Dissociated Response of Aldosterone from Plasma Renin Activity During Prolonged Exercise Under Hypoxia

Abstract

6 healthy male subjects on a fixed salt-diet performed 1 hour ergocycle exercise at 65% of VO2 max in normoxic (N) and hypoxic (H) conditions. Blood samples were taken at intervals for estimations of plasma aldosterone (PAC), angiotensin converting enzyme (ACE), adrenocorticotrophic hormone (ACTH) and catecholamine concentrations. Plasma volume reductions with exercise were similar in N (4.3 +/- 1%) and H (4.0 +/- 1%). PRA response to exercise was increased by hypoxia while PAC and plasma catecholamine rose to a similar extent in both conditions. Increases in ACTH concentration occurred at the end of exercise but no difference was found between high and low altitudes. Plasma ACE remained unchanged throughout exercise in either condition. These results indicate that hypoxemia interferes with PRA-mediated aldosterone secretion. The variations in plasma ACTH levels during exercise in hypoxia do not appear responsible for this interference.

The serum angiotensin-converting enzyme and angiotensin II response to altered posture and acute exercise, and the influence of ACE genotype

“…Our data confirm that Ang II levels rise in response to exercise, as has been previously suggested (Aldigier et al 1993;Bouissou et al 1988;Braith et al 1999;Fyhrquist et al 1983;Kinugawa et al 1997;Kosunen and Pakarinen, 1976;Kraemer et al 1999;Miura et al 1994). Our data are contributory, however, as they help delineate its timecourse more completely, demonstrating rapid rises in response to exercise.…”

“…Some clarification of existing data is thus provided. Bouissou et al (1988) also studied males, using an exercise stimulus of similar nature (bicycle ergometer) and workload (65% of _ V O 2max ), although of longer duration (1 h). They found no change in ACE activity.…”

“…This suggests that exercise-related changes in ACE activity may be of greater importance than basal activity. To date, whether such changes occur at all, or whether they might be ACE-genotype dependent, is not clear; studies relating to the impact of exercise on ACE activity are sparse (Aldigier et al 1993;Bouissou et al 1988;Fyhrquist et al 1983;Miura et al 1994), and their negative findings attributable to small sample size [6-8 subjects (Aldigier et al 1993;Bouissou et al 1988;Miura et al 1994)] and inconsistent stimulus [33 subjects from three different marathons (Fyhrquist et al 1983)]. No studies have yet examined the impact of genotype on any such putative changes.…”

“…Studies of the changes in Ang II levels with exercise have, however, been similarly sparse and difficult to interpret, having used unstandardised stimuli (Fyhrquist et al 1983) or exhaustive resistance exercise likely to induce a Ôstress responseÕ (Kraemer et al 1999), and mixed-sex cohorts (Kinugawa et al 1997) or diseased subjects (Braith et al 1999), often in very small numbers (Bouissou et al 1988). Meanwhile, although resting Ang II levels have been reported to be independent of ACE genotype in sedentary subjects (Chadwick et al 1997;Harrap et al 1993), no studies have yet addressed any association of ACE genotype with exercise-related change in Ang II levels.…”

Angiotensin-Converting Enzyme and Genetics at High Altitude

“…ACE activity is reduced in dogs (Leuenberger et al, 1978) and rats (Jin et al, 1987) in response to acute hypoxia, but not in humans (Colice and Ramirez, 1985, Milledge and Catley, 1987, Bouissou et al, 1988, Millar et al, 1995. Reduced transpulmonary angiotensin I conversion does occur in hypoxia (Jackson, Narkates andOparil, 1986, Peacock andMatthews, 1992) however, and the decreased level of ACE associated with the I allele could have advantageous effects in a number of ways.…”