Evidence for temperature-mediated regional increases in cerebral blood flow during exercise

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Evidence for temperature-mediated regional increases in cerebral blood flow during exercise. / Caldwell, Hannah Grace; Coombs, Geoff B; Howe, Connor A; Hoiland, Ryan L; Patrician, Alexander; Lucas, Samuel J E; Ainslie, Philip N.

I: Journal of Physiology, Bind 598, Nr. 8, 2020, s. 1459-1473.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Caldwell, HG, Coombs, GB, Howe, CA, Hoiland, RL, Patrician, A, Lucas, SJE & Ainslie, PN 2020, 'Evidence for temperature-mediated regional increases in cerebral blood flow during exercise', Journal of Physiology, bind 598, nr. 8, s. 1459-1473. https://doi.org/10.1113/JP278827

APA

Caldwell, H. G., Coombs, G. B., Howe, C. A., Hoiland, R. L., Patrician, A., Lucas, S. J. E., & Ainslie, P. N. (2020). Evidence for temperature-mediated regional increases in cerebral blood flow during exercise. Journal of Physiology, 598(8), 1459-1473. https://doi.org/10.1113/JP278827

Vancouver

Caldwell HG, Coombs GB, Howe CA, Hoiland RL, Patrician A, Lucas SJE o.a. Evidence for temperature-mediated regional increases in cerebral blood flow during exercise. Journal of Physiology. 2020;598(8):1459-1473. https://doi.org/10.1113/JP278827

Author

Caldwell, Hannah Grace ; Coombs, Geoff B ; Howe, Connor A ; Hoiland, Ryan L ; Patrician, Alexander ; Lucas, Samuel J E ; Ainslie, Philip N. / Evidence for temperature-mediated regional increases in cerebral blood flow during exercise. I: Journal of Physiology. 2020 ; Bind 598, Nr. 8. s. 1459-1473.

Bibtex

@article{8fe89c04cb1449f0a401219a77253ef2,
title = "Evidence for temperature-mediated regional increases in cerebral blood flow during exercise",
abstract = "Key points: Aerobic exercise elicits increases in cerebral blood flow (CBF), as well as core body temperature; however, the isolated influence of temperature on CBF regulation during exercise has not been investigated The present study assessed CBF regulation and neurovascular coupling during submaximal cycling exercise and temperature-matched passive heat stress during isocapnia (i.e. end-tidal (Formula presented.) was held constant) Submaximal cycling exercise and temperature-matched passive heat stress provoked ∼16% increases in vertebral artery blood flow, independent of changes in end-tidal (Formula presented.) and blood pressure External carotid artery blood flow increased by ∼43% during both exercise and passive heat stress, with no change in internal carotid artery blood flow Neurovascular coupling (i.e. the relationship between local increases in cerebral metabolism and appropriately matched increases in regional cerebral blood flow) is preserved during both exercise and temperature-matched passive heat stress. Abstract: Acute moderate-intensity exercise increases core temperature (Tc; +0.7-0.8°C); however, such exercise increases cerebral blood flow (CBF; +10-20%) mediated via small elevations in arterial (Formula presented.) and metabolism. The present study aimed to isolate the role of Tc from (Formula presented.) on CBF regulation during submaximal exercise. Healthy adults (n = 11; 10 males/one female; 26 ± 4 years) participated in two interventions each separated by ≥48 h: (i) 60 min of semi-recumbent cycling (EX; 50% workload max) and (ii) 75 min of passive heat stress (HS; 49°C water-perfused suit) to match the exercise-induced increases in Tc (EX: Δ0.75 ± 0.33°C vs. HS: Δ0.77 ± 0.33°C, P = 0.855). Blood flow (Q) in the internal and external carotid arteries (ICA and ECA, respectively) and vertebral artery (VA) (Duplex ultrasound) was measured. End-tidal (Formula presented.) and (Formula presented.) were effectively clamped to resting values within each condition. The QICA was unchanged with EX and HS interventions (P = 0.665), consistent with the unchanged end-tidal (Formula presented.) (P = 0.327); whereas, QVA was higher throughout both EX and HS (EX: Δ16 ± 21% vs. HS: Δ16 ± 23%, time effect: P = 0.006) with no between condition differences (P = 0.785). These increases in QVA contributed to higher global CBF throughout both EX and HS (EX: Δ12 ± 20% vs. HS: Δ14 ± 14%, time effect: P = 0.029; condition effect: P = 0.869). The QECA increased throughout both EX and HS (EX: Δ42 ± 58% vs. HS: Δ53 ± 28%, time effect: P < 0.001; condition effect: P = 0.628). Including blood pressure as a covariate did not alter these CBF findings (all P > 0.05). Overall, these data provide new evidence for temperature-mediated elevations in posterior CBF during exercise that are independent of changes in (Formula presented.) and blood pressure.",
keywords = "Cerebrovascular, Exercise, Temperature",
author = "Caldwell, {Hannah Grace} and Coombs, {Geoff B} and Howe, {Connor A} and Hoiland, {Ryan L} and Alexander Patrician and Lucas, {Samuel J E} and Ainslie, {Philip N}",
note = "(Ekstern)",
year = "2020",
doi = "10.1113/JP278827",
language = "English",
volume = "598",
pages = "1459--1473",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "8",

