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Impaired Oxygen Uptake Kinetics Related to Reduced Peripheral Oxygen Extraction in Heart Failure with Preserved Ejection Fraction
Author(s) -
Hearon Christopher M.,
Sarma Satyam,
Dias Katrin A.,
Hieda Michinari,
Levine Benjamin D.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.588.17
Subject(s) - cardiology , medicine , heart failure with preserved ejection fraction , oxygen , heart failure , ejection fraction , kinetics , peripheral , vo2 max , heart rate , treadmill , chemistry , blood pressure , physics , organic chemistry , quantum mechanics
Background The amount of time needed to increase oxygen utilization to sufficiently meet metabolic demand (V̇O 2 kinetics) is impaired in heart failure (HF) with reduced ejection fraction, and is an independent predictor of HF mortality. However, it is not known if V̇O 2 kinetics are slowed in heart HF patients with preserved ejection fraction (HFpEF). We tested the hypothesis that V̇O 2 kinetics are slowed during submaximal exercise (equivalent to activities of daily living) in HFpEF patients, and that slower V̇O 2 kinetics are related to impaired peripheral oxygen extraction. Methods Eighteen healthy controls (69±6 years, 10 females) and eighteen HFpEF patients (68±7 years, 10 females) were studied during submaximal (~30% predicted max) and peak treadmill exercise. Cardiac output (Q c , acetylene rebreathing), pulmonary oxygen uptake (V̇O 2 , Douglas bags), and arterial‐venous oxygen difference (a‐v O 2 diff ) were measured during exercise. Breath‐by‐breath V̇O 2 uptake was measured continuously at the onset and throughout submaximal exercise, and V̇O 2 kinetics quantified as the time needed to for V̇O 2 to rise to ~63% of steady state V̇O 2 (mean response time, MRT). Results During submaximal exercise, absolute oxygen demand was similar between groups (V̇O 2 : Control: 0.81±0.1, HFpEF: 0.85±0.2 L/min; P=0.54) however, HFpEF patients had substantially slowed V̇O 2 kinetics (MRT: Control: 40.1±14.2, HFpEF: 65.4±27.7 s; P=0.002), and >50% greater accumulated oxygen deficit compared to controls (Control: 400±173, HFpEF: 693±392 mL; P=0.007). At peak exercise, HFpEF patients had lower relative V̇O 2 (Control: 22.2±4.0, HFpEF: 14.6±3.1 mL/kg/min; P<0.001), preserved peak Q c (Control: 13.4±4.0, HFpEF: 13.9±3.5 L/min; P=0.68), and reduced peripheral oxygen extraction (a‐v O 2 diff : Control: 12.7±2.9, HFpEF: 10.4±2.1 mL/dL; P=0.01). When stratified by MRT, HFpEF patients with a MRT >60s demonstrated impaired peripheral oxygen extraction that was apparent during submaximal exercise compared to HFpEF patients with a MRT <60s (submaximal a‐v O 2 diff : MRT<60s: 9.7±2.1, MRT>60s: 7.9±1.1 mL/dL; P=0.03). Conclusions HFpEF patients have slowed V̇O 2 kinetics during exercise that are due in part to impaired peripheral oxygen utilization. This finding supports growing evidence that peripheral oxidative capacity is a primary contributor to exercise intolerance in HFpEF leading to substantial oxygen deficit even during activities of daily living. Further, MRT can lend important insight into the pathophysiology of exercise intolerance in individual HFpEF patients, and identify patients with severe peripheral limitations to exercise capacity. Support or Funding Information NIH: AG017479, F32‐HL137285 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .