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Cardiovascular deconditioning after long duration spaceflight is especially challenging in women who have a lower orthostatic tolerance (OT) compared with men. We hypothesized that an exercise prescription, combining supine aerobic treadmill exercise in a lower body negative pressure (LBNP) chamber followed by 10 min of resting LBNP, three to four times a week, and flywheel resistive training every third day would maintain orthostatic tolerance (OT) in women during a 60-day head-down-tilt bed rest (HDBR). Sixteen women were assigned to two groups (exercise, control). Pre and post HDBR OT was assessed with a tilt/LBNP test until presyncope. OT time (mean ± SE) decreased from 17.5 ± 1.0 min to 9.1 ± 1.5 min (−50 ± 6%) in control group (P

Introduction: Spaceflight simulation studies like confinement in small volume habitat with limited physical activity have reported even after 60 days an abnormal arterial wall adaptation with increase thickness or stiffness. The purpose of the current study was to determine the effects on blood vessel and organ structure of 40 days of isolation in a huge habitat with intensive physical activity. Method: Data were collected from 14 individuals (7 male) who isolated in a cavern for 40-days while performing normal daily activities without time references. Ultrasound assessments were performed pre- and post-isolation using a teleoperated system with eight different acoustic windows to obtain 19 measurements on 12 different organ/vascular structures which included the common carotid artery, femoral artery, tibial artery, jugular vein, portal vein, bile duct, kidney, pancreas, abdominal aorta, cervical and lumbar vertebral distance, and Achilles tendon. Results: Common carotid artery measures, including the intima media thickness, stiffness index, and the index of reflectivity measured from the radiofrequency signal, were not changed with isolation. Similarly, no differences were found for femoral artery measurements or measurements of any of the other organs/vessels assessed. There were no sex differences for any of the assessments. Discussion: Results from this study indicate a lack of physiological effects of 40- days of isolation in a cavern, contrary to what observed in previous 60 days confinement. This suggests a potential protective effect of sustained physical activity, or reduced environmental stress inside the huge volume of the confined facility. [ABSTRACT FROM AUTHOR]

Circadian rhythm has an influence on several physiological functions that contribute to athletic performance. We tested the hypothesis that circadian rhythm would affect blood pressure (BP) responses but not [O.sub.2] uptake (V[O.sub.2]) kinetics during the transitions to moderate and heavy cycling exercises. Nine male athletes (peak [??][O.sub.2]: 60.5 [+ or -] 3.2 ml x [kg.sup.-1] x [min.sup.-1]) performed multiple rides of two different cycling protocols involving sequences of 6-min bouts at moderate or heavy intensities interspersed by a 20-W baseline in the morning (7 AM) and evening (5 PM). Breath-by-breath [??][O.sub.2] and beat-by-beat BP estimated by finger cuff plethysmography were measured simultaneously throughout the protocols. Circadian rhythm did not affect [??][O.sub.2] onset kinetics determined from the phase II time constant ([[tau].sub.2]) during either moderate or heavy exercise bouts with no prior priming exercise ([[tau].sub.2] moderate exercise: morning 22.5 [+ or -] 4.6 s vs. evening 22.2 [+ or -] 4.6 s and T2 heavy exercise: morning 26.0 [+ or -] 2.7 s vs. evening 26.2 [+ or -] 2.6 s, P > 0.05). Priming exercise induced the same robust acceleration in [??][O.sub.2] kinetics during subsequent moderate and heavy exercise in the morning and evening. A novel finding was an overshoot in BP (estimated from finger cuff plethysmography) in the first minutes of each moderate and heavy exercise bout. After the initial overshoot, BP declined in association with increased skin blood flow between the third and sixth minute of the exercise bout. Priming exercise showed a greater effect in modulating the BP responses in the evening. These findings suggest that circadian rhythm interacts with priming exercise to lower BP during exercise after an initial overshoot with a greater influence in the evening associated with increased skin blood flow. blood pressure control; oxidative metabolism; postexercise hypotension doi: 10.1152/ajpheart.00762.2010.

