Peak Exercise and Post‐Exercise Recovery Oxygen Uptake and Muscle Oxygenation in Patients with Heart Failure and Preserved Ejection Fraction and Healthy Matched Adults
Authors: Boyes Natasha , Eckstein Janine , Pylypchuk Stephen , Lahti Dana , Butcher Scotty J , Marciniuk Darcy D , Dewa Dalisizwe M.K. , Wells Calvin R , Haykowsky Mark J , Tomczak Corey R 
Published: June 2021

Background

Exercise intolerance and muscle dysfunction characterize heart failure with preserved ejection fraction (HFpEF). Exercise intolerance, as measured by low peak oxygen uptake (VO2), and slow post‐exercise VO2 recovery are predictors of mortality. The relationship between peak exercise and recovery VO2 and muscle oxygenation is unknown in this population.

Purpose

We tested the hypothesis that post‐exercise VO2 recovery would be slower in patients with HFpEF compared to controls, and that slower post‐exercise VO2 recovery would be related to slower muscle oxygenation recovery in patients with HFpEF.

Methods

Eight patients with HFpEF and 8 healthy age‐and sex‐matched controls completed a stationary cycling peak exercise test to volition fatigue followed by 5‐min of passive recovery. Pulmonary VO2 (gas exchange via metabolic cart) and muscle oxygenation (tissue muscle oxygenation index, TOI) and deoxygenated hemoglobin (HHb via near infrared spectroscopy) were sampled continuously during the exercise test and recovery. Breath‐by‐breath VO2 data were linearly interpolated to 1‐s intervals, and both VO2 and NIRS data were averaged into 5‐s time bins. VO2 recovery data were mono‐exponentially curve‐fitted (OriginPro, 2017) to yield a recovery time constant (tau) and amplitude change. TOI and HHb at end‐exercise, end‐recovery, and the amplitude change were calculated as 10‐s averages. Statistical analyses included independent t‐tests and stepwise multiple regression. Significance was accepted at P<0.05.

Results

Peak VO2 (15.8 ± 5.9 vs. 24.6 ± 6.6 mL/kg/min, P = 0.011) and VO2 recovery amplitude (−10.0 ± 4.9 vs. −15.1 ± 4.2 mL/kg/min, P = 0.041) were significantly lower in patients with HFpEF compared to matched controls. However, there were no differences between groups in VO2 recovery tau (98 ± 43 vs. 71 ± 16 s, P = 0.122) nor in any TOI or HHb parameter (all P>0.05). Stepwise regression by group to predict peak VO2 yielded a positive regression using both peak‐exercise HHb and VO2 recovery amplitude in HFpEF (R2 = 0.957, P<0.001) but only VO2 recovery amplitude in controls (R2 = 0.947, P<0.001). The same parameters predicted VO2 recovery tau in HFpEF (R2 = 0.940, P = 0.001) with no significant finding in controls (P>0.05).

Conclusions

Slower post‐exercise VO2 recovery in patients with HFpEF compared to their healthy counterparts was not confirmed with these data, although this may be largely influenced by the elevated variance in the HFpEF group, or the mild‐moderate HFpEF severity. Regression analyses suggest that the level of muscle deoxygenation, i.e., the level of O2 extraction, during peak exercise may be a more important contributor to peak VO2 in patients with HFpEF compared to their healthy counterparts. The latter may suggest a muscle‐based limitation in HFpEF not observed in healthy controls.

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.