Exercise training in chronic heart failure: beneficial effects on cardiac (11)C-hydroxyephedrine PET, autonomic nervous control, and ventricular repolarization.

Abnormalities of autonomic nervous function are associated with a poor prognosis of patients with chronic heart failure (CHF). We studied the effects of a 6-mo exercise training program on Q-T interval dispersion, heart rate and blood pressure variability, baroreflex sensitivity, myocardial blood flow (MBF), and presynaptic sympathetic innervation in 13 patients with New York Heart Association class II-III heart failure. METHODS: MBF was measured with the H(2)(15)O and C(15)O technique. Cardiac presynaptic innervation was studied by (11)C-hydroxyephedrine (HED) retention assessed with PET. Heart rate and blood pressure variability and baroreflex sensitivity were tested with the phenylephrine method. All studies were performed before and after a 6-mo exercise training program. The exercise capacity was determined by spiroergometry, and Q-T dispersion was measured from a standard 12-lead electrocardiogram. RESULTS: Q-T dispersion was reduced after the training period (mean +/- SEM, from 52 +/- 5 to 36 +/- 5 ms [P = 0.01]). Global (11)C-HED retention improved from 0.228 +/- 0.099 to 0.263 +/- 0.066 s(-1) (P < 0.05). Global MBF was not affected by training, but MBF increased in areas of low initial perfusion in patients with coronary artery disease (from 0.382 +/- 0.062 to 0.562 +/- 0.083 mL/g/min [P < 0.005]). The high-frequency spectrum and total R-R interval variability increased (from 4.53 +/- 0.30 to 5.02 +/- 0.36 ms(2) [P < 0.05] and from 3.60 +/- 0.34 to 4.31 +/- 0.37 ms(2) [P < 0.005], respectively). Both changes correlated significantly with the observed change in (11)C-HED retention. There was a significant reduction of total and a near-significant reduction of low-frequency (LF) systolic blood-pressure (SBP) variability (from 4.89 +/- 1.03 to 3.18 +/- 0.48 [P < 0.05] and from 2.79 +/- 0.38 to 1.76 +/- 0.24 [P = 0.059], respectively). The decrease in LF SBP variability correlated inversely with the enhancement of (11)C-HED retention (r = -0.66; P < 0.05). Baroreflex sensitivity increased from 5.83 +/- 0.82 to 10.15 +/- 1.66 ms/mm Hg (P < 0.05). CONCLUSION: Exercise training induces beneficial changes in functional and imaging measures of cardiovascular autonomic nervous control. These observations point to a training-induced shift toward normalization of the compensatory autonomic nervous imbalance in CHF.     

Muscle sympathetic nerve activation during the Valsalva maneuver: interpretive and analytical caveats

INTRODUCTION: We investigated the relationship between arterial pressure and muscle sympathetic nerve activity (MSNA) to test the hypothesis that the Valsalva maneuver may be used to estimate magnitudes of sympathetic baroreflex activation. METHODS: We recorded the ECG, beat-by-beat arterial pressure, and MSNA in 33 subjects (25 men and 8 women, aged 18-25 yr) who performed three Valsalva maneuvers at 40 mmHg expiratory pressure for 15 s. Valsalva phases were identified and the magnitude of pressure changes were correlated with MSNA. Arterial pressure-MSNA relations were probed further with beat-by-beat linear regression analysis after subjects had been separated into responders (n = 20) and non-responders (n = 13) (> or < 10 mmHg decrease in diastolic pressure, respectively). RESULTS: We detected no significant correlations among the magnitudes of either systolic or diastolic pressure reductions and total MSNA. Slopes relating MSNA to beat-by-beat diastolic pressure decreases were greater (p = 0.01) for responders (-3.4 bursts x min(-1) x mmHg(-1)) than non-responders (0.8 bursts x min(-1) x mmHg(-1)), but total MSNA during straining was not different between the two groups. With both groups combined, total MSNA during phase II and III was positively correlated to both systolic (r = 0.41) and diastolic (r = 0.57) pressure during phase IV. CONCLUSIONS: Sympathetic activation during the Valsalva maneuver does not necessarily reflect arterial baroreflex mechanisms alone. Phase IV increases of arterial pressure correlate positively to MSNA during phase II and III, and therefore gross estimations of sympathetic neural activation are possible through examination of terminal arterial pressure elevations after release from strain.     

