The autonomic and rate pressure product responses of tai chi practitioners.

BACKGROUND: Spectral analysis of autonomic nervous system activity can provide insight into cardiovascular function. Rate pressure product is the parameter often targeted pharmacologically to decrease the incidence of myocardial events. AIM: The purpose of this study was to investigate whether or not Tai Chi Chuan practitioners would demonstrate autonomic responses that would be more cardioprotective when compared to non-trained controls. MATERIALS AND METHODS: This was a cross-sectional study that measured the autonomic responses and rate pressure product of 2 groups of subjects; a Tai Chi Chuan trained (n = 13) and non-trained sedentary controls (n = 13) at rest and during 2 stressor phases that simulated functional activities of daily living. RESULTS: The Tai Chi group maintained a greater parasympathetic outflow at rest and during the isometric grip stressor phase (P<0.05). Sympathetic outflow, systolic blood pressure and rate pressure product were significantly lower in the Tai Chi group at rest, during the isometric grip and standing stressor phases (P<0.05). CONCLUSION: Although a cause-and-effect relationship cannot be concluded in this study, the Tai Chi group was able to demonstrate efficiency of the myocardium with suppressed rate pressure product values and autonomic responses that favored parasympathetic outflow. This type of training may complement non-pharmacological anti-hypertensive therapy.

Impact of aerobic training on cardiovascular reactivity to and recovery from challenge.

OBJECTIVE: To test the hypothesis that aerobic, but not strength, training would lead to attenuated reactivity to and more rapid recovery from cognitive and orthostatic challenge and that deconditioning would reverse this effect. METHODS: We conducted a randomized controlled trial contrasting the effects of aerobic versus strength training on heart rate, four indices of RR interval variability, and blood pressure reactivity to and recovery from psychological and orthostatic challenge in 149 healthy, young, sedentary adults. Subjects were randomized to 12-week aerobic or strength training programs and studied before and after training and again after 4 weeks of sedentary deconditioning. The data were analyzed by performing a Group (aerobic versus strength) by Session (study entry, post training, and deconditioning), by Period (baseline, speech, Stroop, math, tilt) three-way analysis of variance with prespecified contrasts of the effect of group assignment on reactivity and recovery. RESULTS: Aerobic capacity increased in response to conditioning and decreased after deconditioning in the aerobic, but not the strength, training group. However, the two groups did not differ on heart rate, RR interval variability, or blood pressure reactivity to or recovery from laboratory challenge. CONCLUSIONS: These findings, from the largest randomized controlled trial to address this matter to date, raise doubts about attenuation of reactivity or enhancement of recovery as a putative mechanism underlying the cardioprotective effects of aerobic exercise. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT00365196.

Association of body fat percentage and heart rate variability measures of sympathovagal balance.

AIMS: We tested the hypothesis that body fat percentage determines cardiac sympathovagal balance in healthy subjects. MAIN METHODS: Heart rate variability (HRV) measurements were made of the standard deviation of the normal-normal RR intervals (SDNN) and the low frequency/high frequency (LF/HF) ratio, from time domain and fast Fourier transform spectral analysis of electrocardiogram RR intervals during trials of uncontrolled and controlled (paced) breathing at 0.2Hz. Body fat percentage was measured by dual energy x-ray absorptiometric (DEXA) scanning. Significance of differences between uncontrolled and controlled (paced) breathing was determined by analysis of variance and correlations between body fat percentage and HRV measurements by Pearson's coefficient at P<0.05. KEY FINDINGS: Percent body fat was negatively correlated with LF/HF during the uncontrolled breathing (r=-0.56, two-tailed P<0.05, one-tailed P<0.01) but not during the paced breathing trial (r=-0.34, (P>0.1). SIGNIFICANCE: We conclude that sympathetic activity produced by paced breathing at 0.2Hz can obscure the relationship between body fat percentage and sympathovagal balance and that high body fat percentage may be associated with low sympathetic modulation of the heart rate in healthy adolescent/young adult males.

