Abstract

Arterial stiffness is associated with cerebral flow pulsatility. Arterial stiffness increases following acute resistance exercise (RE). Whether this acute RE-induced vascular stiffening affects cerebral pulsatility remains unknown. Purpose: To investigate the effects of acute RE on common carotid artery (CCA) stiffness and cerebral blood flow velocity (CBFv) pulsatility. Methods: Eighteen healthy men (22 ± 1 yr; 23.7 ± 0.5 kg·m−2) underwent acute RE (5 sets, 5-RM bench press, 5 sets 10-RM bicep curls with 90 s rest intervals) or a time control condition (seated rest) in a randomized order. CCA stiffness (β-stiffness, Elastic Modulus (Ep)) and hemodynamics (pulsatility index, forward wave intensity, and reflected wave intensity) were assessed using a combination of Doppler ultrasound, wave intensity analysis and applanation tonometry at baseline and 3 times post-RE. CBFv pulsatility index was measured with transcranial Doppler at the middle cerebral artery (MCA). Results: CCA β-stiffness, Ep and CCA pulse pressure significantly increased post-RE and remained elevated throughout post-testing (p < 0.05). No changes in MCA or CCA pulsatility index were observed (p > 0.05). There were significant increases in forward wave intensity post-RE (p < 0.05) but not reflected wave intensity (p > 0.05). Conclusion: Although acute RE increases CCA stiffness and pressure pulsatility, it does not affect CCA or MCA flow pulsatility. Increases in pressure pulsatility may be due to increased forward wave intensity and not pressure from wave reflections.

Highlights

  • Increases in arterial stiffness with age and/or disease increases risk for cardiovascular events such as myocardial infarction and stroke (Sutton-Tyrrell et al, 2005; Mitchell et al, 2010)

  • Recent studies note a strong assocation between arterial stiffness, pressure/flow pulsatility and cerebral perfusion (Kwater et al, Abbreviations: resistance exercise (RE), Resistance exercise; cerebral blood flow velocity (CBFv), Cerebral blood flow velocity; repetition maximum (RM), Repetition maximum; SBP, Systolic blood pressure; diastolic brachial blood pressure (DBP), Diastolic blood pressure; common carotid artery (CCA), Common carotid artery; intima-media thickness (IMT), Intima-media thickness; mean arterial pressure (MAP), Mean arterial pressure; pulsatility index (PI), Pulsatility index; WIA, Wave intensity analysis; negative area (NA), Negative area; Ep, Elastic modulus; β, β Stiffness index, PP, Pulse pressure; Aix, Augmentation index; Wave separation analyses (WSA), Wave separation analysis; Pf, Forward wave pressure; Pb, Backwards wave pressure; middle cerebral artery (MCA), Middle cerebral artery; transcranial Doppler (TCD), Transcranial Doppler; CVRi, Cerebrovascular resistance index. 2009; Tarumi et al, 2011; Webb et al, 2012)

  • Post-hoc analyses revealed brachial SBP significantly increased immediately following RE and remained elevated for all post-RE time points compared to baseline (p < 0.05; Table 1)

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Summary

Introduction

Increases in arterial stiffness with age and/or disease increases risk for cardiovascular events such as myocardial infarction and stroke (Sutton-Tyrrell et al, 2005; Mitchell et al, 2010). Increased arterial stiffness contributes to target organ damage such as renal dysfunction and retinal damage (Katsi et al, 2012; Safar et al, 2012). The elastic properties of the large central arteries (i.e., aorta and carotid) function to dampen the amplitude of fluctuations in pressure and flow, thereby preventing transmission of excess energy into target organs (Mitchell et al, 2011). Repeated exposure of the cerebral vasculature to pulsatile pressure/flow may precipitate microvascular hypoperfusion and subsequent ischemia contributing to rarefaction, white matter hyperintensities and cerebrovascular impairment (Mitchell et al, 2005). Recent studies note a strong assocation between arterial stiffness, pressure/flow pulsatility and cerebral perfusion

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