Recovery pattern of baroreflex sensitivity after exercise

PURPOSE: To test the association between exercise mode and the recovery pattern of baroreflex sensitivity (BRS) after exercise. METHODS: The study population included healthy male subjects (N = 12, age: 31 +/- 3 yr). Four different interventions were performed in a randomized order: 1) aerobic exercise session on a bicycle ergometer, 2) light resistance exercise session, 3) heavy resistance exercise session, and 4) control intervention with no exercise. All interventions lasted 40 min. R-R intervals and continuous blood pressure were measured before (10 min) and 30-180 min after the interventions. BRSLF was calculated by the transfer function method from the low-frequency band (LF, 0.04-0.15 Hz) of the R-R intervals and systolic blood pressure spectra. RESULTS: BRSLF had blunted until 30 min after aerobic and light resistance exercise (11.1 +/- 4.3 and 10.0 +/- 3.6 vs 17.5 +/- 7.0 ms.mm Hg(-1), P = 0.002 for both, compared with the control intervention, respectively). However, BRSLF was significantly blunted until 60 min after heavy resistance exercise (9.3 +/- 2.3 vs 15.1 +/- 4.7 ms.mm Hg(-1), P = 0.005, compared with the control intervention). The high-frequency power of R-R intervals (0.15-0.4 Hz) was significantly reduced, and the LF power of systolic blood pressure oscillation was significantly augmented 30 min after heavy resistance exercise (P < 0.01 for both), whereas both indices were restored to the control level by 30 min after aerobic and light resistance exercise. CONCLUSION: BRS after acute exercise is associated with exercise intensity, showing relatively rapid recovery after aerobic and light resistance exercise and delayed recovery after heavy resistance exercise. The delayed BRS pattern after heavy resistance exercise is regulated by delicate interplay between the withdrawal of vagal outflow and the probably increased sympathetic vasomotor tone documented by measurements of heart rate and blood pressure variability.     

Head rotation during upright tilt increases cardiovagal baroreflex sensitivity

INTRODUCTION: Vestibular activation of semicircular canals has been linked to increased activity of parasympathetic neurons and has been proposed as a contributing factor to orthostatic intolerance. However, the functional consequences of head yaw rotation during orthostasis on human autonomic function have not been documented. The purpose of this study was to determine the effects of voluntary head rotation on autonomic function during upright tilt. METHODS: ECG, beat-by-beat finger arterial pressure, respiratory rate, PetCO2, and cerebral blood flow velocity were recorded in 10 healthy subjects. Subjects were studied supine and during two separate 5-min periods of upright tilt to 70 degrees with and without continuous head yaw rotation (180 degrees at 0.25 Hz). Breathing frequency was controlled strictly at 0.25 Hz during each trial and data were analyzed in both time and frequency domains. Cross-spectral techniques (transfer functions) were used to assess cardiovagal baroreflex sensitivity and dynamic cerebral autoregulation. RESULTS: Head rotation during upright tilt increased transfer function magnitude between systolic pressure and R-R interval at the low frequency (0.04-0.15 Hz) from 8.1 +/- 2.3 to 10.4 +/- 1.6 ms x mmHg(-1) (p = 0.04), but did not affect estimates of vagal-cardiac efferent activity or cerebral blood flow velocity, hemodynamic oscillations, or dynamic cerebral autoregulation. CONCLUSIONS: Increased cardiovagal baroreflex sensitivity in conjunction with preserved cerebral autoregulation suggests that head rotation during upright tilt is unlikely to trigger orthostatic instability in normal, healthy humans.     

Carotid-cardiac baroreflex response and LBNP tolerance following resistance training.

