Abstract
This study investigated the influence of ventilation on sympathetic action potential (AP) discharge patterns during varying levels of high chemoreflex stress. In seven trained breath-hold divers (age 33 ± 12 yr), we measured muscle sympathetic nerve activity (MSNA) at baseline, during preparatory rebreathing (RBR), and during 1) functional residual capacity apnea (FRCApnea) and 2) continued RBR. Data from RBR were analyzed at matched (i.e., to FRCApnea) hemoglobin saturation (HbSat) levels (RBRMatched) or more severe levels (RBREnd). A third protocol compared alternating periods (30 s) of FRC and RBR (FRC-RBRALT). Subjects continued each protocol until 85% volitional tolerance. AP patterns in MSNA (i.e., providing the true neural content of each sympathetic burst) were studied using wavelet-based methodology. First, for similar levels of chemoreflex stress (both HbSat: 71 ± 6%; P = NS), RBRMatched was associated with reduced AP frequency and APs per burst compared with FRCApnea (both P < 0.001). When APs were binned according to peak-to-peak amplitude (i.e., into clusters), total AP clusters increased during FRCApnea (+10 ± 2; P < 0.001) but not during RBRMatched (+1 ± 2; P = NS). Second, despite more severe chemoreflex stress during RBREnd (HbSat: 56 ± 13 vs. 71 ± 6%; P < 0.001), RBREnd was associated with a restrained increase in the APs per burst (FRCApnea: +18 ± 7; RBREnd: +11 ± 5) and total AP clusters (FRCApnea: +10 ± 2; RBREnd: +6 ± 4) (both P < 0.01). During FRC-RBRALT, all periods of FRC elicited sympathetic AP recruitment (all P < 0.001), whereas all periods of RBR were associated with complete withdrawal of AP recruitment (all P = NS). Presently, we demonstrate that ventilation per se restrains and/or inhibits sympathetic axonal recruitment during high, and even extreme, chemoreflex stress.NEW & NOTEWORTHY The current study demonstrates that the sympathetic neural recruitment patterns observed during chemoreflex activation induced by rebreathing or apnea are restrained and/or inhibited by the act of ventilation per se, despite similar, or even greater, levels of severe chemoreflex stress. Therefore, ventilation modulates not only the timing of sympathetic bursts but also the within-burst axonal recruitment normally observed during progressive chemoreflex stress.
Highlights
NEW & NOTEWORTHY The current study demonstrates that the sympathetic neural recruitment patterns observed during chemoreflex activation induced by rebreathing or apnea are restrained and/or inhibited by the act of ventilation per se, despite similar, or even greater, levels of severe chemoreflex stress
The central motor hypothesis has been studied in humans mainly under normoxic and normocapnic conditions (St Croix et al 1999) or low levels of hypercapnia (Seals et al 1993), raising the possibility that potentiation of central pathways associated with the drive to breathe and sympathetic inhibition with breathing may be augmented with concurrent chemoreflex activation
Observations arguing against this possibility are provided from our earlier study (Steinback et al 2010a), in which the very large sympathetic responses occurring during prolonged apnea at functional residual capacity (FRC), performed by elite breath-hold divers, were acutely inhibited by a two-breath rebreathe protocol performed immediately following the apnea, despite a sustained chemoreflex stimulus
Summary
NEW & NOTEWORTHY The current study demonstrates that the sympathetic neural recruitment patterns observed during chemoreflex activation induced by rebreathing or apnea are restrained and/or inhibited by the act of ventilation per se, despite similar, or even greater, levels of severe chemoreflex stress. The possible factors affecting the sympathoinhibitory effect of ventilation during chemoreflex stimulation may include central pathways that coordinate respiratory drive with sympathetic inhibition Evidence for such pathways has been difficult to www.jn.org find in humans (St Croix et al 1999), whereby MSNA is inhibited during inspiration (or at high lung volumes) and increases during expiration (or at low lung volumes) (Eckberg et al 1985; Seals et al 1993); current evidence in the intact human argues against a significant role played by central respiratory drive on the ventilatory modulation of MSNA (Seals et al 1993; St Croix et al 1999). Whether neural recruitment is restrained and/or inhibited in the presence of ventilation remains unknown
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