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.     

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.     

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.     

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.     

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)     

Exercise training improves left ventricular isovolumic relaxation

PURPOSE: Left ventricular (LV) diastolic function is an important determinant of aerobic fitness. The purpose of this paper was to investigate the relationship between aerobic fitness and the rate and extent of isovolumic LV relaxation. METHODS: Two series of experiments were performed utilizing both human and animal models. In the first series of experiments, the relationship between LV diastolic time intervals and exercise capacity was assessed in two groups of collegiate men (N = 18) with variable peak run times (Bruce protocol). In the second series of experiments, the extent of LV relaxation was examined in sedentary and exercise-trained rats (treadmill running), using an isolated, isovolumic heart preparation. Subsequent morphological assessment was also performed in rats. RESULTS: At rest, men with greater peak treadmill time had a shorter resting LV isovolumic relaxation time (R-R interval adjusted 1000 ms) (long duration runners, 84+/-5 ms vs short duration runners, 105+/-7 ms, P < 0.05) despite a similar LV diastolic interval. Peak treadmill time was inversely correlated to LV isovolumic relaxation time (R-R interval adjusted 1000 ms) (r = -0.55; P < 0.02). In animal studies (N = 26), the LV pressure-volume relationship was shifted rightward in exercise-trained rats (P = 0.003). Exercise-trained rats had an increased LV inner diameter (sedentary, 5.1+/-0.35 mm vs exercise-trained, 6.1+/-0.28 mm, P < 0.05) and a thicker interventricular septum (sedentary, 1.52+/-0.06 mm vs exercise-trained, 1.72+/-0.09 mm, P < 0.05). CONCLUSION: This study suggests that both the rate and extent of LV isovolumic relaxation is enhanced with exercise training. Further study is required to understand the interrelationship between exercise and diastolic function.     

Reduced baroreceptor reflex sensitivity and increased blood pressure variability at 2400 m simulated cabin altitude

In a hypobaric chamber nine healthy volunteers were exposed to an atmospheric pressure corresponding to 2400 m above sea level. This is similar to the lowest air pressure encountered inside pressurized commercial airplanes. Heart rate and blood pressure were monitored beat-to-beat in the supine position with a non-invasive device. Blood pressure variability and heart rate variability were measured in the mid-frequency band; subsequently, baroreceptor reflex sensitivity (BRS) was calculated with the transfer-function method. Compared with baseline, there were reduced BRS and increased blood pressure variability at 2400 m (16.5 +/- 3.1 vs. 13.2 +/- 2.0 ms x mm Hg(-1) and 5.4 +/- 1.3 vs. 8.2 +/- 1.1 mm Hg, respectively; p < 0.05). We conclude that autonomic cardiovascular control was disturbed during acute exposure to an air pressure corresponding to 2400 m.     

The effect of a one-year lifestyle intervention program on carotid intima media thickness

This study assesses the impact of a year long lifestyle intervention program on carotid intima media thickness (CIMT) in 60 subjects, at-risk for or with coronary artery disease. We calculated mean CIMT at baseline (0.731 +/- 0.151 mm) and 1 year (0.720 +/- 0.129 mm), overall CIMT change and the relationship of CIMT change to the number (0-5) of achieved Heart Health Index (HHI) measures (body mass index < 25 kg/m2, exercise > or = 150 min/wk, blood pressure < 140/90 mm Hg, LDL-Cholesterol < 100 mg/dL, fiber intake > 25 g/d). CIMT was unchanged (-0.011 +/- 0.118 mm; p = 0.48); however, there was a trend toward CIMT decrease (-0.025 +/- 0.120 mm vs. +0.033 +/- 0.102 mm; p = 0.10) between subjects with HHI Score > or = 3 (n = 45) compared to those with an HHI Score < 3 (n = 15) at 1 year. These findings suggest atherosclerosis progression can be blunted with a lifestyle intervention that fully leverages nonpharmacologic approaches to cardiovascular risk reduction.     