The purpose of this study was to examine the effect of lower body resistance training on cardiovascular control mechanisms and blood pressure maintenance during an orthostatic challenge. Lower body negative pressure (LBNP) tolerance, carotid-cardiac baroreflex function (using neck chamber pressure), and calf compliance were measured in eight healthy males before and after 19 wk of knee extension and leg press training. Resistance training sessions consisted of four or five sets of 6-12 repetitions of each exercise, performed two times per week. Training increased strength 25 +/- 3 (SE)% (P = 0.0003) and 31 +/- 6% (P = 0.0004), respectively, for the leg press and knee extension exercises. Average fiber size in biopsy samples of m. vastus lateralis increased 21 +/- 5% (P = 0.0014). Resistance training had no significant effect on LBNP tolerance. However, calf compliance decreased in five of the seven subjects measured, with the group average changing from 4.4 +/- 0.6 ml.mm Hg-1 to 3.9 +/- 0.3 ml.mm Hg-1 (P = 0.3826). The stimulus-response relationship of the carotid-cardiac baroreflex response shifted to the left on the carotid pressure axis as indicated by a reduction of 6 mm Hg in baseline systolic blood pressure (P = 0.0471). In addition, maximum slope increased from 5.4 +/- 1.3 ms.mm Hg-1 before training to 6.6 +/- 1.6 ms.mm Hg-1 after training (P = 0.0141). Our results suggest the possibility that high resistance, lower extremity exercise training can cause a chronic increase in sensitivity and resetting of the carotid-cardiac baroreflex.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlated neurocardiologic and fitness changes in athletes interrupting training

PURPOSE: We studied nine male Dutch top marathon skaters during a 1-month interruption of their training schedules after their last contest in the winter to investigate a possible decline in baroreflex sensitivity. METHODS: Before and after this period, a maximal exercise test was done, and at days 0, 4, 7, 14, and 28 neurocardiologic measurement sessions--heart rate and noninvasive baroreflex sensitivity, recumbent and tilt--were performed. RESULTS: Interruption of training resulted in a significant and relevant decrease in the maximal oxygen uptake (from 65.7 +/- 5.8 to 61.6 +/- 4.7 mL O2 x kg(-1) x min(-1); P = 0.03), most likely associated with decreased competitive possibilities. Resting heart rate modestly increased (from 54.6 +/- 7.2 to 58.8 +/- 7.5 bpm), however, not significantly. Heart rate during 60 degrees tilt increased considerably (from 70.1 +/- 6.1 to 80.1 +/- 9.1 bpm; P = 0.01), possibly due to a decrease in blood volume and an increase in cardiopulmonary baroreflex gain. Arterial baroreflex sensitivity decreased significantly in the recumbent (from 13.3 +/- 5.4 to 9.8 +/- 3.8 ms x mm Hg(-1), P = 0.04), but not in the 60 degrees tilt position (from 6.7 +/- 2.0 to 6.0 +/- 2.5 ms x mm Hg(-1)). The relative decrease in baroreflex sensitivity and maximal oxygen uptake correlated significantly (r = 0.71, P = 0.02). CONCLUSIONS: In summary, our data show that correlated detrimental changes in fitness and baroreflex sensitivity are measurable in these athletes after a month of interruption of training.     

Cardiovascular regulation response to hypoxia during stepwise decreases from 21% to 15% inhaled oxygen

INTRODUCTION: The classical view states that hypoxia beyond an oxygen concentration of about 17% induces tachycardia. However, few studies have investigated the dose-dependent effects of acute normobaric hypoxia on autonomic nervous regulation of the cardiovascular system. Therefore, we evaluated the effects of stepwise hypoxia on cardiovascular neural regulation and postulated that acute normobaric hypoxia causes vagal withdrawal and sympathetic activation from 17% 02. METHODS: There were 18 healthy men who were exposed to acute stepwise normobaric hypoxia (21%, 19%, 17%, 15% 02). Spectral analysis of the RR interval and BP variability were used. RESULTS: BP was not altered. Heart rate significantly increased at 15% (21%, 59 +/- 2; 15%, 62 +/- 2 bpm). The low-frequency power of systolic BP variability (an index of vasomotor sympathetic nerve activity) significantly increased at 15% (21%, 6.1 +/- 1.3; 15%, 9.9 +/- 1.3 mmHg2). The low-frequency power of the RR interval variability significantly increased from 17% (21%, 1036 +/- 233; 17%, 1892 +/- 409; 15%, 1966 +/- 362 ms2), However, the high-frequency power of RR interval variability (an index of cardiac parasympathetic nerve activity) did not change. Associated with these changes, the ratio of low- to high-frequency power of RR interval variability as an index of relative cardiac autonomic balance significantly shifted toward sympathetic dominance (21%, 1.5 +/- 0.3; 15%, 2.2 +/- 0.3). All indices of cardiac baroreflex function (transfer function and sequence gains) were unchanged. DISCUSSION: These results suggest that acute exposure to normobaric mild hypoxia (O2 > or = 15%) induces increases in sympathetic vasomotor activity and cardiac sympathetic dominance resulting in an increased heart rate. However, 15% O2 hypoxia might not induce changes in static BP, vagal activity, or spontaneous arterial-cardiac baroreflex function.     

