Xiangrong Shi

Autonomic nervous system control of the heart : endurance exercise training

The purpose of this study was to assess hemodynamic responses to lower body negative pressure (LBNP) to -45 torr with selective cardiac parasympathetic (using atropine sulphate), sympathetic efferent (using metoprolol tartrate), and combined (atropine+metoprolol) blockade prior to and following 8 months of endurance exercise training in eight young men. Training resulted in significant increases of maximal oxygen uptake (27%) and blood volume (16%) and a decrease of baseline heart rate (HR, from 66 +/- 4 to 57 +/- 4 bpm). This training related bradycardia was exclusively determined by an enhanced vagal tone as there was no significant difference in intrinsic HR pre- to post-training and only atropine (pre: 100 +/- 3 vs post: 101 +/- 3 bpm), not metoprolol (pre: 56 +/- 3 vs post: 49 +/- 4 bpm), abolished the HR difference. The reflex tachycardia in the control experiment was significantly diminished following training. However, the increase in HR at LBNP -45 torr between pre- and post-training was similar after either atropine (+13 +/- 2 vs +14 +/- 1 bpm) or metoprolol (+8 +/- 1 vs +8 +/- 1 bpm). Reflex tachycardia was greater during atropine than metoprolol blockade and the sum of the HR increase during selective blockade (21 and 22 bpm) was greater when compared with the control (no blockade, 16 +/- 2 vs 11 +/- 2 bpm). There was no difference pre- to post-training in SV or Qc response to -45 torr LBNP during the control condition. However, selective beta 1-receptor blockade resulted in a greater decrease in SV to -45 torr LBNP post-training compared to pre-training (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Chronic physical activity mitigates cerebral hypoperfusion during central hypovolemia in elderly humans

This study sought to test the hypothesis that orthostasis-induced cerebral hypoperfusion would be less severe in physically active elderly humans (ACT group) than in sedentary elderly humans (SED group). The peak O(2) uptake of 10 SED (67.1 +/- 1.4 yr) and 9 ACT (68.0 +/- 1.1 yr) volunteers was determined by a graded cycling exercise test (22.1 +/- 1.2 vs 35.8 +/- 1.3 ml.min(-1).kg(-1), P < 0.01). Baseline mean arterial pressure (MAP; tonometry) and middle cerebral arterial blood flow velocity (V(MCA); transcranial Doppler) were similar between the groups (SED vs. ACT group: 91 +/- 3 vs. 87 +/- 3 mmHg and 54.9 +/- 2.3 vs. 57.8 +/- 3.2 cm/s, respectively), whereas heart rate was higher and stroke volume (bioimpedance) was smaller in the SED group than in the ACT group. Central hypovolemia during graded lower body negative pressure (LBNP) was larger (P < 0.01) in the ACT group than in the SED group. However, the slope of V(MCA)/LBNP was smaller (P < 0.05) in the ACT group (0.159 +/- 0.016 cm/s/Torr) than in the SED group (0.211 +/- 0.008 cm/s/Torr). During LBNP, the SED group had a greater augmentation of cerebral vasomotor tone (P < 0.05) and hypocapnia (P < 0.001) compared with the ACT group. Baseline MAP variability and V(MCA) variability were significantly smaller in the SED group than in the ACT group, i.e., 0.49 +/- 0.07 vs. 1.04 +/- 0.16 (mmHg)(2) and 1.06 +/- 0.19 vs. 4.24 +/- 1.59 (cm/s)(2), respectively. However, transfer function gain, coherence, and phase between MAP and V(MCA) signals (Welch spectral estimator) from 0.08-0.18 Hz were not different between SED (1.41 +/- 0.18 cm.s(-1).mmHg(-1), 0.63 +/- 0.06 units, and 38.03 +/- 6.57 degrees ) and ACT (1.65 +/- 0.44 cm.s(-1).mmHg(-1), 0.56 +/- 0.05 units, and 48.55 +/- 11.84 degrees ) groups. We conclude that a physically active lifestyle improves the intrinsic mechanism of cerebral autoregulation and helps mitigate cerebral hypoperfusion during central hypovolemia in healthy elderly adults.