Qt dispersion in soccer players during exercise testing

Screening for cardiac health should involve relevant parameters or indices that are easy and inexpensive to obtain. Various cardiac adaptation mechanisms develop during regular exercise that are affected by many factors, and these are reflected on a surface electrocardiogram. QT dispersion has been considered a surrogate for heterogeneity of repolarization, leading to ventricular arrhythmias. We compared QT parameters between athletes and sedentary subjects. A total of 225 men were assessed, comprising a group of professional soccer players and sedentaries. Each subject underwent supine 12-lead electrocardiographic examinations and exercise testing by ergospirometry. QT parameters were taken at rest and at peak exercise. Peak oxygen consumption was considerably higher in the athletes than in the controls (59.3 +/- 5.6 vs. 44.3 +/- 2.4 ml/kg/min, mean +/- SD, p < 0.001). QT parameters at rest: There were significant differences in heart-rate-corrected rest maximal QT duration (413.9 +/- 50.5 vs. 445.3 +/- 45.7 ms, p < 0.001) and in heart-rate-corrected rest minimum QT duration (380.5 +/- 51.2 vs. 409.5 +/- 46.7 ms, p < 0.001). QT parameters at peak exercise: maximal QT duration at peak exercise (253.9 +/- 20.8 vs. 261.7 +/- 26.2, p = 0.02), QT dispersion at peak exercise (25.2 +/- 9.1 vs. 29.5 +/- 15.8 ms, p = 0.04), heart-rate-corrected QT dispersion at peak exercise (44.6 +/- 16.4 vs. 52.6 +/- 28.3 ms, p = 0.03) differed significantly between professional soccer players and controls. QT dispersion and corrected QT dispersion at peak exercise are lower in athletes than in controls. Athletes and other subjects identified with a long QT interval should be examined at regular intervals.     

Effects of short- and long-term detraining on the metabolic response to endurance exercise

Changes in the metabolic response to an endurance exercise were studied (18 rowing km at 75 % of maximal aerobic velocity) during detraining in ten rowers previously highly-trained. Maximal aerobic velocity (VO2 max) and the metabolic response to exercise were determined in the 1 st, 24 th, and 47 th week (training), and in the 52 nd, 76 th, and 99 th week (detraining). Over the decrease of VO2 max, detraining induced a biphasic alteration of the previously observed training adaptations: 1-short-term detraining (5 weeks) resulted in a lower adipose tissue triglyceride (TG) delivery during exercise (p = 0.029), but this one did not represent a direct metabolic limit to exercise since the liver TG delivery increased (p = 0.039), allowing that total fatty acid concentration remained unchanged (12.1 +/- 2.4 vs. 11.8 +/- 2.1 mmol/l; weeks 47 vs. 52); 2-long-term detraining (52 weeks) altered even more the metabolic response to exercise with a decreased total fatty acid concentration during exercise (week 99: 10.6 +/- 2.0 mmol/l; p = 0.022), which induced a higher glycolysis utilization. At this moment, a hemolytic response to endurance exercise was observed through haptoglobin and transferrin concentration changes (weeks 47 vs. 99; p = 0.029 and 0.027, respectively), which resulted probably from higher red blood cell destruction. Endurance-trained athletes should avoid detraining periods over a few weeks since alterations of the metabolic adaptations to training may become rapidly chronic after such delays.     

Skeletal muscle oxidative capacity and exercise tolerance in rats with heart failure

