Exhaustive exercise-induced tissue hypoxia does not change endothelin and big endothelin plasma levels in normal volunteers

Abstract

Chronic hypoxia has been shown to increase plasma endothelin levels. The current study was undertaken to examine the effect of exerciseinduced tissue hypoxia on plasma levels of endothelin-1 (ET-1) and its precursor big endothelin-1 (Big-ET-1). After approval by the local ethical committee an incremental dynamic exercise test was performed in 12 physically trained volunteers (aged 20 to 40 years), using an electrically braked bicycle ergometer. The protocol included a step-wise increase of the workload until a heart rate of 130/min was reached, followed by a maintenance period of 25 min, and a further stepwise increase until exhaustion. Blood was drawn before, at several time points during, and 5 min after termination of the study for determination of ET-1, Big-ET-1, plasma renin activity (PRA), angiotensin converting enzyme (ACE), norepinephrine, epinephrine, and lactate. Lactate levels at baseline were 14.5 ؎ ؎ 1.6 mg/dL (mean ؎ ؎ SEM), which increased to 76.5 ؎ 4.8 mg/dL at the time of exhaustion (P < < .01). Baseline values for ET-1 and Big-ET-1 were 0.264 ؎ ؎ 0.061 and 0.637 ؎ ؎ 0.130 fmol/ml, respectively, which remained essentially unaltered throughout the exercise test. PRA was 1.46 ؎ ؎ 0.45 ng/mL/h before exercise and increased to 3.55 ؎ ؎ 0.96 ng/mL/h at exhaustion (P < < .001). Norepinephrine and epinephrine were also increased at exhaustion. The study demonstrates that exhaustive physical exercise with acute development of pronounced tissue hypoxiain contrast to chronic hypoxia-does not influence the release of ET-1 or Big-ET-1 or the conversion of the precursor to the active compound. Unlike endothelin, circulating renin and the catecholamines were markedly stimulated by this maneuver. Am

Endothelin-1 concentration in plasma is increased after jogging but decreased after cycling in healthy men

“…The finding in the present study of decreased plasma ET-1 levels after cycling is in agreement with the data of Richter et al [9], whereas others reported no change [19][20][21][22] or even an increase in ET-1 plasma concentrations in young athletes performing 30 min of strenuous cycling [8]. These discrepancies may be due to the small numbers of subjects investigated [21] or to differences in the protocols used, e.g., intensity of exercise [8], time of blood sampling after performance [20], or assays used for ET measurements [20,21].…”

Endothelin Stimulates Glucose Uptake and GLUT4 Translocation via Activation of Endothelin ETA Receptor in 3T3-L1 Adipocytes

“…It is now well accepted that the plasma ET-1 level is significantly elevated under hypoxic conditions (30). It has also been reported that exercise tends to elevate ET-1 in plasma and in major organs such as heart and kidney (31)(32)(33)(34), although these results are not as conclusive as the hypoxia studies (35). So far, there is no report on whether hypoxia/exercise-induced increase in ET-1 is linked to glucose metabolism.…”

The acute effects of exercise and glucose ingestion on circulating angiotensin-converting enzyme in humans

“…It is possible that subject age (children vs adults) and the particular exercise parameters used in the current study and that by Fyhrquist et al (1983) [non-incremental and thus of sustained lower intensity than Lenz et al (1998) and Arvay et al (1982)] can explain the differences between studies. Thus, it is possible that higher intensity exercise may elicit an acute response of circulating ACE activity in adults.…”

“…Previous studies conducted in a normoxic environment using asymptomatic individuals have reported a reduction in circulating ACE activity in response to a steady-state plus incremental exercise protocol in adults (Lenz et al 1998), an increase in circulating ACE activity in response to incremental exercise in children (Avray et al 1982), and no change in response to a marathon run in adults (Fyhrquist et al 1983). It is possible that subject age (children vs adults) and the particular exercise parameters used in the current study and that by Fyhrquist et al (1983) [non-incremental and thus of sustained lower intensity than Lenz et al (1998) and Arvay et al (1982)] can explain the differences between studies.…”

“…Circulating ACE activity seems to fall during low-intensity (50 W) exercise performed under conditions of hypoxia, possibly as a result of changes in renal haemodynamics (Milledge and Catley 1982). Thirty minutes of submaximal exercise followed by incremental exercise to exhaustion has also produced a fall in circulating ACE activity (Lenz et al 1998). In contrast, circulating ACE activity has been shown to remain unchanged following a marathon run (Fyhrquist et al 1983).…”