TY - JOUR
T1 - Effects of electrical muscle stimulation on cerebral blood flow
AU - Ando, Soichi
AU - Takagi, Yoko
AU - Watanabe, Hikaru
AU - Mochizuki, Kodai
AU - Sudo, Mizuki
AU - Fujibayashi, Mami
AU - Tsurugano, Shinobu
AU - Sato, Kohei
N1 - Funding Information:
This study was supported in part by the Japan Society for the Promotion of Science KAKENHI (Grant Number: 16H03230) to Soichi Ando. Authors have used the grant for acquiring the experimental data. The founder was not involved in the design, method, data collection and analysis, interpretation of data, and writing the manuscript.
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/12
Y1 - 2021/12
N2 - Background: Electrical muscle stimulation (EMS) induces involuntary muscle contraction. Several studies have suggested that EMS has the potential to be an alternative method of voluntary exercise; however, its effects on cerebral blood flow (CBF) when applied to large lower limb muscles are poorly understood. Thus, the purpose of this study was to examine the effects of EMS on CBF, focusing on whether the effects differ between the internal carotid (ICA) and vertebral (VA) arteries. Methods: The participants performed the experiments under EMS and control (rest) conditions in a randomized crossover design. The ICA and VA blood flow were measured before and during EMS or control. Heart rate, blood pressure, minute ventilation, oxygen uptake, and end-tidal partial pressure of carbon dioxide (PETCO2) were monitored and measured as well. Results: The ICA blood flow increased during EMS [Pre: 330 ± 69 mL min−1; EMS: 371 ± 81 mL min−1, P = 0.001, effect size (Cohen’s d) = 0.55]. In contrast, the VA blood flow did not change during EMS (Pre: 125 ± 47 mL min−1; EMS: 130 ± 45 mL min−1, P = 0.26, effect size = 0.12). In the EMS condition, there was a significant positive linear correlation between ΔPETCO2 and ΔICA blood flow (R = 0.74, P = 0.02). No relationships were observed between ΔPETCO2 and ΔVA blood flow (linear: R = − 0.17, P = 0.66; quadratic: R = 0.43, P = 0.55). Conclusions: The present results indicate that EMS increased ICA blood flow but not VA blood flow, suggesting that the effects of EMS on cerebral perfusion differ between anterior and posterior cerebral circulation, primarily due to the differences in cerebrovascular response to CO2.
AB - Background: Electrical muscle stimulation (EMS) induces involuntary muscle contraction. Several studies have suggested that EMS has the potential to be an alternative method of voluntary exercise; however, its effects on cerebral blood flow (CBF) when applied to large lower limb muscles are poorly understood. Thus, the purpose of this study was to examine the effects of EMS on CBF, focusing on whether the effects differ between the internal carotid (ICA) and vertebral (VA) arteries. Methods: The participants performed the experiments under EMS and control (rest) conditions in a randomized crossover design. The ICA and VA blood flow were measured before and during EMS or control. Heart rate, blood pressure, minute ventilation, oxygen uptake, and end-tidal partial pressure of carbon dioxide (PETCO2) were monitored and measured as well. Results: The ICA blood flow increased during EMS [Pre: 330 ± 69 mL min−1; EMS: 371 ± 81 mL min−1, P = 0.001, effect size (Cohen’s d) = 0.55]. In contrast, the VA blood flow did not change during EMS (Pre: 125 ± 47 mL min−1; EMS: 130 ± 45 mL min−1, P = 0.26, effect size = 0.12). In the EMS condition, there was a significant positive linear correlation between ΔPETCO2 and ΔICA blood flow (R = 0.74, P = 0.02). No relationships were observed between ΔPETCO2 and ΔVA blood flow (linear: R = − 0.17, P = 0.66; quadratic: R = 0.43, P = 0.55). Conclusions: The present results indicate that EMS increased ICA blood flow but not VA blood flow, suggesting that the effects of EMS on cerebral perfusion differ between anterior and posterior cerebral circulation, primarily due to the differences in cerebrovascular response to CO2.
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U2 - 10.1186/s12868-021-00670-z
DO - 10.1186/s12868-021-00670-z
M3 - Article
C2 - 34775960
AN - SCOPUS:85119350283
VL - 22
JO - BMC Neuroscience
JF - BMC Neuroscience
SN - 1471-2202
IS - 1
M1 - 67
ER -