PURPOSE: Past research has shown the development of exercise intolerance after myocardial infarction (MI). The purpose of this study was to test the hypothesis that reductions in oxidative enzyme activity, in a variety of skeletal muscles, coincide with the development of exercise intolerance in a rat model of chronic heart failure (CHF) induced by MI. METHODS: The animals were initially divided into two groups: sham-operated controls (Sham) and animals in which a MI was surgically induced. MI rats were then subdivided into two groups according to left ventricular end-diastolic pressure (LVEDP): <20 mm Hg [small MI (SMI)] and > 20 mm Hg [large MI (LMI)]. Exercise tolerance was measured by performing a progressive run to fatigue test (RTF). Citrate synthase (CS), 3-hydroxyacyl CoA dehydrogenase (HADH), and malate dehydrogenase (MDH) activities were measured in six hindlimb muscles. RESULTS: After approximately 6 wk of recovery, LVEDP differed among groups (P < 0.05): Sham (1 +/- 1 mm Hg, N = 7), SMI (7 +/- 2 mm Hg, N = 7), and LMI (30 +/- 2 mm Hg, N = 6). RTF was 20 +/- 1 min for Sham, 25 +/- 3 min for SMI, and 11 +/- 2 min for LMI (P < 0.05 for LMI vs Sham, SMI). Significant reductions in enzyme activity were found for all three enzymes in the red portion of the gastrocnemius muscles of LMI. However, no significant correlation was found between RTF and CS, HADH, or MDH in any muscle of the three groups of animals. DISCUSSION: The results of the present study demonstrate that severe left ventricular dysfunction is associated with reductions in exercise tolerance and modest decreases in oxidative enzyme activities in selected muscles. It does not appear, however, that the development of exercise intolerance in CHF and oxidative enzyme activities are mechanistically related to one another.     

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.     

Effects of exercise training on cardiovagal and sympathetic responses to Valsalva's maneuver

PURPOSE: We tested the hypothesis that a strictly-controlled program of aerobic conditioning would increase vagal and decrease sympathetic responses to Valsalva straining. METHODS: Eleven young men performed a maximal aerobic capacity test, controlled frequency breathing (0.25 Hz), and three Valsalva maneuvers before and after 4 wk of exercise training on a cycle ergometer (30 min at > or = 70% max heart rate, 3 sessions. week-1). During controlled breathing and Valsalva straining, we recorded the electrocardiogram, noninvasive beat-by-beat arterial pressure, and peroneal nerve muscle sympathetic traffic at the popliteal fossa (pre- and postexercise sympathetic recordings were obtainable in 7 of 11 subjects). Vagal-cardiac tone was estimated from R-R interval standard deviations during controlled frequency breathing. Cardiovagal baroreflex sensitivity was derived from increases of R-R intervals as functions of increases in systolic pressures with linear regression analysis during phase IV pressure increases, and sympathetic sensitivity was derived from the quotient of total muscle sympathetic nerve activity and diastolic pressure changes during phase II pressure reductions. RESULTS: Exercise training increased VO2 max (3.38 +/- 0.10 pre-, and 3.64 +/- 0.11 L. min-1 postexercise; mean +/- SE; P = 0.04), R-R interval standard deviations (75 +/- 0.12 pre- and 94 +/- 0.14 ms postexercise; mean +/- SE; P = 0.03), and cardiovagal baroreflex sensitivity (15.0 +/- 1.1 pre-, and 25.0 ms. mm Hg-1 +/- 4.0 postexercise; mean +/- SE; P = 0.03). Exercise training did not change baseline sympathetic traffic (P = 0.31) or sympathetic nerve responses to diastolic pressure reductions (P = 0.12). CONCLUSIONS: Exercise training affects vagal and sympathetic mechanisms differently: cardiovagal baroreflex sensitivity is increased, but sympathetic responses to arterial pressure decreases are unchanged.     

Relationship between exercise-induced myocardial ischemia and reduced left ventricular distensibility in patients with nonobstructive hypertrophic cardiomyopathy.

