Cerebral oxygenation decreases during exercise in humans with beta-adrenergic blockade

TY - JOUR

T1 - Cerebral oxygenation decreases during exercise in humans with beta-adrenergic blockade

AU - Seifert, T.

AU - Rasmussen, P.

AU - Secher, Niels H.

AU - Nielsen, H.B.

PY - 2009

Y1 - 2009

N2 - AIM: Beta-blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. METHODS: Acting as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non-selective beta-blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near-infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences. RESULTS: Arterial lactate and cardiac output increased to 15.3 +/- 4.2 mM and 20.8 +/- 1.5 L min(-1) respectively (mean +/- SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 +/- 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 +/- 6 vs. 69 +/- 8 beats min(-1)) and at exercise exhaustion, cardiac output (16.6 +/- 3.6 L min(-1)) and arterial lactate (9.4 +/- 3.7 mM) were attenuated with a reduction in exercise capacity from 239 +/- 42 to 209 +/- 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 +/- 10 mmHg; P < 0.05). CONCLUSION: Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity Udgivelsesdato: 2009/7

AB - AIM: Beta-blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. METHODS: Acting as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non-selective beta-blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near-infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences. RESULTS: Arterial lactate and cardiac output increased to 15.3 +/- 4.2 mM and 20.8 +/- 1.5 L min(-1) respectively (mean +/- SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 +/- 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 +/- 6 vs. 69 +/- 8 beats min(-1)) and at exercise exhaustion, cardiac output (16.6 +/- 3.6 L min(-1)) and arterial lactate (9.4 +/- 3.7 mM) were attenuated with a reduction in exercise capacity from 239 +/- 42 to 209 +/- 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 +/- 10 mmHg; P < 0.05). CONCLUSION: Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity Udgivelsesdato: 2009/7

M3 - Journal article

SN - 1748-1708

VL - 196

SP - 295

EP - 302

JO - Acta Physiologica (Print Edition)

JF - Acta Physiologica (Print Edition)

IS - 3

ER -