Cerebral lactate uptake during exercise is driven by the increased arterial lactate concentration
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Cerebral lactate uptake during exercise is driven by the increased arterial lactate concentration. / Siebenmann, Christoph; Sørensen, Henrik; Bonne, Thomas Christian; Zaar, Morten; Aachmann-Andersen, Niels Jacob; Nordsborg, Nikolai Baastrup; Nielsen, Henning Bay; Secher, Niels H.; Lundby, Carsten; Rasmussen, Peter.
In: Journal of Applied Physiology, Vol. 131, No. 6, 2021, p. 1824-1830.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Cerebral lactate uptake during exercise is driven by the increased arterial lactate concentration
AU - Siebenmann, Christoph
AU - Sørensen, Henrik
AU - Bonne, Thomas Christian
AU - Zaar, Morten
AU - Aachmann-Andersen, Niels Jacob
AU - Nordsborg, Nikolai Baastrup
AU - Nielsen, Henning Bay
AU - Secher, Niels H.
AU - Lundby, Carsten
AU - Rasmussen, Peter
N1 - CURIS 2021 NEXS 376
PY - 2021
Y1 - 2021
N2 - Exercise facilitates cerebral lactate uptake, likely by increasing arterial lactate concentration and hence the diffusion gradient across the blood brain barrier. However, non-specific β-adrenergic blockade by propranolol has previously reduced the arterio-jugular venous lactate difference (AVLac) during exercise, suggesting β-adrenergic control of cerebral lactate uptake. Alternatively, we hypothesize that propranolol reduces cerebral lactate uptake by decreasing arterial lactate concentration. To test that hypothesis, we evaluated cerebral lactate uptake taking changes in arterial concentration into account. Nine healthy males performed incremental cycling exercise to exhaustion with and without intravenous propranolol (18.7 ± 1.9 mg). Lactate concentration was determined in arterial and internal jugular venous blood at the end of each workload. To take changes in arterial lactate into account we calculated the fractional extraction (FELac) defined as AVLac divided by the arterial lactate concentration. Arterial lactate concentration was reduced by propranolol at any workload (p<0.05), reaching 14 ± 3 and 11 ± 3 mmol l-1 during maximal exercise without and with propranolol, respectively. While AVLac and FELac increased during exercise (both P < 0.05), they were both unaffected by propranolol at any workload (P = 0.68 and P = 0.26) or for any given arterial lactate concentration (P = 0.78 and P = 0.22). These findings support that, while propranolol may reduce cerebral lactate uptake, this effect reflects the propranolol-induced reduction in arterial lactate concentration and not inhibition of a β-adrenergic mechanism within the brain. We hence conclude that cerebral lactate uptake during exercise is directly driven by the increasing arterial concentration with work rate.
AB - Exercise facilitates cerebral lactate uptake, likely by increasing arterial lactate concentration and hence the diffusion gradient across the blood brain barrier. However, non-specific β-adrenergic blockade by propranolol has previously reduced the arterio-jugular venous lactate difference (AVLac) during exercise, suggesting β-adrenergic control of cerebral lactate uptake. Alternatively, we hypothesize that propranolol reduces cerebral lactate uptake by decreasing arterial lactate concentration. To test that hypothesis, we evaluated cerebral lactate uptake taking changes in arterial concentration into account. Nine healthy males performed incremental cycling exercise to exhaustion with and without intravenous propranolol (18.7 ± 1.9 mg). Lactate concentration was determined in arterial and internal jugular venous blood at the end of each workload. To take changes in arterial lactate into account we calculated the fractional extraction (FELac) defined as AVLac divided by the arterial lactate concentration. Arterial lactate concentration was reduced by propranolol at any workload (p<0.05), reaching 14 ± 3 and 11 ± 3 mmol l-1 during maximal exercise without and with propranolol, respectively. While AVLac and FELac increased during exercise (both P < 0.05), they were both unaffected by propranolol at any workload (P = 0.68 and P = 0.26) or for any given arterial lactate concentration (P = 0.78 and P = 0.22). These findings support that, while propranolol may reduce cerebral lactate uptake, this effect reflects the propranolol-induced reduction in arterial lactate concentration and not inhibition of a β-adrenergic mechanism within the brain. We hence conclude that cerebral lactate uptake during exercise is directly driven by the increasing arterial concentration with work rate.
KW - Faculty of Science
KW - Anaerobic
KW - Brain
KW - Metabolism
KW - Perfusion
KW - Propranolol
U2 - 10.1152/japplphysiol.00505.2021
DO - 10.1152/japplphysiol.00505.2021
M3 - Journal article
C2 - 34734784
VL - 131
SP - 1824
EP - 1830
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 6
ER -
ID: 283840194