Abstract
Background: Arterial and central venous blood pressures are reduced following exercise, which contributes to exercise being a key anti-hypertensive therapy and facilitates expansion of blood volume. However, the effects of exercise intensity, duration and exercising limb on post-exercise hypotension and hypervolaemic responses are not resolved. Therefore, the purposes of this study were to identify the acute (<24 h) profiles of arterial blood pressure and blood volume for (i) endurance (END) compared with repeated high-intensity exercise (RHIE) performed with the lower body (RHIELower), and (ii) RHIELower compared with the upper body (RHIEUpper). It was hypothesised that post-exercise hypotension and plasma volume expansion would be similar between END and RHIELower, whereas RHIEUpper would stimulate a smaller response compared to RHEILower.
Methods: Twelve untrained males (age: 23 ± 3 y; body mass: 72.4 ± 12.8 kg, : 43.6 ± 7.6 mL•kg-1•min-1, mean ± SD) completed one END (50 min at 65% ), one RHIELower and one RHIEUpper exercise trial (both RHIE, five 30-s maximal sprints with 4.5-min recovery) in balanced order, ~2 wk apart. Measurements were taken at baseline, during exercise (cycle ergometry), continuously (beat-to-beat blood pressure) or at 15-min intervals (haemoglobin and haematocrit) throughout the first 3-h seated recovery, then at 8 and 22 h. Responses were modelled for key parameters (e.g., nadir) before inferential analysis for effects of exercise intensity and limb using a pre-post crossover model.
Results: RHIELower stimulated a larger post-exercise hypotensive response (AUC) than did END (7540 ± 3853 vs. 3897 ± 2757 mm Hg•min, p=0.05, CI: 20 – 6764 mm Hg•min), whereas similar responses were evident for exercising different limbs (RHIEUpper 6420 ± 3947, p=0.48, CI: -5157 - 2635 mm Hg•min). In contrast, arterial blood pressure at 22 h was reduced after END (-8 ± 8 mm Hg) but not after RHIELower (0 ± 7 mm Hg, p=0.04, CI: 0.6 - 15 mm Hg) or RHIE Upper. Plasma volume expansion at 22 h was similar (CI: -5 – 5%) for END (+5 ± 5%) and RHIELower (+5 ± 5%), as well as for RHIEUpper (5 ± 7%, CI: -8 – 6%).
Conclusions: The different post-exercise hypotension responses between endurance and RHIE, implicates peripheral dilatory factors associated with exercise intensity. Yet, the similar hypotensive responses between lower- and upper-body RHIE implicates a central component unrelated to the vascular bed used during the exercise. At 22 h, the decreased blood pressure after endurance exercise indicates that the sympathetic nervous system and stress hormones may still be elevated or that a lack of endothelial function following RHIE may occur. Similar plasma volume expansion 22 h following exercise irrespective of exercise intensity and exercising limb indicates that a variety of exercise regimes might be acceptable in inducing hypervolaemia, and was not obviously related to different hypotensive responses. These findings collectively allow a better comprehension of the training response to different exercise stimuli, along with providing evidence for the use of a variety of exercise regimes that could be used by different populations (hypertensive, time constrained, paraplegic) to access the health benefits of exercise.