Effect of G-suit protection on carotid-cardiac baroreflex function

INTRODUCTION: To test the hypothesis that G-suit inflation could increase cardiac chronotropic responses to baroreceptor stimulation and enhance baroreflex buffering of BP, the carotid-cardiac baroreflex response of 12 subjects was measured across two levels of lower body negative pressure (LBNP = 0 and 50 mm Hg) and two levels of G-suit inflation (0 and 50 mm Hg) in random order. METHODS: Carotid-cardiac baroreflex stimulation was delivered via a silastic neck pressure cuff and responsiveness quantified by determination of the maximum slope of the stimulus-response function between R-R intervals (ms) and their respective carotid distending pressures (mmHg). RESULTS: Mean +/- SE baseline control baroreflex responsiveness was 3.8+/-0.4 ms x mm Hg(-1). LBNP reduced the baroreflex response to 2.7+/-0.4 ms x mm Hg(-1), but G-suit inflation with LBNP restored the baroreflex response to 4.3+/-0.6 ms x mm Hg(-1). CONCLUSIONS: These results suggest that, in addition to increased venous return and elevated peripheral resistance, G-suit inflation may provide protection against the debilitating effects of blood distribution to the lower extremities during orthostatic challenges such as standing or high +Gz acceleration by increasing cardiovascular responsiveness to carotid baroreceptor stimulation.     

Effects of repeated Valsalva maneuver straining on cardiac and vasoconstrictive baroreflex responses

INTRODUCTION: We hypothesized that repeated respiratory straining maneuvers (repeated SM) designed to elevate arterial BPs (arterial baroreceptor loading) would acutely increase baroreflex responses. METHODS: We tested this hypothesis by measuring cardiac baroreflex responses to carotid baroreceptor stimulation (neck pressures), and changes in heart rate and diastolic BP after reductions in BP induced by a 15-s Valsalva maneuver in 10 female and 10 male subjects at 1, 3, 6, and 24 h after performing repeated SM. Baroreflex responses were also measured in each subject at 1, 3, 6, and 24 h at the same time on a separate day without repeated SM (control) in a randomized, counter-balanced cross-over experimental design. RESULTS: There was no statistical difference in carotid-cardiac and peripheral vascular baroreflex responses measured across time following repeated SM compared with the control condition. Integrated cardiac baroreflex response (deltaHR/ deltaSBP) measured during performance of a Valsalva maneuver was increased by approximately 50% to 1.1 +/- 0.2 bpm x mm Hg(-1) at 1 h and 1.0 +/- 0.1 bpm x mm Hg(-1) at 3 h following repeated SM compared with the control condition (0.7 +/- 0.1 bpm x mm Hg(-1) at both 1 and 3 h, respectively). However, integrated cardiac baroreflex response after repeated SM returned to control levels at 6 and 24 h after training. These responses did not differ between men and women. CONCLUSIONS: Our results are consistent with the notion that arterial baroreceptor loading induced by repeated SM increased aortic, but not carotid, cardiac baroreflex responses for as long as 3 h after repeated SM. We conclude that repeated SM increases cardiac baroreflex responsiveness which may provide patients, astronauts, and high-performance aircraft pilots with protection from development of orthostatic hypotension.     