Many studies have demonstrated that reduced left ventricular (LV) diastolic distensibility plays a key role in the pathophysiology of hypertrophic cardiomyopathy (HCM). However, the relationship between myocardial ischemia and reduced LV distensibility in HCM remains unclear. We aimed to clarify the relationship between exercise-induced ischemia and reduced LV distensibility in patients with HCM. METHODS: Twenty patients with HCM and 5 age-matched control subjects underwent stress-redistribution (201)Tl myocardial scintigraphy and biventricular cardiac catheterization and echocardiography at rest and during exercise. Scintigraphic defect analysis was interpreted using Berman's 20-segment model. The summed stress score (SSS) was calculated as the sum of scores of the 20 LV segments and the summed difference score (SDS) was calculated as the sum of differences between each of the 20 LV segments on stress and rest images. RESULTS: Patients were divided into 2 groups according to the (201)Tl defect as follows: 9 patients with an SSS on (201)Tl of >or=10 and an SDS on (201)Tl of >or=5 (ischemic group) and 11 patients with an SSS of <10 or an SDS of <5 (nonischemic group). The absolute increases from rest to peak exercise in LV end-diastolic pressure (LVEDP) and pulmonary artery wedge pressure were significantly greater (15.5 +/- 5.2 vs. 7.6 +/- 5.5 mm Hg and 17.3 +/- 5.0 vs. 8.9 +/- 5.0 mm Hg, P < 0.01, respectively), and the percentage changes from rest to peak exercise in the maximum first derivative of LV pressure and LV pressure half-time were significantly smaller in the ischemic HCM group compared with the nonischemic HCM group (70% +/- 24% vs. 123% +/- 43% and -32% +/- 6.4% vs. -44% +/- 9.4%, P < 0.01, respectively). However, the end-diastolic dimensions did not differ between the 2 HCM groups. One of the 9 patients in the ischemic group, as revealed by fill-in on (201)Tl scintigraphy, showed increased (18)F-FDG uptake in the anteroseptal wall. CONCLUSION: Some HCM patients show a significant increase in LVEDP without chamber dilatation, indicating reduced LV diastolic distensibility. Myocardial ischemia may at least in part contribute to this condition.     

Baroreflex sensitivity during static exercise in individuals with Down Syndrome

INTRODUCTION: Individuals with Down syndrome (DS) have altered heart rate (HR) and blood pressure (BP) responses to orthostatic challenges and isometric handgrip (IHG) exercise, suggesting possible alteration in baroreflex sensitivity. PURPOSE: This study investigated baroreflex sensitivity (BRS) as a potential mechanism contributing to chronotropic incompetence during IHG in persons with DS. METHODS: Heart rate and BP were continually recorded in 12 individuals with DS and 10 controls, at rest and during 2 min of IHG, at 30% of maximal voluntary contraction (MVC). Spontaneous BRS was derived via the sequence method. RESULTS: No differences were seen in HR at rest between groups. Systolic BP (SBP) was significantly lower in the DS group at rest (106.1+/- 2.9 vs 116.5+/- 3.9 mm Hg, P < 0.05) and during IHG (123.9+/- 4.6 vs 150.1+/- 5.3 mm Hg, P<0.001). A significant group-by-task interaction was found for both change in HR and change in SBP with IHG, because of an attenuated HR and SBP response to IHG in participants with DS (P<0.05). When controlling for resting SBP, the DS group had a lower BRS at rest (16.0+/-1.7 vs 21.2+/-4.2 ms.mm Hg, P< 0.05) and during IHG (7.8 +/-1.0 vs 12.1+/- 2.6 ms.mm Hg, P< 0.05). CONCLUSIONS: Individuals with DS have lower BRS at rest and during IHG than controls and this may be related to their attenuated HR response during perturbation.     

DLCO response to experimental cycle-run succession in triathletes.

BACKGROUND: We still know relatively little about the factors that define the ability to perform a good run after cycling in triathlon, however, and the perception of discomfort during the first minutes of this post-cycling running has yet to be satisfactorily explained. The pulmonary diffusion capacity for carbon monoxide (DLCO) has been demonstrated to be impaired after the cycle-run succession. Numerous causes have been suggested to explain this phenomenon, but the exact mechanism has not yet been determined. METHODS: Thirteen young male triathletes participated in four different exercise trials: 30 min of cycling followed by 20 min of running (C-R, 1 min rest between C and R), 30 min of running followed by 20 min of running (R-R, 1 min rest between R and R), 30 min of cycling (C), and 30 min of running (R). DLCO and alveolar volume were simultaneously measured during 9 sec of breath-holding before and 10 min after exercise. The transfer coefficient (KCO=DLCO/VA) was then calculated. During all trials, ventilatory data were collected every minute using an automated breath-by-breath system. RESULTS: The results showed that 1) C-R and C induced significant and identical decreases in DLCO and KCO in post-trial compared with pre-trial measurement (40.41+/-2.24 vs 43.49+/-2.36 ml x min(-1) x mm Hg(-1), p<0.01, and 39.37+/-2.16 vs 42.99+/-2.38 ml x min(-1) x mm Hg(-1), p<0.02, for C-R and C, respectively) and 2) there were no DLCO decreases in post-trial compared with pre-trial measurement in R-R and R. CONCLUSIONS: We concluded that cycling exercise in itself seems to increase the immediate post-exercise DLCO impairment.     