Effects of acute nitric oxide synthase inhibition on lower leg vascular function in chronic tetraplegia.

BACKGROUND/OBJECTIVE: To improve our understanding of the lower-leg vascular responses of nitric oxide synthase inhibition in persons with tetraplegia. PARTICIPANTS: Six people with chronic tetraplegia and 6 age-matched controls. METHODS: Lower-leg relative vascular resistance and venous volume variation were obtained by venous occlusion plethysmography and blood pressure by auscultation at baseline. Postintravenous infusion of the nitric oxide synthase inhibitor NG-nitro-L-arginine-methyl-ester (1 mg x kg(-1) or placebo on separate days. RESULTS: At baseline in the group with tetraplegia compared with controls, mean arterial pressure and relative vascular resistance of the leg were significantly lower. After nitric oxide synthase inhibition, mean arterial pressure and lower leg vascular resistance were significantly elevated in both groups. There were no group or intervention differences in venous volume variation. CONCLUSION: These preliminary results suggest that nitric oxide synthase inhibition with 1 mg x kg(-1) N(G)-nitro-L-arginine-methyl-ester normalizes seated blood pressure and lower leg vascular resistance to control group baseline levels.

Cold face test in persons with spinal cord injury: age versus inactivity.

INTRODUCTION: Persons with spinal cord injury (SCI) reflect a model of precocious aging and inactivity; as such, these individuals manifest well-appreciated cardiovascular abnormalities. We aimed to determine the influence of inactivity in persons with SCI, and the influence of age in healthy controls, on cardiovascular autonomic responses to the cold face test (CFT). METHODS: Subjects recruited (n = 42) included 18 controls: 10 young (25 +/- 2 years) and 8 old (50 +/- 6 years), and 24 subjects with chronic SCI: 17 with tetraplegia (C3-C8 44 +/- 7 years) and 7 with paraplegia (T5-T10 36 +/- 8 years). Heart rate (HR) and blood pressure were collected continuously: 2-min pre-CFT, 1-min CFT and 2-min post-CFT. Time-frequency (wavelet) analysis of HR (HFln) was used as an estimate of vagal cardiac modulation. RESULTS: The HR response to the CFT differed significantly among the SCI group (4.1 +/- 8.8 bpm) and the young (-7.7 +/- 5.9 bpm; P \ 0.001) and old (-6.8 +/- 10.7 bpm; P \ 0.01). The HFln response was reduced in the SCI (0.01 +/- 1.59) as compared with the young controls (1.50 +/- 1.50; P \ 0.05), but was not different from the old controls (0.69 +/- 1.39). The bradycardia did not differ among the young and old controls; however, the vagal response was attenuated in the old compared with the young. These data suggest that age does not significantly alter the heart rate response to the CFT, but attenuates the vagal response. CONCLUSION: In the SCI group, the paradoxical heart rate response to facial cooling and the lack of vagal activation suggest that abnormal autonomic cardiovascular reflexive control may result from profound inactivity and/or from the spinal cord injury per se.

Effects of high-carbohydrate and high-fat dietary treatments on measures of heart rate variability and sympathovagal balance.

AIMS: We tested the hypothesis that respiratory quotient (RQ) determines sympathovagal balance associated with metabolism of stored and dietary energy substrates. MAIN METHODS: Six 18-20 year-old African-American males were studied after two control pretreatments of fasting and post-treatments of metabolizing high-fat and high-carbohydrate beverages. RQ, heart rate (HR), energy expenditure (EE) and blood pressure (BP) were recorded at rest and repeated 1 h-3 h after ingesting isocaloric high-carbohydrate and high-fat beverages. Sympathovagal modulation of HR was quantified by the low frequency/high frequency (LF/HF) ratio from fast Fourier transform (spectral) analysis of the electrocardiogram RR intervals during paced breathing at 0.2 Hz. Significance of differences of peak post-treatment values from controls was evaluated by analysis of covariance and of correlations by linear regression at P<0.05. KEY FINDINGS: The high-carbohydrate and high-fat treatments increased RQ, EE, HR and LF/HF with significant interactions between covariates. LF/HF values were not significant after eliminating covariance of RQ, EE and HR for the control vs. high-fat and for the high-fat vs. high-carbohydrate and after eliminating covariance of EE and HR for the control vs. high-carbohydrate treatments. Across the RQ values, correlations were significant for EE and LF/HF. SIGNIFICANCE: These findings imply that high RQ and sympathetic modulation produced by metabolizing carbohydrate is associated with high resting energy expenditure. We conclude that respiratory quotient may be an important determinant of the LF/HF ratio in the heart rate variability spectrum, likely, by a respiratory chemosensory mechanism.

