Effects of Prior Heavy Exercise in Heart Failure with Preserved Ejection Fraction on V̇O2 Kinetics
Authors: Boyes Natasha G. , Eckstein Janine , Pylypchuk Stephen , Butcher Scotty J. , Marciniuk Darcy D. , Dewa Dalisizwe M.K. , Wells Calvin R. , Haykowsky Mark J. , Tomczak Corey R. 
Published: June 2021

Exercise intolerance and muscle dysfunction characterize heart failure with preserved ejection fraction (HFpEF). Prior heavy exercise (“priming”) speeds pulmonary oxygen uptake (V̇O2p) kinetics in older adults. The mechanism behind speeding of V̇O2p kinetics following priming is either through increased oxygen delivery to the exercising muscles or increased intracellular metabolic activity; the former remains dominant in older and diseased populations.

PURPOSE

We tested the hypothesis that priming would not speed V̇O2p on‐kinetics in patients with HFpEF due to muscle dysfunction commonly found in patients with HFpEF.

METHODS

Eight HFpEF patients, 4 high‐fit (CTL‐HF), and 5 low‐fit age‐matched controls (CTL‐LF) performed 3 repetitions of 2 exercise transitions: MOD1, rest to 4‐min moderate‐intensity cycling; and MOD2, MOD1 preceded by 2‐min heavy‐intensity cycling and 5‐min rest. V̇O2p (oxidative metabolism; pulmonary gas exchange), heart rate (HR, cardiac function; ECG), total peripheral resistance (TPR, vascular function; ModelFlow), and tissue oxygenation of the vastus lateralis (TOI, muscle oxygen delivery; near‐infrared spectroscopy) on‐kinetics were measured, linearly interpolated, time‐aligned, and averaged. V̇ O2p and HR were curve‐fitted using a monoexponential equation to yield a time constant (tau). ΔTPR and ΔTOI were calculated from baseline at 15s, 30s, and end‐exercise. Significance was P<0.05.

RESULTS

HFpEF V̇O2p on‐kinetics (tau 45 ± 15 s) were slower than CTL‐HF (25 ± 6 s) but not CTL‐LF (50 ± 19 s; P=0.008). MOD2 V̇O2p on‐kinetics (tau 37 ± 14 s) were faster than MOD1 (47 ± 19 s), pooled across groups (P=0.039). Although not statistically significant, the priming effect was notably smaller in HFpEF compared to control groups (9% in HFpEF, 33% in low‐fit controls, and 30% faster in high‐fit controls). HR on‐kinetics were slower following priming in all groups (MOD1 tau 34 ± 21 vs. MOD2 44 ± 27 s; P=0.001), suggesting cardiac output as an unlikely assistant to the observed speeding in V̇O2p on‐kinetics across groups. TPR was lower in CTL‐HF throughout exercise compared to HFpEF (all P<0.038) and at 30s and end‐exercise compared to CTL‐LF (all P<0.032), pooled across conditions with no effect of priming. TOI in CTL‐HF increased at 15–30s (all P≤0.024) while HFpEF patients and CTL‐LF had decreased TOI at 15–30s in MOD1 (all P≤0.024). The latter suggests lower oxygen delivery at early exercise onset compared to CTL‐HF. Priming reduced TOI in HFpEF at 30s (P=0.033) and CTL‐HF throughout exercise (all P<0.05), suggesting either lower muscle oxygen delivery or greater mitochondrial activity following priming.

CONCLUSION

Slow HFpEF V̇O2p on‐kinetics may not be speeded by priming exercise. Heart rate and vascular responses to priming may not account for speeding of V̇O2p on‐kinetics in older adults. Intracellular mechanisms may limit HFpEF exercise tolerance.

Support or Funding Information

Canadian Institutes of Health Research

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.