The primary objective of this study was to determine whether cardiovascular compensatory response phenotypes exist in the face of a reduced perfusion pressure challenge to exercising muscle oxygen delivery (O2D), and whether these responses might be exercise intensity (EI) dependent. Ten healthy men (19.5 ± 0.4 yr) completed two trials of progressive forearm isometric handgrip exercise to exhaustion (24.5 N increments every 3.5 min) in each of forearm above and below heart level [forearm arterial perfusion pressure (FAPP) difference of 29.5 ± 0.97 mmHg]. At the end of each EI, measurements of forearm blood flow (FBF; ml/min) via brachial artery Doppler and echo ultrasound, mean arterial blood pressure (MAP; mmHg) via finger photoplethysmography, and exercising forearm venous effluent via antecubital vein catheter revealed distinct cardiovascular response groups: n = 6 with compensatory vasodilation vs. n = 4 without compensatory vasodilation. Compensatory vasodilators were able to blunt the perfusion pressure-evoked reduction in submaximal O2D in the arm-above-heart condition, whereas nonvasodilators did not (-22.5 ± 13.6 vs. -65.4 ± 14.1 ml O2/min; P < 0.05), and in combination with being able to increase O2 extraction, nonvasodilators defended submaximal V̇o2 and experienced less of an accumulated submaximal O2D deficit (-80.7 ± 24.7 vs. -219.1 ± 36.0 ml O2/min; P < 0.05). As a result, the compensatory vasodilators experienced less of a compromise to peak EI than nonvasodilators (-24.5 ± 3.5 N vs. -52.1 ± 8.9 N; P < 0.05). In conclusion, in the forearm exercise model studied, vasodilatory response phenotypes exist that determine individual susceptibility to hypoperfusion and the degree to which aerobic metabolism and exercise performance are compromised.

Within individuals, critical power appears sensitive to manipulations in O2 delivery. We asked whether interindividual differences in forearm O2 delivery might account for a majority of the interindividual differences in forearm critical force impulse (critical impulse), the force analog of critical power. Ten healthy men (24.6 ± 7.10 years) completed a maximal effort rhythmic handgrip exercise test (1 sec contraction‐2 sec relaxation) for 10 min. The average of contraction impulses over the last 30 sec quantified critical impulse. Forearm brachial artery blood flow (FBF; echo and Doppler ultrasound) and mean arterial pressure (MAP; finger photoplethysmography) were measured continuously. O2 delivery (FBF arterial oxygen content (venous blood [hemoglobin] and oxygen saturation from pulse oximetry)) and forearm vascular conductance (FVC; FBF·MAP−1) were calculated. There was a wide range in O2 delivery (59.98–121.15 O2 mL·min−1) and critical impulse (381.5–584.8 N) across subjects. During maximal effort exercise, O2 delivery increased rapidly, plateauing well before the declining forearm impulse and explained most of the interindividual differences in critical impulse (r2 = 0.85, P < 0.01). Both vasodilation (r2 = 0.64, P < 0.001) and the exercise pressor response (r2 = 0.33, P < 0.001) independently contributed to interindividual differences in FBF. In conclusion, interindividual differences in forearm O2 delivery account for most of the interindividual variation in critical impulse. Furthermore, individual differences in pressor response play an important role in determining differences in O2 delivery in addition to vasodilation. The mechanistic origins of this vasodilatory and pressor response heterogeneity across individuals remain to be determined.

