No Effect of N‐acetylcysteine on Histamine‐receptor Mediated Sustained Post‐Exercise Vasodilation in Humans

Abstract

An acute bout of aerobic exercise elicits a sustained post‐exercise vasodilation which is histamine‐receptor mediated. This histaminergic vasodilation appears to be blunted by systemically infused high dose ascorbate, a potent antioxidant. However, ascorbate may catalyze the degradation of histamine in vivo. Therefore, we tested the hypothesis that systemically infusing high dose N‐acetylcysteine, an antioxidant with no known histaminergic interaction, would blunt sustained post‐exercise vasodilation. Eight healthy subjects performed 1 hr of unilateral dynamic knee extension at 60% of peak power on 2 separate days: 1) control, intravenous saline infusion and 2) intravenous N‐acetylcysteine infusion (primer dose, 125 mg kg⁻1 hr⁻1, maintenance dose, 25 mg kg⁻1 hr⁻1). Femoral artery blood flow (Doppler ultrasound) was measured before exercise and for 2h post‐exercise. Femoral vascular conductance was calculated as flow/pressure. Pre‐exercise femoral vascular conductance was similar for both conditions (P = 0.9). Compared with pre‐exercise, femoral vascular conductance was elevated throughout the recovery from exercise for both control (4.0 ± 0.1 ml min‐1 mmHg‐1) and N‐acetylcysteine conditions (4.0 ± 0.1 ml min‐1 mmHg‐1; P < 0.05). Femoral vascular conductance was similar between conditions throughout the recovery from exercise (P = 0.8). Taken together, these results suggest that the inhibition of sustained post‐exercise vasodilation by ascorbate was due to a direct degradative effect on histamine and not to the blunting of exercise‐induced oxidative stress.