Individual differences in compensatory vasodilation impact exercise performance
Authors: Bentley Robert F , Walsh Jeremy J , Fenuta Alyssa M , Drouin Patrick J , Tschakovsky Michael E 
Published: November 2023

INTRODUCTION

It is often stated that oxygen delivery (O2D) demand matching is tightly coupled during submaximal exercise. Traditional research approaches have ignored the potential for unique individual response heterogeneity in this model. Previously when we challenged exercising muscle O2D by having participants perform progressive exercise to peak with exercising forearm perfusion pressure reduced, we found individuals inherently differed in their vasodilatory response to an O2D challenge, with some having compensatory vasodilation while others did not.

PURPOSE

To test the hypothesis that both compensatory and non‐compensatory vasodilation phenotypes are evident in the face of a sudden compromise to exercising muscle O2D. Furthermore, that non‐compensators suffer greater impacts on exercise performance as a result.

METHODS

19 healthy male participants (21.8 ± 2.0 yrs) each completed 3 rhythmic isometric forearm exercise protocols separated by 24 hours. Day 1: Participants completed progressive exercise to peak. The intensity associated with 70% peak forearm vascular conductance (FVC: ml/min/100mmHg) was identified. Day 2: Participants performed steady state exercise at the 70% peak FVC intensity. This ensured that the vasodilatory reserve available to respond to a sudden challenge to O2D was the same across participants. A perfusion pressure‐induced challenge to O2D, which decreases local pressure by ~30 mmHg, was then introduced during the exercise. Day 3: Peak vasodilatory capacity was assessed, as well as perfusion and vasodilatory kinetics during exercise with a perfusion pressure challenge. Forearm blood flow (FBF: ml/min), mean arterial blood pressure (MAP: mmHg); and O2D (ml/O2/min) were measured throughout.

RESULTS

Day 2: 11 participants responded with compensatory vasodilation when steady state O2D was challenged (FVCRELAX: 660 ± 134 vs. 530 ± 124 ml/min/100mmHg, P<0.001) while 8 participants yielded no compensatory response (FVCRELAX: 667 ± 167 vs. 663 ± 165 ml/min/100mmHg, P=0.8). Steady state FBF, O2D, and oxygen consumption (VO2) were all compromised in the non‐compensators (P<0.05), while MAP remained similar between vasodilator response groups (P>0.08). As a result of such compromises, exercise tolerance in a perfusion pressure challenged position was reduced to a greater extent in the non‐compensators compared to an unchallenged position (−92 ± 73 vs. −11 ± 37 N, P=0.01). Day 1: There was no difference in exercise performance (230 ± 26 vs. 245 ± 27 N, P=0.2) nor the intensity associated with 70% peak FVC (168 ± 33 vs. 158 ± 23 N, P=0.4) between non‐compensators and compensators. Day 3: Peak vasodilatory capacity was not different between compensatory and non‐compensatory vasodilators (956 ± 236 vs. 920 ± 364 ml/min/100mmHg, P=0.8). There was no difference in the FBF and FVC kinetic responses to an absolute intensity with a perfusion pressure challenge (all P>0.05).

CONCLUSIONS

Vasodilatory response phenotypes exist which determine inter‐individual differences in O2D and impact exercise performance. A non‐compensation response is not explained by differences in vasodilatory capacity, peak exercise capacity or work rate at which 70% peak vasodilation response occurred.

Support or Funding Information

NSERC