Muscle sympathetic nerve activity and ventilation during exercise in subjects with and without chronic heart failure

Witte, Klaus K.; Notarius, Catherine F.; Ivanov, Joan; Floras, John S.

doi:10.1016/s0828-282x(08)70176-4

Cited by 18 publications

(13 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although we and others show hyperpnea that is accompanied by attenuated gas-exchange occur during exercise in HF compared to healthy individuals (25, 27, 28, 40), we demonstrate in this study that impaired ventilation during exercise across all HF transients compared to controls does not persist during experimental post-exercise recovery. As noted in our present and previous observations (27), we show marked differences in P ET CO 2 in the absence of differences in ventilation (i.e., V E , RR, V T , and VO 2 ) in RCO (no CO 2 ) versus NR in HF at 2 min post-exercise; whereas, during exercise these measures appear similar between RCO and NR.…”

Section: Discussioncontrasting

confidence: 84%

Influence of the Metaboreflex on Pulmonary Vascular Capacitance in Heart Failure

Iterson

Snyder

Johnson

et al. 2016

Medicine &Amp; Science in Sports &Amp; Exercise

View full text Add to dashboard Cite

Purpose An impaired metaboreflex is associated with abnormal ventilatory and peripheral vascular function in heart failure (HF), whereas its influence on cardiac function or pulmonary vascular pressure remain unclear. We aimed to assess whether metabolite-sensitive neural feedback (metaboreflex) from locomotor muscles via post-exercise regional circulatory occlusion (RCO) attenuates pulmonary vascular capacitance (GXCAP) and/or circulatory power (CircP) in HF patients. Methods Eleven HF patients (NYHA class: I/II; ages, 51±15; ejection fraction: 32±9%) and 11 age and gender matched controls (ages, 43±9) completed three cycling sessions (four-minutes, 60% peak oxygen uptake [VO2]). Session one: control trial=normal recovery (NR). Sessions two or three: bilateral upper-thigh pressure tourniquets inflated suprasystolic at end-exercise (RCO) for 2-minute recovery with or without inspired CO2 (RCO+CO2) (randomized). Mean arterial pressure (MAP), heart rate, and VO2 were continuously measured. Estimates of central hemodynamics; CircP=(VO2×MAP)/weight, oxygen pulse index (O2pulseI=(VO2/heart rate)/body surface area), and GXCAP=O2pulseI×end-tidal partial pressure CO2 were calculated. Results At rest and end-exercise, CircP and GXCAP were lower in HF versus controls (P<0.05), with no differences between transients (P>0.05). At 2-minute recovery, GXCAP was lower during RCO versus NR in both groups (72±23 versus 98±20 and 73±34 versus 114±35 mL·beat−1·mm Hg·m−2, respectively; P<0.05); whereas, CircP did not differ between transients (P>0.05). Differences (% and Δ) between baseline and 2-minute recovery amongst transients suggest the metaboreflex attenuates GXCAP in HF. Differences (% and Δ) between baseline and 2-min recovery amongst transients suggest the metaboreflex may attenuate CircP in controls. Conclusion The present observations suggest locomotor muscle metaboreflex activation may influence CircP in controls but not in HF. However, metaboreflex activation may evoke decreases in GXCAP (increased pulmonary vascular pressures) in HF and controls.

show abstract

Section: Discussioncontrasting

confidence: 84%

Influence of the Metaboreflex on Pulmonary Vascular Capacitance in Heart Failure

Iterson

Snyder

Johnson

et al. 2016

Medicine &Amp; Science in Sports &Amp; Exercise

View full text Add to dashboard Cite

show abstract

“…; Witte et al. ). Furthermore, cardiopulmonary reflex is impaired in patients with heart failure (Dibner‐Dunlap et al.…”

Section: Discussionmentioning

confidence: 98%

“…Clinically, cardiopulmonary baroreceptor is particularly important to regulate arterial BP at rest and during exercise. It has been reported that resting MSNA in obesity and patients with heart failure and hypertension is higher than in healthy individuals (Yamada et al 1989;Grassi et al 2003;Witte et al 2008). Furthermore, cardiopulmonary reflex is impaired in patients with heart failure (Dibner-Dunlap et al 1996).…”

