastus lateralis (∆[THb]VL/∆[HHb]VL), respectively.
  
  
  RESULTS
  Following the 12-week intervention, the AIT group exhibited higher oxygen uptake efficiency slope (OUES) and lower VE-VCO2 slope than the MCT and GHC groups. Furthermore, AIT, but not MCT, boosted cardiac output (CO) and increased ∆[THb]FC, ∆[THb]VL, and ∆[HHb]VL during exercise. In multivariate analyses, CO was the dominant predictor of VO(2peak). ∆[THb]FC and ∆[THb]VL, which modulated the correlation between CO and OUES, were significantly correlated with OUES. Simultaneously, ∆[THb]VL was the only factor significantly associated with VE-VCO2 slope. Additionally, AIT reduced plasma brain natriuretic peptide, myeloperoxidase, and interleukin-6 levels and increased the Short Form-36 physical/mental component scores and decreased the Minnesota Living with Heart Failure questionnaire score.
  
  
  CONCLUSIONS
  AIT effectively improves oxygen uptake efficiency by enhancing cerebral/muscular hemodynamics and suppresses oxidative stress/inflammation associated with cardiac dysfunction, and also promotes generic/disease-specific qualities of life in patients with HF.
authors.affiliation: Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital, Keelung, Taiwan.
authors.forename: Tieh-Cheng
authors.initials: TC
authors.lastname: Fu
authors.forename: Chao-Hung
authors.initials: CH
authors.lastname: Wang
authors.forename: Pay-Shin
authors.initials: PS
authors.lastname: Lin
authors.forename: Chih-Chin
authors.initials: CC
authors.lastname: Hsu
authors.forename: Wen-Jin
authors.initials: WJ
authors.lastname: Cherng
authors.forename: Shu-Chun
authors.initials: SC
authors.lastname: Huang
authors.forename: Min-Hui
authors.initials: MH
authors.lastname: Liu
authors.forename: Cheng-Lin
authors.initials: CL
authors.lastname: Chiang
authors.forename: Jong-Shyan
authors.initials: JS
authors.lastname: Wang
mesh_terms: D000368:Aged; D001921:Brain / Q000378:metabolism*; D015444:Exercise / Q000502:physiology*; D005260:Female; D006333:Heart Failure / Q000378:metabolism* / Q000628:therapy*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology*; D016896:Treatment Outcome