Influence of acute dietary nitrate supplementation on oxygen delivery/consumption and critical impulse during maximal effort forearm exercise in males: a randomized crossover trial.

Beetroot juice supplementation (BRJ) should increase nitric oxide bioavailability under conditions of muscle deoxygenation and acidosis that are a normal consequence of the maximal effort exercise test used to identify forearm critical impulse. We hypothesized BRJ would improve oxygen delivery:demand matching and forearm critical impulse performance. Healthy males (20.8 ± 2.4 years) participated in a randomized crossover trial between October 2017 and May 2018 (Queen's University, Kingston, ON). Participants completed 10 min of rhythmic maximal effort forearm handgrip exercise 2.5 h post placebo (PL) vs. BRJ (9 completed PL/BRJ vs. 4 completed BRJ/PL) within a 2 week period. Data are presented as mean ± SD. There was a main effect of drink (PL > BRJ) for oxygen extraction (P = 0.033, ηp2 = 0.351) and oxygen consumption/force (P = 0.017, ηp2 = 0.417). There was a drink × time interaction (PL > BRJ) for oxygen consumption/force (P = 0.035, ηp2 = 0.216) between 75 and 360 s (1.25-6 min) from exercise onset. BRJ did not influence oxygen delivery (P = 0.953, ηp2 = 0.000), oxygen consumption (P = 0.064, ηp2 = 0.278), metabolites ((lactate) (P = 0.196, ηp2 = 0.135), pH (P = 0.759, ηp2 = 0.008)) or power-duration performance parameters (critical impulse (P = 0.379, d = 0.253), W' (P = 0.733, d = 0.097)). BRJ during all-out handgrip exercise does not influence oxygen delivery or exercise performance. Oxygen cost of contraction with BRJ is reduced as contraction impulse is declining during maximal effort exercise resulting in less oxygen extraction.

Influence of acute dietary nitrate supplementation on oxygen delivery/consumption and limit of tolerance during progressive forearm exercise in men: a randomized crossover trial.

Beetroot juice (BRJ) supplementation increases nitric oxide bioavailability with hypoxia and acidosis, characteristics of high-intensity exercise. We investigated whether BRJ improved forearm oxygen delivery:demand matching in an intensity-dependent manner. Healthy men (21 ± 2.5 years) participated in a randomized crossover trial between October 2017 and May 2018 (Queen's University, Kingston, ON, Canada). Participants completed a forearm incremental exercise test to limit of tolerance (IET-LOT) 2.5 h post placebo (PL) versus BRJ (2 completed PL/BRJ vs. 9 completed BRJ/PL) within a 2-week period. Data are presented as mean ± standard deviation. There was a significant main effect of drink (PL < BRJ; P = 0.042, ηp2 = 0.385) and drink × intensity interaction for arteriovenous oxygen difference (PL < BRJ; P = 0.03; ηp2= 0.197; 20%-50% and 90% LOT). BRJ did not influence oxygen delivery (P = 0.893, ηp2 = 0.002), forearm blood flow (P = 0.589, ηp2 = 0.03) (forearm vascular conductance (P = 0.262, ηp2 = 0.124), mean arterial pressure (P = 0.254,ηp2 = 0.128)), oxygen consumption (P = 0.194, ηp2 = 0.179) or LOT (P = 0.432, d = 0.247). In healthy men, BRJ did not improve forearm oxygen delivery (vasodilatory or pressor response) during IET-LOT. Increased arteriovenous oxygen difference at submaximal intensities did not significantly influence oxygen consumption or performance across the entire range of forearm exercise intensities. This study adds to the growing body of evidence that BRJ does not influence small muscle mass blood flow in humans regardless of exercise intensity.

Does a single bout maximal effort forearm exercise test for determining critical impulse result in maximal oxygen delivery and consumption in men? A randomized crossover trial.

In a single bout maximal effort isometric forearm handgrip exercise test (maximal effort exercise test, MXT), contraction impulse exhibits exponential decay to an asymptote equivalent to critical impulse (CI). It is unknown whether oxygen delivery (O2del) and consumption (V˙O2) achieved at CI are maximal. Healthy men participated in a randomized crossover trial at Queen's University (Kingston, ON) between October 2017-May 2018. Participants completed an MXT and forearm incremental exercise test to limit of tolerance (IET-LOT) (7 completed MXT followed by IET-LOT vs. 4 completed IET-LOT followed by MXT) within a 2 week period. Data are presented as mean ± standard deviation. Maximal forearm blood flow (FBF) and O2del were not different in 11 men (21 ± 2.5 years) between MXT and IET-LOT (FBF = 473.8 ± 132.2 mL/min vs. 502.3 ± 152.3 mL/min; P = 0.482, ηp2 = 0.015; O2del = 85.2 ± 23.5 mL/min vs. 92.2 ± 37.0 mL/min; P = 0.456, ηp2 = 0.012). However, MXT resulted in greater maximal V˙O2 than IET-LOT (44.5 ± 15.2 mL/min > 36.8 ± 11.4 mL/min; P = 0.007, ηp2 = 0.09), due to greater oxygen extraction (54.0 ± 10.0% > 44.4 ± 8.6%; P = 0.021, ηp2 = 0.185). As CI was 88.6 ± 8.2% of IET-LOT contraction impulse, maximal O2 cost of contractions in MXT was greater than IET-LOT (0.45 ± 0.14 mL/min/Ns > 0.33 ± 0.09 mL/min/Ns; P < 0.001, ηp2 = 0.166). In healthy men, MXT identifying CI results in similar peak oxygen delivery but greater peak V˙O2 via increased extraction compared to an IET-LOT, indicating increased oxygen cost. MXT-CI may better estimate maximal V˙O2 than traditional IET-LOT for this exercise modality.

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

KEY POINTS: The immediate increase in skeletal muscle blood flow following contraction is greater when the contracting muscle is below vs. above heart level. This has been attributed to muscle pump-mediated venous emptying and subsequent widening of the arterial to venous pressure gradient, which can occur below but not above heart level. However, alternative explanations could include greater rapid onset vasodilatation and/or transmural pressure-mediated mechanical distension of resistance vessels, but these remain unexplored. We demonstrate that active vasodilatation is not responsible for greater post-contraction hyperaemia below the heart. Instead, an increased transmural pressure-mediated mechanical distension of resistance vessels is a key mechanism responsible for this phenomenon. Our findings establish the importance of considering/accounting for local mechanical arteriolar distension effects when investigating exercise hyperaemia. They also inform the application of exercise for rehabilitative purposes and prompt investigation into whether arteriolar distension accompanying vasodilatation is reduced with diseases or ageing, thereby compromising exercising muscle perfusion. 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.