Physiological Role of Endothelin-1 in Nonworking Muscles During Exercise in Healthy Subjects

Abstract

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. However, the role of ET-1 in exercise-induced physiological responses is still to be investigated. The purpose of the present study was to investigate in healthy volunteers whether the ET-1 plasma concentration in nonworking muscles is changed by exercise and to investigate the physiological role of ET-1 during exercise. Bicycle ergometer cardiopulmonary exercise tests were performed in 36 healthy men (mean age, 22.5 years). Blood samples for measuring ET-1 were drawn from the cubital vein during rest and immediately after the exercise test. The ET-1 change ratio was calculated as ET-1 immediately following exercise/ET-1 during the resting state. Cardiac output (CO) was measured during the exercise test by the impedance method. Arterial venous oxygen difference (AVO2D) when CO reached 10L/min or 15L/min was calculated as AVO2D = VO2/CO. Results were as follows: (1) the ET-1 change ratio correlated inversely with exercise time at the anaerobic threshold (r = -0.37, p = 0.03) and peak exercise time (r = -0.35, p = 0.04); (2) the ET-1 change ratio tended toward an inverse correlation with deltaVO2/deltawork rate (r = -0.29, p = 0.09); (3) the ET-1 change ratio correlated positively with AVO2D when CO reached 10L/min (r = 0.42, p = 0.02) and tended toward a positive correlation with AVO2D when CO reached 15 L/min (r = 0.32, p = 0.08). These results indicate that an increase in ET-1 in nonworking muscles may participate in the exercise-induced redistribution of blood flow and in increasing the blood flow to working muscles.

Increased endothelin-1 and diminished nitric oxide levels in blister fluids of patients with intermediate cold type complex regional pain syndrome type 1

“…It is unclear what the effect of disuse on the production of ET-1 and NO could be, but the plasma NOx concentration in healthy young humans significantly increases after exercise, with a significant decrease of ET-1 [41]. In healthy subjects, the physiological role of ET-1 in nonworking muscles during exercise has been described [42]. In healthy women, the ET-1 plasma concentration increases with age, which could be significantly counteracted after exercise [43].…”

Impaired Exercise-Induced Vasodilatation in Chronic Atrial Fibrillation. Role of Endothelium-Derived Nitric Oxide.

“…18 It is possible that the irregularity of the pulsatile flow and pressure in AF similarly depresses NO synthase expression. Third, hemostatic factors such as fibrin monomer and fibrinogen degradation products, 15,19 vasoactive molecules such as angiotensin II 20 and endothelin 21,22 or the autonomic nervous system 23 may also be responsible. Finally, oxidative stress in AF should be considered.…”

Relationship Between Impaired Chronotropic Response, Cardiac Output During Exercise, and Exercise Tolerance in Patients with Chronic Heart Failure

“…CO measurement by an invasive method, the direct Fick method, or thermodilution, seemed to be difficult to perform during an exercise test in an outpatient department. Although the reliability of thoracic bioimpedance has been reported in two of our previous · · · · studies, 15,22) CO measurement using an invasive method is recommended in order to arrive at more definite conclusions.…”