}

RIS

TY - JOUR

T1 - Evidence for temperature-mediated regional increases in cerebral blood flow during exercise

AU - Caldwell, Hannah Grace

AU - Coombs, Geoff B

AU - Howe, Connor A

AU - Hoiland, Ryan L

AU - Patrician, Alexander

AU - Lucas, Samuel J E

AU - Ainslie, Philip N

N1 - (Ekstern)

PY - 2020

Y1 - 2020

N2 - Key points: Aerobic exercise elicits increases in cerebral blood flow (CBF), as well as core body temperature; however, the isolated influence of temperature on CBF regulation during exercise has not been investigated The present study assessed CBF regulation and neurovascular coupling during submaximal cycling exercise and temperature-matched passive heat stress during isocapnia (i.e. end-tidal (Formula presented.) was held constant) Submaximal cycling exercise and temperature-matched passive heat stress provoked ∼16% increases in vertebral artery blood flow, independent of changes in end-tidal (Formula presented.) and blood pressure External carotid artery blood flow increased by ∼43% during both exercise and passive heat stress, with no change in internal carotid artery blood flow Neurovascular coupling (i.e. the relationship between local increases in cerebral metabolism and appropriately matched increases in regional cerebral blood flow) is preserved during both exercise and temperature-matched passive heat stress. Abstract: Acute moderate-intensity exercise increases core temperature (Tc; +0.7-0.8°C); however, such exercise increases cerebral blood flow (CBF; +10-20%) mediated via small elevations in arterial (Formula presented.) and metabolism. The present study aimed to isolate the role of Tc from (Formula presented.) on CBF regulation during submaximal exercise. Healthy adults (n = 11; 10 males/one female; 26 ± 4 years) participated in two interventions each separated by ≥48 h: (i) 60 min of semi-recumbent cycling (EX; 50% workload max) and (ii) 75 min of passive heat stress (HS; 49°C water-perfused suit) to match the exercise-induced increases in Tc (EX: Δ0.75 ± 0.33°C vs. HS: Δ0.77 ± 0.33°C, P = 0.855). Blood flow (Q) in the internal and external carotid arteries (ICA and ECA, respectively) and vertebral artery (VA) (Duplex ultrasound) was measured. End-tidal (Formula presented.) and (Formula presented.) were effectively clamped to resting values within each condition. The QICA was unchanged with EX and HS interventions (P = 0.665), consistent with the unchanged end-tidal (Formula presented.) (P = 0.327); whereas, QVA was higher throughout both EX and HS (EX: Δ16 ± 21% vs. HS: Δ16 ± 23%, time effect: P = 0.006) with no between condition differences (P = 0.785). These increases in QVA contributed to higher global CBF throughout both EX and HS (EX: Δ12 ± 20% vs. HS: Δ14 ± 14%, time effect: P = 0.029; condition effect: P = 0.869). The QECA increased throughout both EX and HS (EX: Δ42 ± 58% vs. HS: Δ53 ± 28%, time effect: P < 0.001; condition effect: P = 0.628). Including blood pressure as a covariate did not alter these CBF findings (all P > 0.05). Overall, these data provide new evidence for temperature-mediated elevations in posterior CBF during exercise that are independent of changes in (Formula presented.) and blood pressure.