Cardiovascular response to lower body negative pressure (LBNP) following endurance training

Eleven sedentary male volunteers were assigned to either an exercise (E) group (n = 6; endurance exercise for 12 weeks) or a control (C) group (n = 5; no exercise). After training, E significantly increased (p less than 0.01) their VO2max (pretraining: 37.0 +/- 2.3; posttraining: 44.6 +/- 2.5), whereas C showed no significant change. Heart rate (HR), arterial blood pressure (BP) and forearm blood flow (FBF) were measured both pre- and posttraining at rest and during 2 levels of LBNP: -10 mm Hg and -40 mm Hg. Both C and E had similar decreases in systolic BP and similar increases in HR and diastolic BP during LBNP when comparing the pre- and posttraining periods. In both groups, FBF significantly decreased during -40 mm Hg of LBNP in the pretraining period. However, after training, E had a significantly attenuated (p less than 0.05) decrease in FBF at -40 mm Hg (pretraining: -45.0 +/- 3.7%; posttraining: -29.8 +/- 3.1%). In C, there was no difference in the response of FBF to -40 mm Hg of LBNP comparing pretraining and posttraining. These findings indicate that endurance exercise training decreases the forearm vasoconstrictor response to high levels of LBNP.     

Is exercise-induced arterial hypoxemia in triathletes dependent on exercise modality?

To determine whether exercise modality affects arterial hypoxemia (EIAH) during training-intensity exercise, 13 triathletes performed 20 min of cycling (C) followed by 20 min of running (R): C-R, and two weeks later, 20 min of R followed by 20 min of C:R-C. Each trial was performed at an intensity slightly above the ventilatory threshold and close to the daily training intensity (75 % of VO2max). Ventilatory data were collected continuously using an automated breath-by-breath system. Partial pressure of oxygen in arterial blood (PaO2) was measured after each C and R segment and arterial oxyhemoglobin saturation (SpO2) was monitored continuously via pulse oximetry. The metabolic rate was similar across modalities and trials, i.e., C-R (53.8 +/- 3.8 vs. 51.1 +/- 5.3 ml.min(-1).kg(-1)) and R-C (52.2 +/- 4.5 vs. 53.2 +/- 4.6 ml.min(-1).kg (-1)). EIAH showed significantly greater severity for R compared to C irrespective of the order (p < 0.05 for both trials). R values of PaO2 (and SpO2) for C-R and R-C were 88.7 +/- 6.0 mm Hg (93.0 +/- 0.6 % SpO2) and 86.6 +/- 7.3 mm Hg (93.5 +/- 0.6 % SpO2) and C values were 93.7 +/- 8.4 mm Hg (95.4 +/- 0.4 % SpO2) and 91.4 +/- 5.4 mm Hg (94.8 +/- 0.3 % SpO2). R ventilatory data described a significantly different breathing pattern than C, with higher respiratory rate (35.9 b.min(-1) vs. 51.1 b.min(-1) for C-R, p < 0.01; and 50.0 b.min(-1) vs. 41.5 b.min(-1) for R-C, p < 0.01) and lower tidal volume (2636 ml vs. 2282 ml for C-R, p < 0.02 and 2272 ml vs. 2472 ml for R-C, p < 0.05). We concluded that EIAH was greater during running than cycling for a similar metabolic rate corresponding to training intensity and that EIAH could thus be considered dependent on exercise modality.     

