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One Session of High‐Intensity Interval Training Acutely Enhances the Sensitivity of Cerebral Vasoreactivity Post‐Exercise in Young Healthy Males
Author(s) -
Martinez Mauricio,
Salvador Paolo,
Schoech Lauren,
Clark Cayla,
Gonzales Joaquin U.,
Rivas Eric
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.04879
Subject(s) - medicine , supine position , cardiorespiratory fitness , high intensity interval training , middle cerebral artery , cerebral blood flow , cardiology , transcranial doppler , anesthesia , ischemia
Background Cardiorespiratory fitness and exercise training are associated with improved cerebral vasoreactivity of the middle cerebral artery (MCA vmean ). High‐intensity interval exercise training (HIIT) is an effective time‐efficient alternative to long‐duration lower‐intensity exercise that offers similar vascular benefits. It is currently unclear whether HIIT acutely alters cerebral cerebrovascular function. Purpose This project tested the hypothesis that a single session of HIIT would enhance cerebrovascular reactivity after exercise. Methods Five healthy active (7‐day activity: 9140±3525 steps·day; VO 2 max: 55±6.3 mLO 2 ·kg·min −1 ) adults (22.4±1.9y, 175.9±5.1cm, 77.1±5.1kg) completed one session of HIIT exercise comprised of four bouts of four‐minute intervals at 65% watt max (between 85–95% maximal heart rate [HR]) with three‐minute recovery between at 15% watt max (between 50–65% HRmax). Transcranial Doppler MCA vmean assessed hypercapnia induced cerebral vasoreactivity using a three‐minute rebreathing technique in a supine rest position, before and 30‐minutes after the HIIT. Dose‐response curves (non‐linear log‐transformed) examined the sensitivity of cerebral vasoreactivity to increased concentrations of the partial pressure of end‐tidal CO 2 (Torr). Parameters derived from the dose‐response curve included half‐maximal effective concentration (EC 50 ), LogEC 50 , and HillSlope. Systemic hemodynamics including mean arterial pressure (MAP), systemic vascular resistance (SVR) and HR were also measured during the rebreathe test. MCA vmean cerebral vascular conductance (CVC) was calculated by MCA vmean /MAP. Paired t‐tests were used to compare the pre‐ to post‐HIIT changes in parameters. Alpha prior was set at P <0.05. Results The sensitivity of cerebral vasoreactivity improved from pre to post‐HIIT exercise as reflected by lower MCA vmean EC 50 (Δ3.0±1.5 Torr, P <0.006) and LogEC 50 (Δ0.03±0.02 Log Torr, P <0.008) post‐exercise. MCA vmean HillSlope showed a trend for significance ( P <0.06). Systemically, MAP (Δ9.6±7.7 mmHg, P <0.02) and SVR (Δ343.2±242.5 dynes·s 1 ·cm 5 , P <0.002) were both lower and HR (Δ18±7 b/min, P <0.002) was increased post‐exercise. When accounted for post‐exercise hypotension, MCA vmean CVC EC 50 (Δ4.2±2.0 Torr, P <0.007) and LogEC 50 (Δ0.04±0.02 Log Torr, P <0.001) were also improved post‐exercise; however, MCA vmean CVC HillSlope was not different ( P =0.30) between conditions. Conclusion These preliminary data suggest that a single session of HIIT exercise may improve the sensitivity of cerebral vasoreactivity in young healthy males. This may in part be due to changes in peripheral hemodynamics such as baroreflex mediated alterations in MAP, SVR, and HR post‐exercise. These preliminary findings give insight into an integrative relationship between cerebral and peripheral blood flow during recovery from high‐intensity exercise and the benefits of HIIT on cerebrovascular health.