Differential responses to CO₂ and sympathetic stimulation in the cerebral and femoral circulations in humans

Abstract

The relative importance of CO 2 and sympathetic stimulation in the regulation of cerebral and peripheral vasculatures has not been previously studied in humans. We investigated the effect of sympathetic activation, produced by isometric handgrip (HG) exercise, on cerebral and femoral vasculatures during periods of isocapnia and hypercapnia. In 14 healthy males (28.1 ± 3.7 (mean ± S.D.) years), we measured flow velocity (V P ; transcranial Doppler ultrasound) in the middle cerebral artery during euoxic isocapnia (ISO, +1 mmHg above rest) and two levels of euoxic hypercapnia (HC5, end-tidal P CO 2 , P ET,CO 2 , = +5 mmHg above ISO; HC10, P ET,CO 2 = +10 above ISO). Each P ET,CO 2 level was maintained for 10 min using the dynamic end-tidal forcing technique, during which increases in sympathetic activity were elicited by a 2-min HG at 30% of maximal voluntary contraction. Femoral blood flow (FBF; Doppler ultrasound), muscle sympathetic nerve activity (MSNA; microneurography) and mean arterial pressure (MAP; Portapres) were also measured. Hypercapnia increasedV P and FBF by 5.0 and 0.6% mmHg −1 , respectively, and MSNA by 20-220%. Isometric HG increased MSNA by 50% and MAP by 20%, with no differences between ISO, HC5 and HC10. During the ISO HG there was an increase in cerebral vascular resistance (CVR; 20 ± 11%), whileV P remained unchanged. During HC5 and HC10 HG,V P increased (13% and 14%, respectively), but CVR was unchanged. In contrast, HG-induced sympathetic stimulation increased femoral vascular resistance (FVR) during ISO, HC5 and HC10 (17-41%), while there was a general decrease in FBF below ISO. The HG-induced increases in MSNA were associated with increases in FVR in all conditions (r = 0.76-0.87), whereas increases in MSNA were associated with increases in CVR only during ISO (r = 0.91). In summary, in the absence of hypercapnia, HG exercise caused cerebral vasoconstriction, myogenically and/or neurally, which was reflected by increases in CVR and a maintainedV P . In contrast, HG increased FVR during conditions of ISO, HC5 and HC10. Therefore, the cerebral circulation is more responsive to alterations in P CO 2 , and less responsive to sympathetic stimulation than the femoral circulation.

Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: Effect of age and 12-week exercise training

“…The exact mechanisms responsible for the increased reactivity are unknown; however, increases in cerebral activation, core temperature (Rasmussen et al 2006) and CO 2 -induced increases in MAP (Ainslie et al 2005) have been suggested. Similar to the findings from this study, Rasmussen et al (2006) observed an approximately twofold increase in hypercapnic reactivity during exercise at 67 % V Á O2 max.…”

Cerebrovascular Reactivity is Increased with Acclimatization to 3,454 M Altitude

“…33,34 In addition, alterations in cerebral autoregulation in response to hypercapnia 35 and hypoxia 7,36,37 have been reported. To overcome the potential influence of MAP, we monitored MAP (Figure 3) continuously throughout the experiments and calculated CVCR (Figure 4) as it has been suggested 20 to reveal direct effects of changes in MAP on CVR.…”

Cerebral Oxygenation in Awake Rats during Acclimation and Deacclimation to Hypoxia: AnIn VivoElectron Paramagnetic Resonance Study

“…3). During normoxia, breathing 5% CO 2 can result in a 13% to 47% increase in CBF (Kim et al, 1999;Ainslie et al, 2005). Breathing 10% CO 2 can stimulate CBF by 81% to 240% (Dutka et al, 2002).…”