Key result
When hyperventilation-related decreases in PetCO2 are prevented, activation of metabolically sensitive skeletal muscle afferent fibers increases cerebral blood flow.
Why the study?
Does preventing hyperventilation-related decreases in PetCO2 during muscle metaboreflex activation increase cerebral blood flow in healthy males?
Does preventing hyperventilation-related decreases in PetCO2 during muscle metaboreflex activation increase cerebral blood flow in healthy males?
Preventing hyperventilation-induced hypocapnia during muscle metaboreflex activation reveals that metabolically sensitive skeletal muscle afferents increase cerebral blood flow.
Findings in healthy males warrant no practice change; leaves open metaboreflex effects on cerebral blood flow in patients.
We investigated the effect of activating metabolically sensitive skeletal muscle afferents (muscle metaboreflex) on cerebral blood flow and the potentially confounding influence of concomitant changes in the partial pressure of arterial carbon dioxide. Eleven healthy males (25 ± 4 yr) performed submaximal leg cycling exercise on a semirecumbent cycle ergometer (heart rate: ∼120 beats/min), and assessments were made of the partial pressure of end-tidal carbon dioxide (PetCO2 ), internal carotid artery blood flow (ICAQ) and conductance (ICACVC), and middle cerebral artery mean blood velocity (MCAvm) and conductance index (MCACVCi).The muscle metaboreflex was activated during cycling with leg blood flow restriction (BFR) or isolated with postexercise ischemia (PEI). In separate trials, PetCO2 was either permitted to fluctuate spontaneously (control trial) or was clamped at 1 mmHg above resting levels (PetCO2 clamp trial). In the control trial, leg cycling with BFR decreased PetCO2 (Δ-4.8 ± 0.9 mmHg vs. leg cycling exercise) secondary to hyperventilation, while ICAQ, ICACVC, and MCAvm were unchanged and MCACVCi decreased. However, in the PetCO2 clamp trial, leg cycling with BFR increased both MCAvm (Δ5.9 ± 1.4 cm/s) and ICAQ (Δ20.0 ± 7.8 ml/min) and attenuated the decrease in MCACVCi, while ICACVC was unchanged. In the control trial, PEI decreased PetCO2 (Δ-7.0 ± 1.3 mmHg vs. rest), MCAvm and MCACVCi, whereas ICAQ and ICACVC were unchanged. In contrast, in the PetCO2 clamp trial both ICAQ (Δ18.5 ± 11.9 ml/min) and MCAvm (Δ8.8 ± 2.0 cm/s) were elevated, while ICACVC and MCACVCi were unchanged. In conclusion, when hyperventilation-related decreases in PetCO2 are prevented the activation of metabolically sensitive skeletal muscle afferent fibers increases cerebral blood flow.
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Prodel et al. (2016) studied Healthy (n=11). Muscle metaboreflex activation with PetCO2 clamp vs. Muscle metaboreflex activation with spontaneous PetCO2 fluctuation (control trial) was evaluated on Cerebral blood flow (middle cerebral artery mean blood velocity and internal carotid artery blood flow). When hyperventilation-related decreases in PetCO2 are prevented, activation of metabolically sensitive skeletal muscle afferent fibers increases cerebral blood flow.
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