Simultaneous arterial pressure recordings improve the detection of endofibrosis

PURPOSE: Exercise improves the diagnostic performance of ankle-to-brachial index (ABI) in the detection of exercise-induced arterial endofibrosis (EIAE). Pressure values for all four limbs are required to calculate ABI, but rapid systemic pressure changes occur during the recovery period from exercise. We checked whether after exercise, ABI calculated from simultaneous measurements was better than from consecutive measurements for differentiating athletes with EIAE from normal athletes. METHODS: We studied 42 normal athletes and 42 athletes suffering from unilateral pain caused by histologically proven EIAE. Bilateral brachial and ankle (ASBP) systolic blood pressure levels were simultaneously measured in the supine position at rest and every minute during the first 4 min of the recovery from incremental maximal exercise. Using receiver operating characteristics curves (ROC), we compared the diagnostic performance of single-leg ASBP and ABI values and between-leg ASBP (DeltaASBP) and ABI (DeltaABI) differences, calculated from simultaneous (simu) versus consecutive (cons) measurements, to discriminate athletes with EIAE from normal athletes. RESULTS: For single-leg postexercise values, ROC curve area was significantly higher for ABIsimu compared with ASBPsimu (P < 0.05, r = 0.91) and ASBPrand (P < 0.05, r = 0.68). Areas (+/- SE of area) of the ROC curves for postexercise Delta ASBPsimu and Delta ABIsimu were 0.97 +/- 0.01 and 0.97 +/- 0.02, respectively, and were higher than areas for postexercise Delta ASBP and Delta ABI calculated from consecutive and random measurements (P < 0.01). Accuracy for postexercise Delta ASBPsimu and Delta ABIsimu in discriminating EIAE from normal athletes was 93% [95% CI; 85-97], with a cutoff point of 22 mm Hg and 0.10, respectively. CONCLUSION: Delta ASBP and/or Delta ABI calculated from simultaneous pressure measurements should be recommended when searching for unilateral EIAE. Whether this result is applicable in the detection of early atherosclerotic lesions in sedentary subjects requires future investigation.     

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.     

Exercise training and autonomic nervous system activity in obese individuals

PURPOSE: This study was designed to investigate the effects of 12 wk of exercise training on autonomic nervous system (ANS) in 18 obese middle-aged men (N = 9) and women (N = 9) (age: 41.6 +/- 1.2 yr; BMI: 27.3 +/- 0.4 kg x m(-2); %fat: 29.6 +/- 1.3%, mean +/- SE). METHODS: Each subject participated in an aerobic exercise training at anaerobic threshold (AT), consisting of 30 min/session, 3 times/wk, for 12 consecutive weeks. The ANS activities were assessed by means of power spectral analysis of heart rate variability (HRV) at resting condition before, at 5 wk, and after the exercise program. RESULTS: The exercise training resulted in a significant decrease in body mass, BMI, and % fat (P < 0.01) but not in lean body mass (P > 0.05) together with a significant increase in the AT VO2 (P < 0.01). Our power spectral data indicated that there were significant increases in the low-frequency component associated with the sympathovagal activity (0.03--0.15 Hz, 348.5 +/- 66.8 vs 694.7 +/- 91.5 ms(2), P < 0.01), the high-frequency vagal component (0.15--0.4 Hz, 146.3 +/- 30.4 vs 347.7 +/- 96.5 ms(2), P < 0.05), and the overall autonomic activity as evaluated by total power (0.03--0.4 Hz, 494.8 +/- 88.5 vs 1042.4 +/- 180.9 ms(2), P < 0.01) of HRV after the training. CONCLUSIONS: Twelve weeks of exercise training has significantly improved both the sympathetic and parasympathetic nervous activities of the obese individuals with markedly reduced ANS activity, suggesting a possible reversal effect of human ANS functions. These favorable changes may also have an influence on the thermoregulatory control over the obesity.     

Effects of exercise load and breathing frequency on heart rate and blood pressure variability during dynamic exercise.

It is known that heart rate (HR) variability decreases with dynamic exercise, but there are only few studies on blood pressure (BP) variability with exercise loads and the effect of breathing pattern has never been investigated. Thus, we studied HR and systolic blood pressure (SBP) signals by spectral analysis (FFT), in 9 healthy subjects, at different breathing frequencies (0.15, 0.2, 0.3, 0.4, 0.5, 0.6 Hz), at rest and during 3 exercise loads (25, 50 and 75% VO2max). BP was measured with a non-invasive device (Finapres) and continuously recorded. The power spectrum of R-R period significantly decreased with exercise loads in the low frequency band (LF: 0.04-0.128 Hz) and in the high frequency band (HF: 0.128-0.65 Hz), but with breathing frequency only in the HF part of the spectrum. The power spectrum of SBP significantly increased with exercise loads in LF and HF bands, and decreased in HF band with increasing breathing frequency. R-R and SBP HF peaks were centered on breathing frequency peaks. Therefore, spectral analysis of HR and SBP confirm the withdrawal of vagal control during exercise, while mechanical effect of respiration on SBP persists. LF/HF ratio of R-R spectral components decreased with increasing load, whereas cardiovascular sympathetic activity is known to rise, suggesting that this ratio is not a good indicator of cardiovascular autonomic modulation during exercise.     