Influence of percutaneous transluminal angioplasty on transcutaneous oxygen pressure in patients with peripheral arterial occlusive disease

PURPOSE: To determine in a prospective controlled trial the effect of percutaneous transluminal angioplasty (PTA) on skin oxygen supply and microcirculation as measured by means of transcutaneous oxygen pressure in patients with disabling lower-limb ischemia compared with that in patients who underwent intraarterial angiography for the assessment of disabling lower-limb ischemia. MATERIALS AND METHODS: Thirty-four patients (17 men, 17 women; mean age, 68.6 years +/- 9.8 [SD]) with peripheral arterial occlusive disease (PAOD) (claudication, n = 15; critical ischemia, n = 19) underwent transcutaneous oxygen pressure measurement at the dorsum of the foot 1 day before PTA, during PTA, 1 day after PTA, and 6 weeks after PTA. Measurements were obtained with the patient in the supine and erect sitting positions, as well as after exercise. Thirty-one patients (21 men, 10 women; mean age, 68.5 years +/- 9.3) with symptomatic PAOD who were undergoing intraarterial angiography served as the control group. RESULTS: Mean pressure before PTA was 31.6 mm Hg +/- 24 in the supine position, 50.8 mm Hg +/- 22 in the sitting position, and 22.2 mm Hg +/- 23 after exercise. Immediately after PTA, a significant increase to 34 mm Hg +/- 20 in the supine position was noted (P <.05). One day after PTA, pressure was 37.3 mm Hg +/- 20 for the supine position and 52 mm Hg +/- 20 for the sitting position. Six weeks after treatment, a further significant increase to 43.9 mm Hg +/- 19 in the supine position, 61 mm Hg +/- 15 in the sitting position, and 44.7 mm Hg +/- 24 after exercise was noted (P <.05). In the control group, a significant pressure decrease immediately after and 1 day after angiography was noted (P <.05). Measurements returned to baseline at 6 weeks follow-up. CONCLUSION: PTA has a positive effect on oxygen supply to the skin in patients with PAOD. Conversely, intraarterial angiography in patients with PAOD deteriorates skin microcirculation temporarily.     

Can relaxation lower metaboreflex-mediated blood pressure elevations?

PURPOSE: Relaxation can lower resting blood pressure, and this investigation sought to determine whether relaxation could reduce mean blood pressure (MBP) elevations produced by postexercise circulatory occlusion (PECO). METHODS: Sixteen volunteers trained with relaxation and were able to decrease MBP at rest by at least 5 mm Hg within 2 min. Subjects performed four tests assigned randomly: i). rest with cuff occlusion, ii). rest and cuff occlusion with relaxation, iii). hand-grip exercise followed by PECO rest with cuff occlusion, and iv) hand-grip exercise followed by PECO with relaxation. Data for HR and MBP were collected using a Finapres; ratings of relaxation and discomfort from cuff occlusion were obtained using a 1- to 10-unit scale. Stroke volume (SV) and HR were collected from six subjects to calculate cardiac output and total peripheral conductance (TPC). Dependent variables were compared using an ANOVA. RESULTS: HR (mean +/-SD) was lower during both relaxation conditions as compared with control (-7 +/- 4 bpm vs -2 +/- 3 bpm; P< 0.05). The MBP was reduced during relaxation alone (-6 +/- 3.7 mm Hg; < 0.05) but not during PECO with relaxation. The rating of relaxation was higher during relaxation (6.8 +/- 1.3 units) versus control (3.5 +/- 1.2 units), but ratings were not different between relaxation conditions. Ratings of discomfort were higher during PECO ( P< 0.05). Relaxation did not significantly alter CO or SV (N= 6). During relaxation alone, TPC was increased (0.046 +/- 0.001 vs 0.049 +/- 0.002 L.min.mm Hg; P< 0.05). However, TPC was significantly increased during PECO with relaxation. CONCLUSIONS: These findings suggest that although relaxation can affect cardiovascular regulation and lower HR and MBP at rest, this central signal cannot lower reflex increases in blood pressure originating from a peripheral metabolic stimulus.