The effect of aerobic training and cardiac autonomic regulation in young adults.

OBJECTIVES: We tested the effect of aerobic exercise on autonomic regulation of the heart in healthy young adults. METHODS: Healthy, sedentary young adults (n = 149; age = 30.4 +/- 7.53 years) were randomized to receive 12 weeks of either aerobic conditioning or strength training. Primary outcomes were heart rate and RR interval variability (RRV) measured before and after training and after 4 weeks of sedentary deconditioning. RRV, a noninvasive index of cardiac autonomic regulation, reflects variability in the intervals between consecutive R waves of the electrocardiogram. RESULTS: Aerobic conditioning but not strength training led to a significant increase in aerobic capacity (3.11 mL/kg/min), a decrease in heart rate (-3.49 beats per minute), and an increase in high-frequency RRV (0.25 natural log msec2), each of which returned to pretraining levels after deconditioning. Significant 3-way interactions, however, revealed autonomic effects only in men. CONCLUSIONS: In sedentary, healthy young adults, aerobic conditioning but not strength training enhances autonomic control of the heart, but post hoc analyses suggested that gender plays a significant role in this exercise-related cardioprotection.

Effect of hypotensive challenge on systemic hemodynamics and cerebral blood flow in persons with tetraplegia.

INTRODUCTION: Individuals with tetraplegia have impaired central control of sympathetic vascular modulation and blood pressure (BP); how this impairment affects cerebral blood flow (CBF) is unclear. OBJECTIVES: To determine if persons with tetraplegia maintain CBF similarly to able-bodied controls after a hypotensive challenge. METHODS: Seven individuals with chronic tetraplegia and seven age-matched, non-SCI control subjects underwent a hypotensive challenge consisting of angiotensin-converting enzyme (ACE) inhibition (1.25 mg enalaprilat) and 45 degrees head-up tilt (HUT). Heart rate (HR), low frequency systolic BP variability (LFsbp), brachial mean arterial pressure (MAP) and middle cerebral artery CBF were measured before and after the challenge. Group differences for the baseline (BL) to post-challenge response were determined by repeated measures ANOVA. RESULTS: HR did not differ between the groups in response to the hypotensive challenge. LFsbp response was significantly reduced in the tetra compared to the control group (-38 +/- 51 vs. 72 +/- 93%, respectively). MAP did not differ between the groups at BL but was significantly lower in the tetra compared to the control group post-challenge (55 +/- 13 vs. 71 +/- 9 mmHg, respectively); the percent change in MAP was significantly greater in the tetra than in the control group (-29 +/- 14.1 vs. -13 +/- 9%, respectively). However, CBF did not differ between the groups at baseline or post-challenge; the percent change in CBF post-challenge was not different between the tetra and control groups (-29 +/- 13.2 vs. -23 +/- 10.3%, respectively). INTERPRETATION: Despite impaired sympathetic vasomotor and BP control, CBF in persons with tetraplegia was comparable to that of control subjects during a hypotensive challenge.

Exercise training improves cardiovascular and autonomic profiles in HIV.