AB - Key points: Aerobic exercise elicits increases in cerebral blood flow (CBF), as well as core body temperature; however, the isolated influence of temperature on CBF regulation during exercise has not been investigated The present study assessed CBF regulation and neurovascular coupling during submaximal cycling exercise and temperature-matched passive heat stress during isocapnia (i.e. end-tidal (Formula presented.) was held constant) Submaximal cycling exercise and temperature-matched passive heat stress provoked ∼16% increases in vertebral artery blood flow, independent of changes in end-tidal (Formula presented.) and blood pressure External carotid artery blood flow increased by ∼43% during both exercise and passive heat stress, with no change in internal carotid artery blood flow Neurovascular coupling (i.e. the relationship between local increases in cerebral metabolism and appropriately matched increases in regional cerebral blood flow) is preserved during both exercise and temperature-matched passive heat stress. Abstract: Acute moderate-intensity exercise increases core temperature (Tc; +0.7-0.8°C); however, such exercise increases cerebral blood flow (CBF; +10-20%) mediated via small elevations in arterial (Formula presented.) and metabolism. The present study aimed to isolate the role of Tc from (Formula presented.) on CBF regulation during submaximal exercise. Healthy adults (n = 11; 10 males/one female; 26 ± 4 years) participated in two interventions each separated by ≥48 h: (i) 60 min of semi-recumbent cycling (EX; 50% workload max) and (ii) 75 min of passive heat stress (HS; 49°C water-perfused suit) to match the exercise-induced increases in Tc (EX: Δ0.75 ± 0.33°C vs. HS: Δ0.77 ± 0.33°C, P = 0.855). Blood flow (Q) in the internal and external carotid arteries (ICA and ECA, respectively) and vertebral artery (VA) (Duplex ultrasound) was measured. End-tidal (Formula presented.) and (Formula presented.) were effectively clamped to resting values within each condition. The QICA was unchanged with EX and HS interventions (P = 0.665), consistent with the unchanged end-tidal (Formula presented.) (P = 0.327); whereas, QVA was higher throughout both EX and HS (EX: Δ16 ± 21% vs. HS: Δ16 ± 23%, time effect: P = 0.006) with no between condition differences (P = 0.785). These increases in QVA contributed to higher global CBF throughout both EX and HS (EX: Δ12 ± 20% vs. HS: Δ14 ± 14%, time effect: P = 0.029; condition effect: P = 0.869). The QECA increased throughout both EX and HS (EX: Δ42 ± 58% vs. HS: Δ53 ± 28%, time effect: P < 0.001; condition effect: P = 0.628). Including blood pressure as a covariate did not alter these CBF findings (all P > 0.05). Overall, these data provide new evidence for temperature-mediated elevations in posterior CBF during exercise that are independent of changes in (Formula presented.) and blood pressure.

KW - Cerebrovascular

KW - Exercise

KW - Temperature

UR - http://www.scopus.com/inward/record.url?scp=85079221805&partnerID=8YFLogxK

U2 - 10.1113/JP278827

DO - 10.1113/JP278827

M3 - Journal article

C2 - 31912506

AN - SCOPUS:85079221805

VL - 598

SP - 1459

EP - 1473

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 8

ER -

ID: 253079990