Abstract
Aorta effectively buffers cardiac pulsatile fluctuation generated from the left ventricular (LV) which could be a mechanical force to high blood flow and low-resistance end-organs such as the brain. A dynamic orthostatic challenge may evoke substantial cardiac pulsatile fluctuation via the transient increases in venous return and stroke volume (SV). Particularly, this response may be greater in endurance-trained athletes (ET) who exhibit LV eccentric remodeling. The aim of this study was to determine the contribution of aortic compliance to the response of cerebral blood flow fluctuation to dynamic orthostatic challenge in ET and age-matched sedentary (SED) young healthy men. ET (n = 10) and SED (n = 10) underwent lower body negative pressure (LBNP) (−30 mmHg for 4 min) stimulation and release the pressure that initiates a rapid regain of limited venous return and consequent increase in SV. The recovery responses of central and middle cerebral arterial (MCA) hemodynamics from the release of LBNP (~15 s) were evaluated. SV (via Modeflow method) and pulsatile and systolic MCA (via transcranial Doppler) normalized by mean MCA velocity (MCAv) significantly increased after the cessation of LBNP in both groups. ET exhibited the higher ratio of SV to aortic pulse pressure (SV/AoPP), an index of aortic compliance, at the baseline compared with SED (P < 0.01). Following the LBNP release, SV was significantly increased in SED by 14 ± 7% (mean ± SD) and more in ET by 30 ± 15%; nevertheless, normalized pulsatile, systolic, and diastolic MCAv remained constant in both groups. These results might be attributed to the concomitant with the increase in aortic compliance assessed by SV/AoPP. Importantly, the increase in SV/AoPP following the LBNP release was greater in ET than in SED (P < 0.01), and significantly correlated with the baseline SV/AoPP (r = 0.636, P < 0.01). These results suggest that the aortic compliance in the endurance athletes is able to accommodate the additional SV and buffer the potential increase in pulsatility at end-organs such as the brain.
Highlights
Exaggerated hemodynamic fluctuation would be a profound mechanical force to high blood flow and lowresistance end-organs (O’rourke and Safar, 2005; Mitchell, 2008)
In left ventricular (LV) characteristics, LV end-diastolic dimension (LVEDd), LVESd, Left ventricular mass (LVM), LVM index (LVMi), posterior wall thicknesses (PWT), and interventricular septum (IVST) were significantly greater in endurance-trained athletes (ET) than SED, as expected
Mean and diastolic MCA velocity (MCAv) did not differ between the groups; whereas, the systolic and pulsatile MCAv in ET were significantly lower than SED (Table 2) with higher stroke volume (SV)/AoPP (2.2 ± 0.4 vs 2.7 ± 0.3 ml/mmHg, P < 0.01)
Summary
Exaggerated hemodynamic fluctuation would be a profound mechanical force to high blood flow and lowresistance end-organs (e.g., the brain and kidneys) (O’rourke and Safar, 2005; Mitchell, 2008). Smaller cardiac ejection (e.g., SV) is likely to be associated with smaller cerebrovascular hemodynamic fluctuation and vice versa (Sugawara et al, 2017) It is well-known that chronic endurance training induces the eccentric remodeling (e.g., increased chamber size) and superior compliance characteristics of the LV (Levine et al, 1991; Pluim et al, 2000; Scharhag et al, 2002; Caselli et al, 2011; Tomoto et al, 2015). Postural alteration evokes drastic gravitational hemodynamic changes such as greater pulsatile fluctuations of blood flow and blood pressure In this context, postural alteration-related volume loading (e.g., increased venous return) may cause the substantial change in SV in endurance-trained athletes. It is unknown the impact of rapid postural change on central and cerebral hemodynamics in endurance-trained individuals
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