OBJECTIVES: Human immunodeficiency virus (HIV) is associated with cardiovascular (CV) and autonomic dysfunction, however the effects of fitness on vascular and autonomic mechanisms in HIV disease are unknown. METHODS: We studied forty-eight subjects (40.4 +/- 4.2 years) in a cross-sectional design matched for age, gender, BMI, and fitness. Participants were assigned to 1 in 4 groups: 1) Healthy Unfit (HU), 2) Healthy Fit (HF), 3) HIV Positive Unfit (HPU), and 4) HIV Positive Fit (HPF). Fitness was assessed via open-circuit spirometry; arterial compliance and autonomic modulations were measured via applanation tonometry and power spectral analysis, respectively, and baroreflex sensitivity was obtained using the alpha index. RESULTS: Arterial compliance was augmented in HPF vs. HPU [7.4 +/- 1.9 mmHg x second vs. 4.4 +/- 1.7 mmHg x second (P = 0.006)]. Parasympathetic modulation was higher in HPF vs. HPU [2244.5 +/- 2997.6 msecond(2) vs. 489.1 +/- 552.9 msecond(2) (P < 0.05)]. Sympathetic modulation was lower in HPF vs. HU [4.7 +/- 5.0 mmHg(2) vs. 12.9 +/- 9.7 mmHg(2) (P < 0.05)]. Baroreflex sensitivity was higher in HPF vs. HPU [17.3 +/- 10.2 msecond/mmHg vs. 7.4 +/- 3.8 msecond/mmHg (P = 0.003)], and HPF vs. HU [17.3 +/- 10.2 msecond/mmHg vs. 6.2 +/- 3.0 msecond/mmHg (P = 0.004)]. CONCLUSIONS: Augmentations in arterial compliance and baroreflex sensitivity associated with fitness portent an improved CV and autonomic profile for HIV-positive individuals. Physical activity may be an adjuvant method to enhance the overall vascular health in HIV-compromised individuals.

Aerobic exercise attenuates inducible TNF production in humans.

Aerobic exercise reduces coronary heart disease risk, but the mechanisms of this protection are not fully understood. Atherosclerosis is an inflammatory disease mediated by monocyte-derived macrophages, which accumulate in arterial plaques and become activated to release factors, including cytokines, that cause damage. Here we studied the effects of aerobic training on monocyte production of tumor necrosis factor (TNF) in whole blood ex vivo. Healthy young sedentary adults (n = 61, age 20-45 yr) were randomized to a moderate- (M) or a high- (H) intensity 12-wk training program. Whole blood was extracted before and after training, and then it was stimulated by addition of lipopolysaccharide (LPS); inducible TNF was measured in the plasma. Data were analyzed according to intention to treat principles using a random-effect model to determine the impact of training group on maximal aerobic capacity and LPS-stimulated TNF after correcting for covariates. Analyses revealed improvement in aerobic capacity in both the H (9%) and the M (7%) groups. However, aerobic training led to significant (P < 0.001) decreases in TNF release only in the H group. These data suggest that in healthy young adults, a 12-wk high-intensity aerobic training program downregulates blood monocyte production of stimulated cytokine release.

Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation.

Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.

Arterial stiffness in persons with paraplegia.

BACKGROUND: Arterial stiffness recently has been identified as an independent risk factor for cardiovascular disease. An accurate and noninvasive estimate of arterial stiffness can be made through close examination of the pulse wave contour, and is expressed as the augmentation index (AI). Increased stiffness is associated with increased systolic blood pressure (SBP), pulse pressure, and reduced baroreceptor sensitivity. The purpose of this study was to compare the common carotid AI in participants with paraplegia vs able-bodied controls as well as compare group differences for blood pressure while supine and in response to gravitational stress. PARTICIPANTS: Study participants were 19 healthy individuals with paraplegia (below T6) and 9 able-bodied controls matched for age, height, and weight. METHODS: An electronic tilt table was used for testing responses to gravitational stress at 4 angles (-10 degrees, 10 degrees, 35 degrees, and 75 degrees). AI was assessed at each angle of tilt using an externally applied high-fidelity strain-gauge transducer placed over the right common carotid artery. RESULTS: AI was augmented in the group with paraplegia compared with the able-bodied group (8.0 +/- 3.9 vs 6.7 +/- 2.8, respectively; P < 0.05). Supine blood pressure and the SBP response to tilt did not differ between the groups, and there were no tilt-angle effects on SBP. CONCLUSION: In normotensive persons with paraplegia, AI was increased significantly compared with matched able-bodied controls, which may suggest the premature development of arterial disease in this population.

