Cerebrovascular Reactivity in Resistance Trained Young Men

Abstract

Cerebrovascular reactivity is a measure of cerebrovascular function and is often used as an indicator of cerebrovascular health. There is evidence that habitual exercise can influence cerebrovascular reactivity; however, the effect of habitual exercise has only been examined in aerobic trained individuals or under the context of cardiorespiratory fitness. Therefore, the purpose of our study was to investigate the effect of chronic resistance training on cerebrovascular reactivity. We recruited 22 young men, including 11 untrained (UT; age = 27 ± 4 yr) and 11 resistance trained (RT; age = 24 ± 4 yr) individuals. Middle cerebral artery velocity (MCAv), beat‐to‐beat mean arterial blood pressure (MAP), and end‐tidal CO2 (ETCO2) were continuously monitored during a stepped hypercapnia protocol. In order to account for the influence of blood pressure on MCAv, cerebrovascular conductance index (CVCi) was calculated as MCAv/MAP × 100. MCAv, MAP, and CVCi reactivities were calculated as the linear relationship between each respective variable and ETCO2. There were no group differences in MCAv, MAP, CVCi, or ETCO2 during baseline or any level of the stepped hypercapnia (p > 0.05 for all). There was a trend for RT adults to have a higher MCAv reactivity, compared to UT adults (RT: 2.4 ± 0.4 cm/s/mmHg vs. UT: 1.7 ± 0.2 cm/s/mmHg; p = 0.06); however, there were no group differences in CVCi reactivity (RT: 1.5 ± 0.6 cm/s/mmHg2 vs. UT: 1.6 ± 0.2 cm/s/mmHg2; p = 0.41). Additionally, the MAP response to hypercapnia differed between the groups, as RT adults had a greater MAP reactivity compared with UT adults (RT: 0.98 ± 0.40 mmHg/mmHg vs. UT: 0.25 ± 0.08 mmHg/mmHg; p < 0.05). In conclusion, chronic resistance training likely influences cerebrovascular reactivity, as RT individuals had a larger MAP reactivity and a trend for greater MCAv reactivity, compared with UT individuals. Our results suggest that in young men, chronic resistance training may influence the hemodynamic response to a physiological stimulus, such as hypercapnia.Support or Funding InformationSupported by National Institute of Health grant HL118154This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.