Dipyridamole myocardial SPECT with low heart rate response indicates cardiac autonomic dysfunction in patients with diabetes

BACKGROUND: Because dipyridamole is used to assess heart rate (HR) variability, we investigated whether a low HR response during dipyridamole single photon emission computed tomography (SPECT) in patients with diabetes indicates the presence of cardiac autonomic neuropathy (CAN). METHODS AND RESULTS: Subjects were 61 non-insulin-dependent diabetes patients without perfusion defects, myocardial infarction, or arrhythmia who underwent thallium 201 SPECT imaging. The control group comprised 28 subjects without diabetes. HR was measured during infusion of dipyridamole at a rate of 0.14 mg/kg/min, and peak-baseline ratios of 1.20 or less were defined as low. CAN severity was classified by standard autonomic function tests as severe (n = 22), mild (n = 19), or none (n = 20). HR ratios were significantly attenuated in patients with diabetes compared with those in control subjects (1.22 +/- 0.12 vs 1.32 +/- 0.12, P <.001). Among the patients with diabetes, HR ratios decreased as CAN severity increased from none (1.32 +/- 0.10) to mild (1.23 +/- 0.12, P <.05) to severe (1.13 +/- 0.08, P <.005). There was good correlation between HR ratio and R-R interval ratio to deep breathing and to Valsalva, and patients with low HR ratios showed an attenuated response to both tests (all P <.001). The sensitivity and specificity of HR ratios in the detection of CAN were 77% and 74% for severe CAN and 63% and 90% for mild-to-severe CAN, respectively. CONCLUSIONS: In patients with diabetes who have normal dipyridamole SPECT results, an attenuated HR response observed during stress indicates a high likelihood of CAN. Further work that assesses these results in diabetes patients with coronary artery disease is warranted.     

Effects of acute exercise on attenuated vagal baroreflex function during bed rest.

We measured carotid baroreceptor-cardiac reflex responses in six healthy men, 24 h before and 24 h after a bout of leg exercise during 6 degrees head-down bed rest to determine if depressed vagal baroreflex function associated with exposure to microgravity environments could be reversed by a single exposure to acute intense exercise. Baroreflex responses were measured before bed rest and on day 7 of bed rest. An exercise bout consisting of dynamic and isometric actions of the quadriceps at graded speeds and resistances was performed on day 8 of bed rest and measurements of baroreflex response were repeated 24 h later. Vagally-mediated cardiac responses were provoked with ramped neck pressure-suction sequences comprising pressure elevations to +40 mm Hg, followed by serial, R-wave triggered 15 mm Hg reductions, to -65 mm Hg. Baroreceptor stimulus-cardiac response relationships were derived by plotting each R-R interval as a function of systolic pressure less the neck chamber pressure applied during the interval. Compared with pre-bed rest baseline measurements, 7 d of bed rest decreased the gain (maximum slope) of the baroreflex stimulus-response relationship by 16.8 +/- 3.4% (p < 0.05). On day 9 of bed rest, 24 h after exercise, the maximum slope of the baroreflex stimulus-response relationship was increased (p < 0.05) by 10.7 +/- 3.7% above pre-bed rest levels and 34.3 +/- 7.9% above bed rest day 7. Our data verify that vagally-mediated baroreflex function is depressed by exposure to simulated microgravity and demonstrate that this effect can be acutely reversed by exposure to a single bout of intense exercise.     

Endurance training alters arterial baroreflex function in dogs

The present study was designed to determine whether 12 wk of daily exercise alter autonomic neural control of the heart during baroreflex stimulation in healthy dogs. We studied 16 untrained and 12 endurance-trained anesthetized dogs which were instrumented to measure arterial blood pressure (AP), carotid sinus baroreceptor pressure (CBP), electrocardiogram (ECG), heart rate (HR), and R-R interval (RR). The arterial baroreflex was studied during hypertension caused by i.v. bolus infusion of phenylephrine, hypotension caused by i.v. bolus infusion of nitroprusside, and bilateral carotid occlusion (BCO) in which carotid sinus pressure was reduced to 41 +/- 2 mm Hg (mean +/- SEM). Arterial baroreflex sensitivity, which was assessed by determining the change in heart interval (i.e., change in RR) per unit change in systolic AP (delta RR/delta AP), was significantly lower during the hypertensive challenge in the trained dogs compared to the untrained dogs (2.2 +/- 0.3 vs 6.8 +/- 1.5 ms.mm Hg-1, respectively). Similarly, the delta RR/delta AP was substantially lower during the hypotensive challenge in trained dogs vs the untrained dogs (1.2 +/- 0.3 vs 1.8 +/- 0.4 ms.mm Hg-1, respectively). In addition, the HR response to the BCO was significantly less in trained dogs (22 +/- 2 bpm) vs untrained dogs (32 +/- 5 bpm). The open-loop gain (Go), which was used to quantitate the effectiveness of the carotid baroreflex to increase mean systemic AP during BCO, was similar in both untrained and trained dogs (2.9 +/- 0.6 and 2.4 +/- 0.5, respectively). These data indicate that, while endurance training significantly reduces the HR component of the arterial baroreflex, the arterial pressure response apparently is not altered.     