High-frequency modulation of heart rate variability during exercise in patients with COPD.

STUDY OBJECTIVES: To evaluate cardiac autonomic modulation in patients with COPD during peak exercise. METHODS: Fifty-three patients with COPD (mean FEV(1), 35% predicted [SD, 11% predicted]; mean PaO(2), 68 mm Hg [SD, 11 mm Hg]; mean PaCO(2), 40 mm Hg [SD, 7 mm Hg]; mean age, 61 years [SD, 10 years]; 26 women and 27 men) and 14 healthy control subjects aged 60 years (SD, 8 years) [seven women and seven men] were studied at rest and during ramped bicycle ergometry to their volitional peak. Patients were not receiving autonomic medications other than inhaled beta-agonist agents and/or anticholinergic agents. Control subjects were not receiving any medications. Cardiac autonomic modulation was assessed via time-frequency analysis (Wigner-Ville) of ECG-derived heart rate variability as the power in the low-frequency (LF) band (ie, 0.04 to 0.15 Hz) and the high-frequency (HF) band (ie, > 0.15 to 0.4 Hz) averaged from > 3 min at rest and minutes 2 through 5 of their exercise period. RESULTS: Patients with COPD had a significantly increased mean, ln-transformed HF band from rest to peak exercise (9.9 ms(2) [SD, 1.4 ms(2)] vs 10.7 ms(2) [SD, 1.4 ms(2)], respectively; p < 0.01), while the HF band was unchanged for the control group (10.7 ms(2) [SD, 1.5 ms(2)] vs 10.4 ms(2) [1.3 ms(2)], respectively; difference not significant). The mean ln-transformed LF band was significantly increased from rest to peak exercise in patients with COPD (10.9 ms(2) [SD, 1.5 ms(2)] vs 11.5 ms(2) [SD, 1.4 ms(2)], respectively; p < 0.01) and in control subjects (10.9 ms(2) [SD, 1.5 ms(2)] vs 11.5 ms(2) [SD, 1.3 ms(2)], respectively; p < 0.01). The mean LF/HF ratio was significantly decreased from rest to peak exercise in patients with COPD (3.1 [SD, 1.5] vs 2.5 [SD, 1.0], respectively; p < 0.01) and was increased in control subjects (1.9 [SD, 0.8] vs 2.4 [1.0], respectively; p < 0.01). When expressed in normalized units ([absolute power of the components]/[total power - very low frequency power] x 100), the HF band was again significantly greater during peak exercise than at rest in the patients with COPD and was unchanged during peak exercise for the control group. Autonomic changes were not significantly correlated with age, gender, body mass index, spirometry, lung volumes, resting gas exchange, or oxygen saturation during exercise. CONCLUSION: These data suggest that, in contrast to control subjects, the balance of sympathetic to parasympathetic cardiac modulation decreases in patients with COPD during maximal volitional exercise.

Arterial stiffness increases during obstructive sleep apneas.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) appears to be an independent risk factor for diurnal systemic hypertension, but the specific biologic markers for this association have not been well established. Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans. However, arterial stiffness has not been measured in association with obstructive apneas in patients with OSA, nor related to systemic blood pressure (BP) activity in this setting. Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA, by demonstrating that (1) arterial stiffness increases acutely in association with obstructive apnea and hypopnea, and that (2) such increased stiffness may occur in the absence of acute BP increase. DESIGN: Prospective, cross-sectional. SETTING: A tertiary-care university-based sleep and ventilatory disorders center. PATIENTS: Forty-four normo- and hypertensive adult patients (11 women, 33 men) with polysomnographically diagnosed moderate to severe OSA. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography. Arterial augmentation index (AAI), a measure of arterial stiffness, was calculated as the ratio of augmented systolic BP (SBP) to pulse pressure and expressed as a percentage for the following conditions: awake, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events, and the first 15 cardiac cycles following apnea termination ("post apnea"). Mean AAI (+/-SD) for the group was significantly increased during NREM sleep from early apnea to late apnea (12.02 +/- 2.70% vs 13.35 +/- 3.54%, p<0.05, ANOVA). During REM (analyzed in 20 patients), MI again significantly increased from early apnea to late apnea (11.75 +/- 2.81% vs 13.43 +/- 4.97%). Conversely, neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM (SBP 130 +/- 14 mmHg vs 129 +/- 14 mmHg) or REM (SBP 128 +/- 22 mmHg vs 127 +/- 21 mmHg). CONCLUSIONS: Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep, in the absence of measurable BP change. These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implications concerning cardiovascular sequelae in patients with OSA.

