Caitlin A Dow1, Brian L Stauffer1,2,3, Danielle L Brunjes1, Jared J Greiner1, Christopher A DeSouza1,2. 1. Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, CO, 80309, USA. 2. Department of Medicine, University of Colorado Anschutz Medical Center, Aurora, CO, 80045, USA. 3. Denver Health Medical Center, Denver, CO, 80204, USA.
Abstract
NEW FINDINGS: What is the central question of this study? Does aerobic exercise training reduce endothelin-1 (ET-1)-mediated vasoconstrictor tone in overweight/obese adults? And, if so, does lower ET-1 vasoconstriction underlie the exercise-related enhancement in endothelium-dependent vasodilatation in overweight/obese adults? What is the main finding and its importance? Regular aerobic exercise reduces ET-1-mediated vasoconstrictor tone in previously sedentary overweight/obese adults, independent of weight loss. Decreased ET-1 vasoconstriction is an important mechanism underlying the aerobic exercise-induced improvement in endothelium-dependent vasodilator function in overweight/obese adults. Endothelin-1 (ET-1)-mediated vasoconstrictor tone is elevated in overweight and obese adults, contributing to vasomotor dysfunction and increased cardiovascular disease risk. Although the effects of habitual aerobic exercise on endothelium-dependent vasodilatation in overweight/obese adults have been studied, little is known regarding ET-1-mediated vasoconstriction. Accordingly, the aims of the present study were to determine the following: (i) whether regular aerobic exercise training reduces ET-1-mediated vasoconstrictor tone in overweight and obese adults; and, if so, (ii) whether the reduction in ET-1-mediated vasoconstriction contributes to exercise-induced improvement in endothelium-dependent vasodilatation in this population. Forearm blood flow (FBF) in response to intra-arterial infusion of selective ETA receptor blockade (BQ-123, 100 nmol min-1 for 60 min), acetylcholine [4.0, 8.0 and 16.0 μg (100 ml tissue)-1 min-1 ] in the absence and presence of ETA receptor blockade and sodium nitroprusside [1.0, 2.0 and 4.0 μg (100 ml tissue)-1 min-1 ] were determined before and after a 3 month aerobic exercise training intervention in 25 (16 men and nine women) overweight/obese (body mass index 30.1 ± 0.5 kg m-2 ) adults. The vasodilator response to BQ-123 was significantly lower (∼25%) and the FBF responses to acetylcholine were ∼35% higher after exercise training. Before the exercise intervention, the co-infusion of acetylcholine plus BQ-123 resulted in a greater vasodilator response than acetylcholine alone; however, after the exercise intervention the FBF response to acetylcholine was not significantly increased by ETA receptor blockade. These results demonstrate that regular aerobic exercise reduces ET-1-mediated vasoconstrictor tone in previously sedentary overweight and obese adults. Moreover, decreased ET-1-mediated vasoconstriction is an important mechanism underlying the aerobic exercise-induced improvement in endothelium-dependent vasodilator function in overweight/obese adults.
NEW FINDINGS: What is the central question of this study? Does aerobic exercise training reduce endothelin-1 (ET-1)-mediated vasoconstrictor tone in overweight/obese adults? And, if so, does lower ET-1 vasoconstriction underlie the exercise-related enhancement in endothelium-dependent vasodilatation in overweight/obese adults? What is the main finding and its importance? Regular aerobic exercise reduces ET-1-mediated vasoconstrictor tone in previously sedentary overweight/obese adults, independent of weight loss. Decreased ET-1 vasoconstriction is an important mechanism underlying the aerobic exercise-induced improvement in endothelium-dependent vasodilator function in overweight/obese adults. Endothelin-1 (ET-1)-mediated vasoconstrictor tone is elevated in overweight and obese adults, contributing to vasomotor dysfunction and increased cardiovascular disease risk. Although the effects of habitual aerobic exercise on endothelium-dependent vasodilatation in overweight/obese adults have been studied, little is known regarding ET-1-mediated vasoconstriction. Accordingly, the aims of the present study were to determine the following: (i) whether regular aerobic exercise training reduces ET-1-mediated vasoconstrictor tone in overweight and obese adults; and, if so, (ii) whether the reduction in ET-1-mediated vasoconstriction contributes to exercise-induced improvement in endothelium-dependent vasodilatation in this population. Forearm blood flow (FBF) in response to intra-arterial infusion of selective ETA receptor blockade (BQ-123, 100 nmol min-1 for 60 min), acetylcholine [4.0, 8.0 and 16.0 μg (100 ml tissue)-1 min-1 ] in the absence and presence of ETA receptor blockade and sodium nitroprusside [1.0, 2.0 and 4.0 μg (100 ml tissue)-1 min-1 ] were determined before and after a 3 month aerobic exercise training intervention in 25 (16 men and nine women) overweight/obese (body mass index 30.1 ± 0.5 kg m-2 ) adults. The vasodilator response to BQ-123 was significantly lower (∼25%) and the FBF responses to acetylcholine were ∼35% higher after exercise training. Before the exercise intervention, the co-infusion of acetylcholine plus BQ-123 resulted in a greater vasodilator response than acetylcholine alone; however, after the exercise intervention the FBF response to acetylcholine was not significantly increased by ETA receptor blockade. These results demonstrate that regular aerobic exercise reduces ET-1-mediated vasoconstrictor tone in previously sedentary overweight and obese adults. Moreover, decreased ET-1-mediated vasoconstriction is an important mechanism underlying the aerobic exercise-induced improvement in endothelium-dependent vasodilator function in overweight/obese adults.
Authors: Tatiana Moro; Camille R Brightwell; Rachel R Deer; Ted G Graber; Elfego Galvan; Christopher S Fry; Elena Volpi; Blake B Rasmussen Journal: J Nutr Date: 2018-06-01 Impact factor: 4.798
Authors: Zachary I Grunewald; Thomas J Jurrissen; Makenzie L Woodford; Francisco I Ramirez-Perez; Lauren K Park; Ryan Pettit-Mee; Thaysa Ghiarone; Scott M Brown; Mariana Morales-Quinones; James R Ball; Kevin F Staveley-O'Carroll; Annayya R Aroor; Paul J Fadel; Pierre Paradis; Ernesto L Schiffrin; Shawn B Bender; Luis A Martinez-Lemus; Jaume Padilla Journal: Hypertension Date: 2019-10-21 Impact factor: 10.190
Authors: Adeola A Sanni-Ajibaye; Anson M Blanks; Cassandra C Derella; Abigayle B Simon; Paula Rodriguez-Miguelez; Jacob Looney; Jinhee Jeong; Jeffrey Thomas; David W Stepp; Neal L Weintraub; Xiaoling Wang; Ryan A Harris Journal: Physiol Rep Date: 2022-05
Authors: Kelly A Stockelman; Anthony R Bain; Caitlin A Dow; Kyle J Diehl; Jared J Greiner; Brian L Stauffer; Christopher A DeSouza Journal: Am J Physiol Heart Circ Physiol Date: 2021-01-08 Impact factor: 4.733
Authors: Isabel Witvrouwen; Dominique Mannaerts; An M Van Berendoncks; Yves Jacquemyn; Emeline M Van Craenenbroeck Journal: Front Physiol Date: 2020-05-08 Impact factor: 4.566