Individual differences in compensatory vasodilation impact exercise performance

It is often stated that oxygen delivery (O 2 D) 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 O 2 D 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 O 2 D 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 O 2 D. 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 O 2 D was the same across participants. A perfusion pressure‐induced challenge to O 2 D, 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 O 2 D (ml/O 2 /min) were measured throughout. RESULTS Day 2: 11 participants responded with compensatory vasodilation when steady state O 2 D was challenged (FVC RELAX : 660 ± 134 vs. 530 ± 124 ml/min/100mmHg, P<0.001) while 8 participants yielded no compensatory response (FVC RELAX : 667 ± 167 vs. 663 ± 165 ml/min/100mmHg, P=0.8). Steady state FBF, O 2 D, and oxygen consumption (VO 2 ) 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 O 2 D 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