Cerebral vasoreactivity during hypercapnia is reset by augmented sympathetic influence

Sympathetic nerve activity influences cerebral blood flow, but it is unknown whether augmented sympathetic nerve activity resets cerebral vasoreactivity to hypercapnia. This study tested the hypothesis that cerebral vasodilation during hypercapnia is restrained by lower-body negative pressure (LBNP)-stimulated sympathoexcitation. Cerebral hemodynamic responses were assessed in nine healthy volunteers [age 25 yr (SD 3)] during rebreathing-induced increases in partial pressure of end-tidal CO(2) (Pet(CO(2))) at rest and during LBNP. Cerebral hemodynamic responses were determined by changes in flow velocity of middle cerebral artery (MCAV) using transcranial Doppler sonography and in regional cerebral tissue oxygenation (ScO(2)) using near-infrared spectroscopy. Pet(CO(2)) values during rebreathing were similarly increased from 41.9 to 56.5 mmHg at rest and from 40.7 to 56.0 mmHg during LBNP of -15 Torr. However, the rates of increases in MCAV and in ScO(2) per unit increase in Pet(CO(2)) (i.e., the slopes of MCAV/Pet(CO(2)) and ScO(2)/Pet(CO(2))) were significantly (P ≤0.05) decreased from 2.62 ± 0.16 cm·s(-1)·mmHg(-1) and 0.89 ± 0.10%/mmHg at rest to 1.68 ± 0.18 cm·s(-1)·mmHg(-1) and 0.63 ± 0.07%/mmHg during LBNP. In conclusion, the sensitivity of cerebral vasoreactivity to hypercapnia, in terms of the rate of increases in MCAV and in ScO(2), is diminished by LBNP-stimulated sympathoexcitation.

Aging and Arterial Blood Pressure Variability during Orthostatic Challenge

Background: It has been demonstrated that a decrease in vagal cardiac function compromises arterial blood pressure (ABP) stability during orthostatic challenge. Augmentations in low-frequency (LF) ABP oscillations are indicative of this change in autonomic hemodynamic control. Aging is associated with diminished arterial baroreflex sensitivity and vagal cardiac dysfunction. However, the effect of aging on the stability of ABP during an orthostatic challenge remains to be elucidated. Objective: The purpose of this study was to investigate ABP stability with aging during central hypovolemia induced by lower-body negative pressure (LBNP). Methods: Graded LBNP up to –40 mm Hg was applied in 16 older (65 ± 3 years of age) and 16 younger (25 ± 3 years of age) healthy adults. ABP variability was analyzed by fast Fourier transform. LF spectral density (0.04–0.15 Hz) was extracted to provide an index of vasomotor responsiveness. Results: Both LF systolic blood pressure (SBP) variability and diastolic blood pressure variability were augmented with LBNP. The rate of increase in LF SBP variability was augmented significantly greater in older as compared with younger subjects (p = 0.049). In addition, LF SBP variability was inversely correlated with decreases in pulse pressure in both age groups (r = –0.84, p = 0.01). The magnitude of the decreases in SBP and pulse pressure during LBNP was significantly affected by age, with the largest changes occurring in older subjects. The altered ABP response that manifested in older individuals was associated with a significant diminution in the reflex tachycardiac response elicited by LBNP. Conclusions: Induction of central hypovolemia via graded LBNP augments LF ABP variability. This increased ABP variability is significantly greater in older individuals. Our data suggest that aging is associated with ABP instability during orthostatic challenge.

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.

A diminished aortic-cardiac reflex during hypotension in aerobically fit young men

We compared the aortic-cardiac baroreflex sensitivity in eight average fit (AF: VO2max = 44.7 +/- 1.3 ml.kg-1 x min-1) and seven high fit (HF: VO2max = 64.1 +/- 1.7 ml.min-1 x kg-1) healthy young men during hypotension elicited by steady state sodium nitroprusside (SN) infusion. During SN mean arterial pressure (MAP) was similarly decreased in AF (-12.6 +/- 1.0 mm Hg) and HF (-12.1 +/- 1.1 mm Hg). However, the increases in heart rate (HR) were less (P < 0.023) in HF (15 +/- 3 bpm) than AF (25 +/- 1 bpm). When sustained neck suction (NS, -22 +/- 1 torr in AF and -20 +/- 1 torr in HF, P > 0.05) was applied to counteract the decreased carotid sinus transmural pressure during SN, thereby isolating the aortic baroreceptors, the increased HR remained less (P < 0.021) in HF (8 +/- 2 bpm) than AF (16 +/- 2 bpm). During both SN infusion and SN+NS, the calculated gains (i.e., delta HR/delta MAP) were significantly greater in AF (2.1 +/- 0.3 and 1.3 +/- 0.2 bpm.mm Hg-1) than HF (1.2 +/- 0.2 and 0.6 +/- 0.2 bpm.mm Hg-1). However, the estimated carotid-cardiac baroreflex sensitivity (i.e., the gain difference between the stage SN and SN + NS) was not different between AF (0.7 +/- 0.2 bpm.mm Hg-1) and HF (0.6 +/- 0.1 bpm.mm Hg-1). These data indicated that the aortic-cardiac baroreflex sensitivity during hypotension was significantly diminished with endurance exercise training.

Physically active lifestyle enhances vagal-cardiac function but not central autonomic neural interaction in elderly humans.