Section: Technical Considerations and Limitationsmentioning

confidence: 99%

Enhanced muscle pump during mild dynamic leg exercise inhibits sympathetic vasomotor outflow

et al. 2014

View full text Add to dashboard Cite

Muscle sympathetic nerve activity (MSNA) is not increased during leg cycling at light and mild intensities, despite activation of central command and the exercise pressor reflex. We determined whether increasing central blood volume and loading the cardiopulmonary baroreceptors modulate sympathetic vasomotor outflow during leg cycling. To this end, we changed the pedaling frequency to enhance skeletal muscle pump. Subjects performed two leg cycle exercises at differential pedal rates of 60 and 80 rpm (60EX and 80EX trials) for two conditions (with and without MSNA measurement). In each trial, subjects completed leg cycling with a differential workload to maintain constant oxygen consumption (VO2). MSNA was recorded via microneurography at the right median nerve of the elbow. Without MSNA measurement, thoracic impedance, stroke volume (SV), and cardiac output (CO) were measured non‐invasively using impedance cardiography. Heart rate and VO2 during exercise did not differ between the 60EX and 80EX trials. Changes in thoracic impedance, SV, and CO during the 80EX trial were greater than during the 60EX trial. MSNA during the 60EX trial was unchanged compared with that at rest (25.8 ± 3.1 [rest] to 28.3 ± 3.4 [exercise] bursts/min), whereas a significant decrease in MSNA was observed during the 80EX trial (25.8 ± 2.8 [rest] to 19.7 ± 2.0 [exercise] bursts/min). These results suggest that a muscle pump‐induced increase in central blood volume, and thereby loading of cardiopulmonary baroreceptors, could inhibit sympathetic vasomotor outflow during mild dynamic leg exercise, despite activation of central command and the exercise pressor reflex.

show abstract

“…Even if no data have yet been reported about autonomic overactivation in CHF stratified by different VE/VCO 2 slope categories, in cross‐sectional studies muscle ergoreceptor overactivity, muscle sympathetic nerve activity, and circulating norepinephrine levels have all been shown to correlate with both VE/VCO 2 slope and peak VO 2. In addition, a derangement in cardiopulmonary reflex control occurs early in the course of CHF . In this regard, Ponikowski et al have described an increased VE/VCO 2 slope even in CHF patients with preserved exercise tolerance, in whom an increased ventilatory response to exercise would not reflect an advanced stage of the disease, but rather a specific hypersensitivity of ventilatory reflex control .…”

Section: Discussionmentioning

confidence: 99%

Different Determinants of Ventilatory Inefficiency at Different Stages of Reduced Ejection Fraction Chronic Heart Failure Natural History

Mezzani

Giordano

Komici

et al. 2017

JAHA

View full text Add to dashboard Cite

BackgroundIt is not known whether determinants of ventilation (VE)/volume of exhaled carbon dioxide (VCO 2) slope during incremental exercise may differ at different stages of reduced ejection fraction chronic heart failure natural history.Methods and Results VE/VCO 2 slope was fitted up to lowest VE/VCO 2 ratio, that is, a proxy of the VE/perfusion ratio devoid of nonmetabolic stimuli to ventilatory drive. VE/VCO 2 slope tertiles were generated from our database (<27.5 [tertile 1], ≥27.5 to <32.0 [tertile 2], and ≥32.0 [tertile 3]), and 147 chronic heart failure patients with repeated tests yielding VE/VCO 2 slopes in 2 different tertiles were selected. Determinants of VE/VCO 2 slope changes across tertile pairs 1 versus 2, 2 versus 3, and 1 versus 3 were assessed by exploring changes in VE and VCO 2 at lowest VE/VCO 2 and those in VE/work rate (W) and VCO 2/W slope. Resting and peak cardiac output (CO) were calculated as VO 2/estimated arteriovenous O2 difference and the CO/W slope analyzed. Notwithstanding a progressively lower W with increasing tertile, VE at lowest VE/VCO 2 and VE/W slope were significantly higher in tertiles 2 and 3 versus tertile 1. Conversely, VCO 2 at lowest VE/VCO 2 and CO/W slope significantly decreased across tertiles, whereas VCO 2/W slope did not. Difference (Δ) in VE/W slope between tertiles accounted for 71% of ΔVE/VCO 2 slope variance, with ΔVCO 2/W slope explaining an additional 26% (model r=0.99; r 2=0.97; P<0.0001). Similar results were obtained substituting ΔVCO 2/W slope with ΔCO/W slope.ConclusionsVentilatory overactivation is the predominant cause of VE/VCO 2 slope increase at initial stages of chronic heart failure, whereas hemodynamic impairment plays an additional role at more‐advanced pathophysiological stages.

show abstract

Muscle sympathetic nerve activity and ventilation during exercise in subjects with and without chronic heart failure

Cited by 18 publications

References 38 publications

Influence of the Metaboreflex on Pulmonary Vascular Capacitance in Heart Failure

Influence of the Metaboreflex on Pulmonary Vascular Capacitance in Heart Failure

Enhanced muscle pump during mild dynamic leg exercise inhibits sympathetic vasomotor outflow

Different Determinants of Ventilatory Inefficiency at Different Stages of Reduced Ejection Fraction Chronic Heart Failure Natural History

Contact Info

Product

Resources

About