PURPOSETo identify if rapid vasodilatory responses differ between individuals with or without type 2 diabetes.METHODS13 males (7 type II diabetics (T2D), 6 healthy controls (CON)) lay supine with the arm at heart level and completed 6 trials of single handgripping contractions (3 trials/day/contraction intensity, on 2 separate days, 1 s contraction duration) at 10, 20, and 40 % of their maximal voluntary contraction (randomly ordered). Forearm brachial artery blood flow (FBF, echo and Doppler ultrasound), mean arterial pressure (MAP, finger photoplethysmography) were measured continuously.RESULTStension‐time integral of single contraction force production (kg·s) vs. FBF relationships were constructed for each individual. There was no difference in the slope (4.7 ± 2.9 vs. 4.8 ± 2.5) or y‐intercept (y‐int) (35.2 ± 32.5 vs. 23.3 ± 15.2) between T2D and CON. However, there was considerable variation in both the slope and y‐int between subjects in each group. T2D coefficient of variation (COV) of slope was 64% and y‐int was 93%. COV for the slope in CON was 52% and y‐int 65%. Despite the variation, the r2 value for each individual was strong, ranging from 0.34–0.7 (σ = 0.51 ± 0.14) in T2D and 0.44–0.97 (σ = 0.76 ± 0.22) in CON.CONCLUSIONOlder males exhibit substantial inter‐individual rapid vasodilatory responses to muscle contraction. These individual differences do not appear to be influenced by type 2 diabetes.

PURPOSETo determine if differences in O2 delivery (O2D) between healthy subjects predicts performance in a critical power (CP) test.METHODS10 healthy male subjects lay supine with the arm at heart level and completed 10 min of rhythmic maximal voluntary contractions (1 s contraction: 2 s relaxation duty cycle). CP was calculated as the average peak contraction force during the last 30 s of the trial where force plateaued. Forearm brachial artery blood flow (FBF) during exercise (echo and Doppler ultrasound) and O2D (FBF x arterial oxygen content ([haemoglobin] from venous blood sample and oxygen saturation from pulse oximetry)) were measured.RESULTSmeans ± SD. A wide range of O2D and CP was observed. O2D 101.5 ± 25.1 ml O2/min (range 70.92–154.1 ml O2/min) & CP 25.4 ± 6.0 kg (range 17.5–34.7 kg). O2D & FBF area under the curve (AUC, ml O2/forearm volume & ml/forearm volume) for the first 200 s of exercise were predictors of CP (r2 = 0.47, 0.48 p ≤ 0.03). However, O2D & FBF total AUC during exercise was the strongest predictors rather than steady state levels achieved (r2 = 0.63, 0.66 p ≤ 0.01).CONCLUSIONSConsiderable inter‐individual differences in oxygen delivery exist during an all out CP test. These differences account for much of the inter‐individual differences in CP, supporting the contention that vasodilatory responsiveness and capacity are important determinants of small muscle mass CP. NSERC

PURPOSETo determine whether vasodilator and/or pressor response phenotypes are present during a perfusion pressure induced perturbation to exercising muscle oxygen delivery (O2D).METHODS10 healthy male subjects (19.5±0.4 yrs) completed two trials of progressive handgrip exercise to exhaustion (2.5kg increments every 3.5 mins) in each forearm above and below heart level (forearm arterial perfusion pressure (FAPP) Δ 29.5±0.97mmHg). Forearm blood flow ((FBF (ml/min); brachial artery Doppler and echo ultrasound), mean arterial blood pressure (MAP (mmHg); finger photoplethysmography) and O2D (ml/O2/min; venous effluents) were measured at the end of each work rate (WR).RESULTSGroup level, Δ FBF was compromised beyond the 5kg WR in above vs. below. There was no vasodilatory (P=0.21) or exercise pressor (P=0.63) response, and submax O2D, submax and peak VO2 and peak WR were compromised by reduced FAPP (all P<0.05). In contrast, individual responses revealed compensatory vasodilators (n=6) and those who did not (n=4). Vasodilators blunted the FAPP‐evoked reduction in submax O2D and VO2 compared to non‐vasodilators (P<0.05), and experienced less of a compromise to peak WR (P<0.05).CONCLUSIONSIn the current model, vasodilatory response phenotypes exist, which determine hypoperfusion susceptibility and the degree to which aerobic metabolism and exercise performance are compromised. NSERC.