Does endurance training affect orthostatic responses in healthy elderly men?

PURPOSE: To investigate the effects and time course of endurance training on the regulation of heart rate (HR), arterial pressure (AP), norepinephrine (NE), and plasma volume (PV) during orthostatic stress in healthy elderly men. METHODS: Thirty-one healthy men (65--75 yr) were randomly allocated into endurance training (N = 20, EX) and control (N = 11, CON) groups. The EX group cycled 3 d x wk(-1) for 30 min at 70% VO(2peak) for 12 wk x VO(2peak) was determined on an electronically braked cycle ergometer, before training and after 4, 8, and 12 wk of endurance training. The immediate (initial 30 s), early steady-state (1 min), and prolonged (5, 10, 15 min) beat-by-beat HR and AP responses during 90 degrees head-up tilt (HUT) were measured at least 3 d after each VO(2peak) test. Spontaneous baroreflex slopes were determined by application of linear regression to sequences of at least three cardiac cycles in which systolic blood pressure (SBP) and R-R interval changed in the same direction. Venous blood was collected during 90 degrees HUT and analyzed for changes in plasma NE concentrations, as well as hematocrit and hemoglobin to determine changes in PV. RESULTS: Endurance training significantly (P < 0.01) increased VO(2peak) (mL x kg(-1) x min(-1)) in EX by 10 +/- 2%. The immediate, early steady-state, and prolonged HR and AP responses and spontaneous baroreflex slopes during 90 degrees HUT were not significantly different (P > 0.05) between EX and CON groups before or after 4, 8, or 12 wk of endurance training. No significant differences (P > 0.05) were observed between EX and CON groups for peak changes in PV during orthostasis before (-15.0 +/- 1.4% vs -11.9 +/- 1.3%) or after 4 (-12.2 +/- 1.0% vs -12.7 +/- 1.4%), 8 (-13.7 +/- 1.2% vs -12.4 +/- 0.7%), and 12 wk (-10.8 +/- 1.6% vs -10.6 +/- 0.6%) of endurance training, suggesting a similar stimulus presented by 90 degrees HUT in both groups. Peak changes in NE concentrations during HUT were similar (P > 0.05) between EX and CON groups before (119 +/- 23 pg x mL(-1) vs 191 +/- 36 pg x mL(-1)) and after 4 (139 +/- 29 pg x mL(-1) vs 146 +/- 25 pg x mL(-1)), 8 (114 +/- 32 pg x mL(-1) vs 182 +/- 41 pg x mL(-1)), and 12 wk (143 +/- 35 pg x mL(-1) vs 206 +/- 42 pg.mL-1) of endurance training. CONCLUSIONS: These data indicate that in healthy elderly men, improvements in VO(2peak) can occur without compromising the regulation of HR, AP, NE, and PV during orthostatic stress.     

