Biomedical subjects

R M Welch-O'Connor

Publications and source records attributed to R M Welch-O'Connor.

5 recordsLinked to original sources

PubMed2000

Differential baroreflex control of heart rate in sedentary and aerobically fit individuals.

PURPOSE: We compared arterial, aortic, and carotid-cardiac baroreflex sensitivity in eight average fit (maximal oxygen uptake, VO2max = 42.2+/-1.9 mL x kg(-1) x min(-1)) and eight high fit (VO2max = 61.9+/-2.2 mL x kg(-1) x min(-1)) healthy young adults. METHODS: Arterial and aortic (ABR) baroreflex functions were assessed utilizing hypo- and hyper-tensive challenges induced by graded bolus injections of sodium nitroprusside (SN) and phenylephrine (PE), respectively. Carotid baroreflex (CBR) sensitivity was determined using ramped 5-s pulses of both pressure and suction delivered to the carotid sinus via a neck chamber collar, independent of drug administration. RESULTS: During vasoactive drug injection, mean arterial pressure (MAP) was similarly altered in average fit (AF) and high fit (HF) groups. However, the heart rate (HR) response range of the arterial baroreflex was significantly attenuated (P < 0.05) in HF (31+/-4 beats x min(-1)) compared with AF individuals (46+/-4 beats x min(-1)). When sustained neck suction and pressure were applied to counteract altered carotid sinus pressure during SN and PE administration, isolating the ABR response, the response range remained diminished (P < 0.05) in the HF population (24+/-3 beats x min(-1)) compared with the AF group (41+/-4 beats x min(-1)). During CBR perturbation, the HF (14+/-1 beats-min(-1)) and AF (16+/-1 beats-min(-1)) response ranges were similar. The arterial baroreflex response range was significantly less than the simple sum of the CBR and ABR (HF, 38+/-3 beats x min(-1) and AF, 57+/-4 beats x min(-1)) in both fitness groups. CONCLUSIONS: These data confirm that reductions in arterial-cardiac reflex sensitivity are mediated by diminished ABR function. More importantly, these data suggest that the integrative relationship between the ABR and CBR contributing to arterial baroreflex control of HR is inhibitory in nature and not altered by exercise training.

Baroreflex↗

PubMed1999

Ventilatory responses to dynamic exercise elicited by intramuscular sensors.

PURPOSE: Eight subjects, aged 27.0+/-1.6 yr, performed incremental workload cycling to investigate the contribution of skeletal muscle mechano- and metaboreceptors to ventilatory control during dynamic exercise. METHODS: Each subject performed four bouts of exercise: exercise with no intervention (CON); exercise with bilateral thigh cuffs inflated to 90 mm Hg (CUFF); exercise with application of lower-body positive pressure (LBPP) to 45 torr (PP); and exercise with 90 mm Hg thigh cuff inflation and 45 torr LBPP (CUFF+PP). Ventilatory responses and pulmonary gas exchange variables were collected breath-by-breath with concomitant measurement of leg intramuscular pressure. RESULTS: Ventilation (VE) was significantly elevated from CON during PP and CUFF+PP at workloads corresponding to > or = 60% CON peak oxygen uptake (VO2peak) and during CUFF at workloads > or = 80% CON VO2peak, P < 0.05. The VO2 at which ventilatory threshold occurred was significantly reduced from CON (2.17+/-0.28 L x min(-1)) to 1.60+/-0.19 L x min(-1), 1.45+/-0.15 L x min(-1), and 1.15+/-0.11 L x min(-1) during CUFF, PP, and CUFF+PP, respectively. The slope of the linear regression describing the VE/CO2 output relationship was increased from CON by approximately 22% during CUFF, 40% during PP, and 41% during CUFF+PP. CONCLUSIONS: As intramuscular pressure was significantly elevated immediately upon application of LBPP during PP and CUFF+PP without a concomitant increase in VE, it seems unlikely that LBPP-induced increases in VE can be attributed to activation of the mechanoreflex. These findings suggest that LBPP-induced reductions in perfusion pressure and decreases in venous outflow resulting from inflation of bilateral thigh cuffs may generate a metabolite sensitive intramuscular ventilatory stimulus.

Adult↗

PubMed1999

Carotid baroreflex function during prolonged exercise.

