INFLUENCES OF BEDREST DECONDITIONING ON ORTHOSTATIC HYPERTENSION RISK

Abstract

Objective: Orthostatic hypertension defined as systolic blood pressure (SBP) increase of more than 20 mmHg when standing up with hypertensive upright SBP heralds increased cardiovascular risk. The phenomenon is caused by sympathetic overactivation and occurs in conditions associated with poor cardiopulmonary fitness or hypovolemia. We hypothesized that head-down tilt bedrest, which induces cardiopulmonary deconditioning, hypovolemia, and sympathetic activation increases the likelihood of experiencing orthostatic hypertension. Design and method: We pooled data from two strict head-down tilt bedrest studies, the 60 days AGBRESA study (n=24, 8 women/ 16 men, 33.3±9 years) and the 30 days SANS countermeasure study (n=47, 20 women/ 27 men, 35±9 years), which both included healthy persons on no medications. In both studies, participants were on controlled sodium diets and caloric intake was adjusted to maintain body weight. Before and immediately after bedrest, we measured supine and upright blood pressure and heart rate during head-up tilt testing. We measured plasma volume using carbon monoxide rebreathing before and after bedrest. Results: Supine SBP was 128±9 mmHg before and 133±10 mmHg after bedrest (p<0.0001). While 5 minutes standing, SBP changed 2±8 mmHg before and 3±8 mmHg after bedrest (p=0.5825). 1 out of 67 participants fulfilled diagnostic criteria of orthostatic hypertension before and 3 out of 57 after bedrest. Supine heart rate was 69±11 bpm before and 79±15 bpm after bedrest (p<0.0001). With standing, heart rate increased 21±12 bpm before and 39±16 bpm after bedrest (p<0.0001). Plasma volume decreased by 367±348 ml with bedrest (p<0.0001). Conclusions: We conclude that in most healthy persons, cardiovascular deconditioning and volume loss associated with long-term bedrest are not sufficient to elicit orthostatic hypertension. There may be a smaller subgroup of susceptible individuals.