Greater post‐contraction hyperaemia below vs. above heart level: the role of active vasodilatation vs. passive mechanical distension of arterioles

Abstract

We tested the hypotheses that increased post‐contraction hyperaemia in higher (H; below heart) vs. lower (L; above heart) transmural pressure conditions is due to (1) greater active vasodilatation or (2) greater transmural pressure‐mediated arteriolar distension. Participants (n = 20, 12 male, 8 female; combined mean age 24.5 ± 2 years) performed a 2 s isometric handgrip contraction, where arm position was maintained within or changed between H and L during contraction, resulting in four starting–finishing arm position conditions (LL, HL, LH, HH). Post‐contraction forearm blood flow (echo and Doppler ultrasound) was higher with contraction release in H vs. L environments (P < 0.05). However, contraction initiated in H did not result in greater vasodilatation (forearm vascular conductance; FVC) than contraction initiated in L, regardless of contraction release condition (peak FVC: LL 217 ± 104 vs. HL 204 ± 92 ml min−1 (100 mmHg)−1, P = 0.313, LH 229 ± 8 vs. HH 225 ± 85 ml min−1 (100 mmHg)−1, P = 0.391; first post‐contraction cardiac cycle FVC: same comparisons, both P = 0.317). However, FVC of the first post‐contraction cardiac cycle was greater for contractions released in H vs. L regardless of pre‐contraction condition (LL 106 ± 67 vs. LH 152 ± 76 ml min−1 (100 mmHg)−1, P < 0.05; HL 80 ± 51 vs. HH 119 ± 58 ml min−1 (100 mmHg)−1, P < 0.05). These findings refute the hypothesis that greater hyperaemia following a single contraction in higher transmural pressure conditions is due to greater active vasodilatation. Instead, our findings reveal a key role for increased transmural pressure‐mediated mechanical distension of arterioles in creating a greater increase in vascular conductance for a given active vasodilatation following skeletal muscle contraction.