The cause of the age-related impairment of arterial baroreflex function remains ill-defined; moreover, it is unknown whether this impairment results from aging per se or from an inactive lifestyle associated with aging. In this study, we sought to: 1) determine whether elderly individuals who maintained an active lifestyle had an enhanced carotid baroreflex function as compared with their sedentary counterparts; and 2) determine whether this difference was due in part to altered function of the arterial baroreceptor and/or altered central modulation. Eight healthy, sedentary (SED, 68 ± 2 yr) and eight physically active (ACT, 68 ± 1 yr) elderly men with peak O2 consumption 25.5 ± 1.2 vs 35.7 ± 2.4 ml/min/kg (P < 0.01), respectively, were assessed with carotid baroreceptor (CBR) function using 5s pulses of neck pressure or suction (ranging from +40 to −80 Torr) delivered to the carotid sinus region at rest and during lower body negative pressure (LBNP) of −15 and −40 Torr. Changes in heart rate (HR) and mean arterial pressure (MAP) were assessed for CBR-HR and CBR-MAP gains, respectively. Overall CBR-HR gains in a range of ∼ 120 mmHg of carotid sinus pressure were greater (P < 0.01) in ACT than SED at rest and during LBNP. The derived peak CBR-HR slopes between ACT and SED at rest were −0.32 ± 0.07 vs −0.11 ± 0.02 bpm/mmHg (P = 0.007), respectively. However, there was no statistical difference (P = 0.37) in CBR-MAP gains between the groups. Neither CBR-MAP (P = 0.08) nor CBR-HR (P = 0.41) gain was augmented by LBNP in the elderly. Conclusion: Active lifestyle enhances the CBR-HR reflex sensitivity as a result of the improved vagal-cardiac function in elderly people. Aging is associated with an absence of central autonomic interaction in the control of blood pressure regardless of physical fitness.

The Influence of Hostility and Family History of Cardiovascular Disease on Autonomic Activation in Response to Controllable versus Noncontrollable Stress, Anger Imagery Induction, and Relaxation Imagery

Autonomic activation in response to controllable versus noncontrollable stress, anger imagery induction, and relaxation imagery was studied among 80 participants between the ages of 18 and 34 years. Participants differed in level of trait hostility and family history of cardiovascular disease. Results were obtained through power spectral analyses of electrocardiograph R-R intervals, which produced an index of autonomic nervous system activation. For both male and female populations, parasympathetic regulation was diminished during anger induction for individuals with high levels of trait hostility and having a family history of cardiovascular disease. Similar results were obtained for women during the uncontrolled stress condition. Based on family history of cardiovascular disease and trait hostility, men responded differentially to relaxation imagery induction, whereas no differences were found among females.

Diminished forearm vasomotor response to central hypervolemic loading in aerobically fit individuals.

The aim of this study was to test the hypothesis that cardiopulmonary baroreflex control of forearm vascular resistance (FVR) during central hypervolemic loading was less sensitive in exercise trained high fit individuals (HF) compared to untrained average fit individuals (AF). Eight AF (age: 24 +/- 1 yr and weight: 78.9 +/- 1.7 kg) and eight HF (22 +/- 1 yr 79.5 +/- 2.4 kg) voluntarily participated in the investigation. Maximal aerobic power (determined on a treadmill), plasma volume and blood volume (Evans blue dilution method) were significantly greater in the HF than AF (60.8 +/- 0.7 vs. 41.2 +/- 1.9 ml.kg-1.min-1, 3.96 +/- 0.17 vs 3.36 +/- 0.08 1, and 6.33 +/- 0.23 vs 5.28 +/- 0.13 1). Baseline heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP, measured by an intraradial catheter or a Finapres finger cuff), forearm blood flow (FBF, plethysmography), and FVR, calculated from the ratio (MAP-CVP)/FBF, were not different between the HF and the AF. Lower body negative pressure (LBNP, -5, -10, -15, and -20 torr) and passive leg elevation (LE, 50 cm) combined with lower body positive pressure (LBPP, +5, +10, and +20 torr) were utilized to elicit central hypovolemia and hypervolemia, respectively. Range of CVP (from LBNP to LE+LBPP) was similar in the AF (from -3.9 to +1.9 mm Hg) and HF (from -4.0 to +2.2 mm Hg). However, FVR/CVP was significantly less in the HF (-1.8 +/- 0.1 unit.mm Hg-1) than AF (-34 +/- 0.1 unit.mm Hg-1). The FVR decrease in response to increase in CVP was significantly diminished in the HF (-1.46 +/- 0.45 unit.mm Hg-1) compared to the AF (-4.40 +/- 0.97 unit.mm Hg-1), and during LBNP induced unloading the FVR/CVP of the HF (-2.01 +/- 0.49 unit.mm Hg-1) was less (P < 0.08) than the AF (-3.28 +/- 0.69 unit.mm Hg-1). We concluded that the cardiopulmonary baroreceptor mediated FVR reflex response was significantly less sensitive to changes in CVP in individuals who practice exercise training.