The present investigation was designed to uncouple the hemodynamic physiological effects of thermoregulation from the effects of a progressively increasing central command activation during prolonged exercise. Subjects performed two 1-h bouts of leg cycling exercise with 1) no intervention and 2) continuous infusion of a dextran solution to maintain central venous pressure constant at the 10-min pressure. Volume infusion resulted in a significant reduction in the decrement in mean arterial pressure seen in the control exercise bout (6.7 +/- 1.8 vs. 11.6+/- 1.3 mmHg, respectively). However, indexes of central command such as heart rate and ratings of perceived exertion rose to a similar extent during both exercise conditions. In addition, the carotid-cardiac baroreflex stimulus-response relationship, as measured by using the neck pressure-neck suction technique, was reset from rest to 10 min of exercise and was further reset from 10 to 50 min of exercise in both exercise conditions, with the operating point being shifted toward the reflex threshold. We conclude that the progressive resetting of the carotid baroreflex and the shift of the reflex operating point render the carotid-cardiac reflex ineffectual in counteracting the continued decrement in mean arterial pressure that occurs during the prolonged exercise.

Adult↗

PubMed1998

Cardiovascular function following reduced aerobic activity.

PURPOSE: The aim of this study was to test the hypothesis that a sustained reduction of physical activity (deconditioning) would alter the cardiovascular regulatory function. METHODS: Nineteen young, healthy volunteers participated in physical deconditioning for a period of 8 wk. Before (pre) and following (post) physical deconditioning, the responses of heart rate (HR), mean arterial pressure (MAP, measured by Finapres), central venous pressure (CVP), stroke volume (SV, Doppler), and forearm blood flow (FBF, plethysmography) were determined during lower body negative pressure (LBNP). The carotid baroreflex (CBR) function was assessed using a train of pulsatile neck pressure (NP) and suction, and the aortic baroreflex control of HR was assessed during steady-state phenylephrine (PE) infusion superimposed by LBNP and NP to counteract the PE increased CVP and carotid sinus pressure, respectively. RESULTS: Active physical deconditioning significantly decreased maximal oxygen uptake (-7%) and LBNP tolerance (-13%) without a change in baseline hemodynamics. Plasma volume (-3% at P = 0.135), determined by Evans Blue dilution, and blood volume (-4% at P = 0.107) were not significantly altered. During LBNP -20 to -50 torr, there was a significantly greater drop of SV per unit decrease in CVP in the post- (14.7 +/- 1.6%/mm Hg) than predeconditioning (11.2 +/- 0.7%/mm Hg) test accompanied by a greater tachycardia. Deconditioning increased the aortic baroreflex sensitivity (pre vs post: -0.61 +/- 0.12 vs -0.84 +/- 0.14 bpm.mm-1 Hg, P = 0.009) and the slope of forearm vascular resistance (calculated from [MAP-CVP]/FBF) to CVP (-2.75 +/- 0.26 vs -4.94 +/- 0.97 PRU/mm Hg, P = 0.086). However, neither the CBR-HR (-0.28 +/- 0.03 VS -0.39 +/- 0.10 bpm.mm-1 Hg) nor the CBR-MAP (-0.37 +/- 0.16 vs -0.25 +/- 0.07 mm Hg/mm Hg) gains were statistically different between pre- and postdeconditioning. CONCLUSIONS: We concluded that the functional modification of the cardiac pressure-volume relationship resulted in the reduced LBNP tolerance, despite the accentuated aortic and cardiopulmonary baroreflex function following deconditioning.

Adult↗

PubMed1996

Arterial and cardiopulmonary baroreflexes in 60- to 69- vs. 18- to 36-yr-old humans.

This study was designed to test the hypothesis that aging diminished baroreflex function during central hypovolemia. Eleven healthy young and eleven older (age 60-69 yr) individuals were assessed by using heart rate (HR) and mean arterial pressure (MAP) responses to neck pressure and suction during rest and lower body negative pressure (LBNP) of -15 Torr. The slope of forearm vascular resistance to central venous pressure during low-level LBNP was assessed as the index of cardiopulmonary baroreflex sensitivity. Baseline cardiovascular variables were not significantly different between the groups. In addition, there was no group difference in cardiopulmonary baroreflex (-3.6 vs. -3.7 units/mmHg for young vs. older, respectively) or carotid baroreflex (-0.39 vs. -0.35 beats.min-1.mmHg-1 and -0.26 vs. -0.35 mmHg/mmHg, for young vs. older, respectively) sensitivity. LBNP did not affect either HR or MAP, whereas it decreased CVP and increased FVR in both groups. LBNP significantly augmented the carotid-HR (-0.47 +/- 0.03 beats.min-1.mmHg-1) and carotid-MAP (-0.42 +/- 0.04 mmHg/mmHg) reflex gains in the young subjects only. We concluded that there was no difference in the discrete baroreflex function between the two age groups; however, the interaction of cardiopulmonary baroreceptors with carotid baroreflex function was absent in the older subjects, suggesting that the central integration of afferent neural inputs from the discrete baroreceptors was altered with aging.

Adult↗