Characteristics and effectiveness of vasodilatory and pressor compensation for reduced relaxation time during...

What is the central question of this study? Reduced relaxation time between contractions in exercise requires increased vasodilatation and/or pressor response to prevent hypoperfusion and potential compromise to exercise tolerance. However, it remains unknown whether and to what extent local vasodilatation and/or systemic pressor compensation occurs and whether the efficacy of compensation is exercise intensity dependent. What is the main finding and its importance? We demonstrate that in a forearm exercise model vasodilatory but not pressor compensation occurs and is adequate to prevent hypoperfusion below but not above ∼40% peak work rate. Inadequate compensation occurs with exercise still well inside the submaximal domain, despite a vasodilatory reserve, and compromises exercise performance. During muscle contraction in rhythmic exercise, muscle blood flow is significantly impeded by microvascular compression. The purpose of this study was to establish the nature and magnitude of vasodilatory and/or pressor compensatory responses during forearm exercise in the face of an increased duration of mechanical microvascular compression, and whether the effectiveness of such compensation was exercise intensity dependent. Seven healthy males (21.0 ± 1.8 years old) completed progressive forearm exercise (24.5 N every 3 min; 2 s contraction-4 s relaxation duty cycle) in two conditions: control (CON), 2 s 100 mmHg forearm cuff inflation during contraction; and impedance (IMP), extension of cuff inflation 2 s beyond contraction. Forearm blood flow (in millilitres per minute); brachial artery Doppler and echo ultrasound), mean arterial blood pressure (in millimetres of mercury; finger photoplethysmography) and exercising forearm venous effluent (antecubital vein catheter) measurements revealed an exercise intensity-dependent compensatory vasodilatation effectiveness whereby increased vasodilatation fully protected forearm blood flow up to the 30% exercise intensity in IMP. Above this exercise intensity, forearm blood flow was defended only in part, although submaximal oxygen uptake was not compromised for any completed work rate. As a result, peak exercise intensity (175 ± 22 versus 196 ± 28 N, P = 0.04) and oxygen delivery (76 ± 14 versus 112 ± 22 ml O₂  min^-1 , P = 0.01) were significantly reduced in IMP compared with CON. In conclusion, reducing relaxation time compromised exercise capacity without compromise to oxygen uptake. Vasodilatory compensation was complete at lower but not higher exercise intensities, whereas pressor compensation was absent. The reasons for the exercise intensity dependence of the efficacy of vasodilatory compensation remain to be determined.