Airway cell composition at rest and after an all-out test in competitive rowers

PURPOSES: This study was designed to assess: a) whether rowing affects airway cell composition, and b) the possible relationship between the degree of ventilation during exercise and airway cells. SUBJECTS AND METHODS: In nine young, nonasthmatic competitive rowers (mean age +/- SD: 16.2 +/- 1.0 yr), induced sputum samples were obtained at rest and shortly after an all-out rowing test over 1000 m (mean duration: 200 +/- 14 s), during which ventilatory and metabolic variables were recorded breath-by-breath (Cosmed K4b, Italy). RESULTS: At rest, induced sputum showed prevalence of neutrophils (60%) over macrophages (40%); after exercise, total cell and bronchial epithelial cell (BEC) counts tended to increase. In the last minute of exercise, mean VE was 158.0 +/- 41.5 L x min(-1), and VO2 x kg(-1) 62 +/- 11 mL x min(-1). Exercise VE correlated directly with postexercise total cell (Spearman rho: 0.75, P < 0.05) an dmacrophage (rho: 0.82, P < 0.05) counts. A similar trend was observed for exercise VE and changes in BEC counts from baseline to postexercise (rho: 0.64, P = 0.11). Exercise VE did not correlate with airway neutrophil counts at rest or after exercise. Expression of adhesion molecules by airway neutrophils, macrophages, and eosinophils decreased after the all-out test. CONCLUSION: Similar to endurance athletes, nonasthmatic competitive rowers showed increased neutrophils in induced sputum compared with values found in sedentary subjects. The trend toward increased BEC postexercise possibly reflected the effects of high airflows on airway epithelium. Airway macrophages postexercise were highest in rowers showing tile most intense exercise hyperpnea, suggesting early involvement of these cells during exercise. However, the low expression of adhesion molecules by all airway cell types suggests that intense short-lived exercise may be associated with a blunted response of airway cells in nonasthmatic well-trained rowers.     

Effect of ipratropium bromide on EIB in children depends on vagal activity

PURPOSE: Ipratropium bromide (IB) has been used to prevent exercise-induced bronchoconstriction (EIB), but its effect varies among individuals. We hypothesized that such variability may reflect individual differences in vagal activity (VA), and therefore determined whether a correlation exists between VA and the effect of IB on EIB in 13.0 (+/-0.8)-yr-old children with asthma and documented EIB. METHODS: Subjects served as their own control and were tested on three occasions in an ambient temperature of 5 degrees C. Visit I included no treatment. In visits II and III (counterbalanced sequence) subjects inhaled either 500 microg IB or 0.9% NaCl as a placebo, 45 min before exercise provocation. Investigators and the subjects were blinded to the inhaled substance. VA was assessed by a 4-s exercise test (3). The ratio of resting ECG R-R-interval at full inspiration to the lowest R-R interval during 4-s cycling was taken as an index of VA. Eight-minute cycling at constant work rate (HR=173+/-4 bpm) at 5 degrees C was used to provoke EIB. A two-factor (treatment x time) repeated-measures ANOVA was used. RESULTS: The exercise-induced drop in FEV1 was similar in the three sessions. However, because the IB caused a 15.7+/-4.1 increase in FEV1 preexercise, the postexercise values after a placebo or no treatment were consistently lower than after IB. The beneficial response to IB, compared with no treatment and with placebo, was positively correlated to VA (for FEV1: r=0.91, P=0.002; and r=0.90, P=0.002, respectively). CONCLUSION: We suggest that the therapeutic effect of IB on exercise-induced asthma may be related to vagal activity.     

Attenuation of human carotid-cardiac vagal baroreflex responses after physical detraining.

Astronauts who are occupied with prelaunch schedules may have to limit their regular physical exercise routines. To assess a potential effect on blood pressure control, carotid baroreceptor-cardiac reflex responses of 16 men (30-45 years of age) were evaluated before and after 2 weeks of exercise detraining that followed 10 weeks of regular scheduled exercise (30 min/d, 4 d/week at 75% Vo2max). At mid-expiration, the subjects held their breath and 40 mm Hg of pressure was applied to a neck chamber for four heart beats, followed by 15-mm Hg, R-wave triggered decrements to -65 mm Hg. Changes of R-R intervals were plotted against carotid distending pressure (systolic-neck chamber pressure). After detraining, the baroreflex stimulus-response relationship had a reduced slope [4.0 +/- 0.5 vs. 2.8 +/- 0.4 msec/mmHg (p = 0.0008)] and range of response [191 +/- 19 vs. 145 +/- 17 ms (p = 0.002)]. In addition, there was a resetting of the relationship on the R-R interval axis. Both the minimum and maximum R-R interval responses to the stimulus were significantly reduced after detraining [953 +/- 32 vs. 909 +/- 36 ms (p = 0.035) and 1145 +/- 36 vs. 1054 +/- 39 (p = 0.002)]. Baseline systolic pressure did not change with detraining (116 +/- 2 vs. 114 +/- 2 mm Hg) and the carotid baroreceptor-cardiac response relationship did not shift on the pressure axis. These results suggest that detraining from regular exercise can compromise vagally-mediated mechanisms of blood pressure regulation.