Relationship between aerobic endurance training and dynamic cerebral blood flow regulation in humans

Abstract

The incidence of orthostatic intolerance is elevated in endurance-trained individuals. We sought to test the hypothesis that aerobic endurance training is associated with an attenuated control of the cerebral vasculature. Endurance trained (ET, n = 13) and age-matched untrained (UT, n = 11) individuals (peak O2 consumption, mean ± SEM; 63 ± 1 vs 42 ± 1 mL/min/kg, P < 0.05) were examined while supine and seated upright. Dynamic cerebral autoregulation (CA) was assessed by calculation of the rate of regulation (RoR) from the arterial blood pressure (ABP) and middle cerebral artery (MCA) mean blood velocity (V mean ) responses to a bilateral thigh cuff release, which evoked a transient hypotension. Cerebral oxygenation (oxyhemoglobin; HbO2 ) was determined with near-infrared spectroscopy. When seated upright, cuff release evoked a greater decrease in ABP (P < 0.001), MCA V mean (P = 0.096) and HbO2 (P < 0.001) in ET compared with UT. However, RoR was similar in ET and UT individuals while seated upright (to 0.193 ± 0.039 vs 0.129 ± 0.029/s, P > 0.05), and there was no significant difference in the relative change in RoR from the supine to upright positions (ΔRoR: -65 ± 7 and -69 ± 7%, for ET and UT, respectively). These findings suggest that aerobic endurance training is not associated with an attenuation in dynamic CA.

Implications of habitual endurance and resistance exercise for dynamic cerebral autoregulation

“…Our finding of no difference in dCA between endurance and sedentary is consistent with results from others using repeated sit–stand manoeuvres (Aengevaeren et al., ) and bilateral thigh cuff release in the upright position (Ichikawa et al., ). However, some authors have reported an increased gain and normalized gain during forced oscillations in MAP produced by repeated squat–stand manoeuvres (Labrecque et al., ) and bilateral thigh cuff release, respectively (Lind‐Holst et al., ) – indicative of a reduced damping ability of the cerebral circulation.…”

“…In comparison to healthy sedentary individuals, endurance‐trained individuals demonstrate larger decreases in MAP, MCAv and cerebral oxygenation during upright thigh cuff release (Ichikawa et al., ) and are more prone to syncope (Levine et al., ) – indicating reduced dCA in endurance athletes during hypotensive challenges. However, Ichikawa et al.…”

“…However, Ichikawa et al. () found no change in rate of regulation in the upright position – functionally significant given the threat orthostasis presents to the cerebral circulation. While comparing studies that used differential analyses is difficult (Tzeng et al., ), we have shown increased TFA‐derived gain during 0.10 Hz MAP oscillations in endurance athletes, utilizing the same technique employed in the current study (Labrecque et al., ).…”

“…Ichikawa et al. (), using the same thigh cuff release method, demonstrated no difference in the slope of the linear regression line of cerebrovascular conductance index over time in the upright position – known as the rate of regulation. Notably, in the same study they reported that the rate of regulation was actually reduced in endurance‐trained individuals in the supine position.…”

Blood flow in internal carotid and vertebral arteries during graded lower body negative pressure in humans

“…Also, an acute hypotension-induced large drop in CBF does not cause syncope even with perfusion pressure below the lower end of the cerebral autoregulation curve (Carey et al 2001b;Ogoh et al 2008Ogoh et al , 2010. In addition, dynamic cerebral autoregulation, one of the CBF regulatory mechanisms, is well preserved in patients with syncope (Carey et al 2001b) and in highly fit athletes who are experiencing orthostatic intolerance (Ichikawa et al 2013). Carbon dioxide levels and indices of cerebrovascular resistance decrease during presyncope, but presyncopal cerebrovascular changes appear to be similar in patients with recurrent vasovagal syncope and in subjects with no previous syncopal symptoms (Carey et al 2001a).…”