The Postexercise Pressor Reflex Is Influenced by Pedal Frequency During Low Intensity Ergometry in Normotensive Healthy Adults
Authors: Randall Nicholas R. , Van Iterson Erik H. , Villarraga Nico , Ziegler Briana , Olson Thomas P. 
Published: November 2023

Introduction

The exercise pressor reflex (EPR) is suggested to be linked to activated group III/IV afferents. However, the predominating mechanical and/or metabolic stimuli by which the EPR is mediated remains unclear. It is suggested that high pedal frequency increases the recruitment of type II muscle fibers, which may result in augmented production of metabolic byproducts as a function of increased anaerobic processes. Therefore, this study tested the hypothesis that compared to low frequency, high pedal frequency will be associated with increased blood pressure during postexercise suprasystolic regional circulatory occlusion (SupraRCO). Further, although subsystolic RCO (SubRCO) during exercise is suggested to provoke venous distension associated with mechanically‐mediated activation of group III/IV afferents, we hypothesized the rise in blood pressure during postexercise SubRCO will be blunted vs postexercise SupraRCO irrespective of pedal frequency.

Methods

Healthy adults (N=13, 6 male, 7 female), age 36±19 yrs participated in 2 days of testing, each consisting of 3 sessions of recumbent cycle ergometry at pedal frequencies of 100 (HIGH) or 35 (LOW) rpm (randomized) at 20 W for 8 min. At cessation of exercise, bilateral upper thigh pressure tourniquets were inflated to SupraRCO (200 mm Hg), SubRCO (90 mm Hg), or no inflation (NR) for 2 min (randomized). Blood pressure via manual sphygmomanometry was measured at rest, end‐exercise, and 2 min postexercise. Mean arterial pressure (MAP) was calculated as (SBP + 2 * DBP)/3.

Results

For both rest and end‐exercise, MAP did not differ across repeated transients for either HIGH or LOW (both P>0.05). However, mean MAP across repeated transients was greater in HIGH vs LOW at end‐exercise (P<0.05). At 2 min postexercise in HIGH, compared to NR (89±8 mm Hg), MAP was higher in SupraRCO (105±18 mm Hg; P=0.02), but not in SubRCO (98±9 mm Hg; P=0.38); whereas MAP did not differ between SupraRCO and SubRCO (P=0.70). Similarly, at 2 min postexercise in LOW, MAP was increased in SupraRCO vs NR (96±10 vs 85±7 mm Hg, respectively; P=0.02); whereas there were no differences between SubRCO (88±7 mm Hg) with either NR (P=0.91) or SupraRCO (P=0.23). Lastly, compared to LOW, MAP was greater in HIGH at 2 min postexercise for both SupraRCO (P<0.01) and SubRCO (P<0.01), but not in NR (P=0.59).

Conclusions

In intact exercising humans it remains challenging to elucidate exact contributions of group III/IV afferents to the EPR. However, these data are consistent with the role of group III/IV afferents in contributing to the EPR in humans. New to this field, our observations suggest that at low fixed workloads, increased pedal frequency augments the postexercise pressor response to both SupraRCO and SubRCO in healthy adults. These data contribute to an improved understanding of specific stimuli associated with the EPR linked to group III/IV afferents in humans.

Support or Funding Information

NHLBI R25 HL115473; NHLBI RO1 HL126638; AHA 16POST30260021