Effect of antioxidants on histamine receptor activation and sustained postexercise vasodilatation in humans

Abstract

An acute bout of aerobic exercise elicits a sustained post-exercise vasodilatation that is mediated by histamine H1 and H2 receptor activation. However, the upstream signaling pathway that leads to post-exercise histamine receptor activation is unknown. We tested the hypothesis that the potent antioxidant ascorbate would inhibit this histaminergic vasodilatation following exercise. Subjects performed 1 hr unilateral dynamic knee extension at 60% of peak power in three conditions: 1) control; 2) intravenous ascorbate infusion; and, 3) ascorbate infusion plus oral H1/H2 histamine receptor blockade. Femoral artery blood flow (Doppler ultrasound) was measured before exercise and for 2 hr post-exercise. Femoral vascular conductance was calculated as flow/pressure. Post-exercise vascular conductance was greater for control condition (3.4 ± 0.1 ml min−1 mmHg−1) compared with ascorbate (2.7 ± 0.1 ml min−1 mmHg−1, P < 0.05) and ascorbate plus H1/H2 blockade (2.8 ± 0.1 ml min−1 mmHg−1, P < 0.05), which did not differ from one another (P = 0.9). Because ascorbate may catalyze the degradation of histamine in vivo, we conducted a follow-up study where subjects performed exercise in two conditions: 1) control and 2) intravenous N-acetylcysteine infusion. Post-exercise vascular conductance was similar for control (4.0 ± 0.1 ml min−1 mmHg−1) and N-acetylcysteine conditions (4.0 ± 0.1 ml min−1 mmHg−1; P = 0.8). Thus, the results in study 1 were due to the degradation of histamine in skeletal muscle by ascorbate, since the histaminergic vasodilatation was unaffected by N-acetylcysteine. Taken together, exercise-induced oxidative stress does not appear to contribute to sustained post-exercise vasodilatation.

Evidence of a broad histamine footprint on the human exercise transcriptome

“…; Romero et al . ). Femoral vascular conductance (ml min −1 mmHg −1 ) was calculated by dividing femoral blood flow by mean arterial pressures.…”

Acute lower leg hot water immersion protects macrovascular dilator function following ischaemia–reperfusion injury in humans

“…Data were averaged across 1 min bins at each indicated time point. Blood velocity measurements were determined from Doppler ultrasound audio recordings using an intensity‐weighted algorithm (custom software), subsequent to demodulation of forward and reverse Doppler frequencies (Buck, Sieck, & Halliwill, ; Romero et al., , , ). Vessel diameter was determined using custom edge‐detection and wall‐tracking software (Black, Cable, Thijssen, & Green, ; Woodman et al., ).…”

<p>Effective prevention of sorafenib-related vascular damage induced adverse events and maintenance of hepatic function by dried bonito broth and histidine</p>

“…The present study also showed that DBB and HIS maintained the PV vascular area, with HIS having a more marked effect (Figure 4). This effect of HIS on venous dilatation has been reported as a histamine-mediated vasodilatation14,21 and has been used clinically to maintain endothelium and smooth muscle function in the human saphenous vein transplant 15. In addition, as previously reported,22–24 our study showed that the maintenance of PV flow contributed to the management of hepatic function, including serum levels of ALB, during chemotherapy (Figure 6).…”