Aerobic exercise attenuates an exaggerated exercise blood pressure response in normotensive young adult African-American men.

An exaggerated exercise blood pressure response (EEBPR) may be associated with an increased risk of hypertension. We hypothesized that aerobic exercise training can decrease EEBPR and the risk for hypertension by decreasing arterial resistance. We studied the effects of aerobic training on the submaximal exercise blood pressure (BP) of eight normotensive young adult African-American men with an EEBPR. Subjects were trained on a stationary bicycle at an intensity of 70% peak oxygen uptake (VO2peak), for 30 min, three times per week, for 8 weeks. BP, heart rate, cardiac output (CO), stroke volume (SV) and total peripheral vascular resistance (TPR) were measured at rest and during submaximal exercise at a work intensity of 50% VO2peak. Significance of the training effects were evaluated by comparing the pre- and post-training measures (t-test, p < 0.05). A 15% post-training increase in VO2peak (34.6 +/- 1.4 to 40 +/- 1.4 ml/kg/min) and a 9.5 ml post-training increase in mean resting stroke volume were found. A 16.2 mmHg decrement in mean systolic BP, an 11.5 mmHg decrement in mean diastolic BP, a 120 dyne/s/cm5 decrement in TPR and a 1.2 l/min increase in CO were detected during the post-training submaximal exercise tests. These results suggest that reductions in TPR may attenuate the EEBPR of normotensive African-American males following an 8-week training regimen of stationary bicycling at 70% VO2peak. Aerobic exercise training may, therefore, reduce the risk of hypertension in normotensive African-American males by the mechanism of a reduction in TPR. Because of the limited number of subjects, the results of this study should be interpreted cautiously pending confirmation by a larger controlled trial.

Effects of lung volume and chemoreceptor activity on blood pressure and R-R interval during the Valsalva maneuver.

STUDY OBJECTIVES: The purpose of the present investigation was to examine the effect of lung volume and inspiration of 100% oxygen on blood pressure and R-R interval responses during the Valsalva maneuver. DESIGN AND PARTICIPANTS: Fourteen healthy subjects completed eight Valsalva maneuvers. Four of the maneuvers were completed after inspiring to total lung capacity while the remaining maneuvers were completed at end-expiratory lung volume. Two maneuvers completed at a given lung volume were performed under hyperoxic conditions while the remaining maneuvers were completed under normoxic conditions. RESULTS: Overall, a significant increase in blood pressure and decrease in R-R interval occurred throughout phases I-IV of the Valsalva maneuvers that were initiated from end-expiratory lung volume as compared to total lung capacity. These changes were accompanied by a concomitant increase in baroreflex sensitivity during phase IV. Furthermore, independent of lung volume the baroreflex response was attenuated under hyperoxic conditions. CONCLUSIONS: We conclude that the lung volume that exists prior to the onset of the maneuver alters the blood pressure and R-R interval response during phases I-IV of the Valsalva maneuver. Furthermore, we suggest that these responses are mediated in part by changes in chemoreceptor activity since the baroreflex was reset and the sensitivity was reduced under hyperoxic conditions. Given these findings, we recommend that lung volume be controlled when patients are completing a Valsalva maneuver to obtain reliable and reproducible measures of blood pressure, R-R interval duration and baroreflex sensitivity.