Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

Abstract

Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PET CO 2 : ϩ10 mmHg, by inhalation of a CO 2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCAϩMMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV O2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCAϩMMA led to the highest MAP, CO, and HR. Moreover, HCAϩMMA increased SV and was associated with the highest MV O2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV O2, and CW, increases of which were smaller during HCAϩMMA than the sum of the increases during HCA and MMA alone (MAP: ϩ28 Ϯ 2 vs. ϩ34 Ϯ 2 mmHg, P Ͻ 0.001; HR: ϩ15 Ϯ 2 vs. ϩ22 Ϯ 3 bpm, P Ͻ 0.01; TPR: ϩ1.1 Ϯ 1.4 vs. ϩ3.0 Ϯ 1.5 mmHg·l·min Ϫ1 , P Ͻ 0.05; MV O2: ϩ50.25 Ϯ 4.74 vs. ϩ59.48 Ϯ 5.37 mmHg·min Ϫ1 ·10 Ϫ2 , P Ͻ 0.01; CW: ϩ59.10 Ϯ 7.52 vs. ϩ63.67 Ϯ 7.71 ml mmHg·min Ϫ1 ·10 Ϫ4 , P Ͻ 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (ϩ2.3 Ϯ 0.4 l/min) and SV (ϩ13 Ϯ 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.hypercapnia; muscle metaboreflex; hypertension; stroke volume; myocardial oxygen consumption REGULATION OF ARTERIAL BLOOD pressure involves the integration of humoral, hormonal, and neurogenic components. For example, whereas hypercapnia has direct humoral vasodilatory effects (19,20), the neurally mediated central chemoreflex increases cardiovascular sympathetic nervous system activity, leading heart rate (HR), stroke volume (SV), cardiac output (CO), vascular resistance, and then blood pressure all to increase (31). During exercise, blood pressure is also regulated by muscle reflexes (2, 17). The muscle metaboreflex forms a second direct excitatory input for the neural control of cardiovascular function (21, 29, 42) that also stimulates sympathetic pathways (29,30,33) leading to increases in HR, SV, CO, vascular resistance, and then blood pressure.It is known that central chemoreflex and muscle metaboreflex signals converge to common areas in the brain (43) and exert similar excitatory effects through the cardiovascular autonomic nervous system. On the other hand, little is known about the hemodynamic effects of muscle metaboreflex activation during hypercapnia. Ponikowski (35) showed that muscle ergoreflex activation was an independent predictor of ventilation sensitivity to hypercapnia in chronic heart failure and argued for the existence of interactions between the muscle metaboreflex and hypercapnic chemoreflex. Despite the likelihood that these two reflexes interact during exercise, this topic received little direct attention before the pioneering work of Lykidis et al. (22,23),...

The impact of tubeless anesthesia versus intubated anesthesia on cerebral oxygen saturation and postoperative cognitive function in patients undergoing video-assisted thoracoscopic surgery: a randomized trial

“…Second, when PaCO 2 changes are in the range of 20–80 mmHg, the oxygen dissociation curve is shifted to the right, the affinity between hemoglobin and oxygen is reduced, the release of oxygen is increased, and the local partial pressure of oxygen is increased ( 43 ). Third, hypercapnia stimulates central chemoreceptors which excite the cardiac sympathetic system, resulting in an increase in HR, stroke volume, cardiac output, and SBP, which increases cerebral perfusion ( 44 ). In addition, the change of HR was also related to StO 2 (R 2 =0.225, B=0.202, P=0.005), as hypercapnia stimulates cardiac sympathetic nerves, increases the HR, enhances myocardial contractility, increases cardiac output, and finally improves cerebral perfusion.…”

On the haemodynamic consequence of the chemoreflex and muscle mechanoreflex interaction in women and men: two tales, one story

“…Therefore, the muscle metaboreflex and/or the MMR may contribute to the haemodynamic consequences resulting from the interaction between the exercise pressor reflex and the CR (Wan et al., 2020). However, while the cardiovascular impact of the metaboreflex:CR interaction has been documented (Delliaux et al., 2015; Edgell & Stickland, 2014; Lykidis et al., 2010; Seals et al., 1991), the haemodynamic consequences of the MMR:CR interaction remain largely unknown (Bruce & White, 2012).…”

The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human

“…However, the cardiovascular consequences of the interaction between the two reflexes was not addressed. Earlier work in humans has altered arterial blood gases (to stimulate chemoreceptors) during post-exercise circulatory occlusion (PECO, to stimulate metabosensitive muscle afferents) or during passive limb movement (to stimulate mechanosensitive muscle afferents), and then focused on the interaction between the CR and the metaboreflex, or the mechanoreflex, component of the EPR at rest (Seals et al 1991;Hanada et al 2003;Gujic et al 2007;Lykidis et al 2010;Bruce & White, 2012;Edgell & Stickland, 2014;Delliaux et al 2015;Silva et al 2018). Unfortunately, taken together the outcome of these studies was somewhat equivocal and this may, at least in part, be because the use of PECO as a surrogate for the EPR activation has clear limitations.…”