We tested the hypotheses that women completing 56 days, 6[degrees] head-down bed-rest (HDBR) would have changes in sensitivity of cardiovascular responses to adrenergic receptor stimulation and that frequent aerobic and resistive exercise would prevent these changes. Twenty-four women, eight controls, eight exercisers (lower body negative pressure treadmill and flywheel resistance exercise), and eight receiving nutritional supplement but no exercise were studied in baseline and during administration of the [beta]-agonist isoproterenol (ISO) and the [alpha]- and [beta]-agonist norepinephrine (NOR). In the control and nutrition groups, HDBR increased heart rate (HR) and reduced stroke volume (SV), and there was a significantly greater increase in HR with ISO after HDBR. In contrast, the HR and SV of the exercise group were unchanged from pre-HDBR. After HDBR, leg vascular resistance (LVR) was greater than pre-HDBR in the exercise group but reduced in control and nutrition. LVR was reduced with ISO and increased with NOR. Changes in total peripheral resistance were similar to those of LVR but of smaller magnitude, perhaps because changes in cerebrovascular resistance index were directionally opposite to those of LVR. There were no changes in sensitivity of the vascular resistance responses to adrenergic stimulation. The HR response might reflect a change in sensitivity or a necessary response to the reduction in SV after HDBR in control and nutrition groups. The reduced peripheral vascular resistance after HDBR might help to explain orthostatic intolerance in women. Exercise was an effective countermeasure to the HDBR effects. vascular resistance; norepinephrine; microgravity; cardiac output

We tested the hypothesis that flow-mediated dilation (FMD) of the brachial artery would be impaired by acute increases in sympathetic nervous system activity (SNA) in models where similar peak shear stress stimulus was achieved by varying the duration of forearm muscle ischemia. Eleven healthy young men were studied under four different conditions, each with its own control: lower body suction (LBS), cold pressor test (CPT), mental arithmetic task (MAT), and activation of muscle chemoreflex (MCR). The duration of ischemia before observation of FMD by ultrasound imaging was 5 min each for control, LBS, and CPT; 3 min for MAT; and 2-min for MCR. Peak shear rate was not different between control and any of the SNA conditions, although total shear in the first minute was reduced in MAT. MCR was the only condition in which brachial artery vasoconstriction was observed before forearm occlusion [4.38 (SD 0.53) vs. control 4.60 (SD 0.53) mm, P < 0.05]; however, diameter increased to the same absolute value as that of the control, so the percent FMD was greater for MCR [9.85 (SD 2.33) vs. control 5.29 (SD 1.50)%]. Blunting of the FMD response occurred only in the CPT model [1.51 (SD 1.20)%]. During SNA, the increase in plasma cortisol from baseline was significant only for MCR; the increase in plasma norepinephrine was significant for MCR, LBS, and CPT; and the increase in epinephrine was significant only for MCR. These results showed that the four models employed to achieve increases in SNA had different effects on baseline brachial artery diameter and that blunted FMD is not a general response to increased SNA. endothelium; shear stress; muscle chemoreflex; cold pressor test; mental stress

The amplitude of low-frequency (LF) oscillations of heart rate (HR) usually reflects the magnitude of sympathetic activity, but during some conditions, e.g., physical exercise, high sympathetic activity results in a paradoxical decrease of LF oscillations of HR. We tested the hypothesis that this phenomenon may result from a feedback inhibition of sympathetic outflow caused by circulating norepinephrine (NE). A physiological dose of NE (100 ng x [kg.sup.-1] x [min.sup.-1]) was infused into eight healthy subjects, and infusion was continued alter [alpha]-adrenergic blockade [with phentolamine (Phe)]. Muscle sympathetic nervous activity (MSNA) from the peroneal nerve, LF (0.04-0.15 Hz) and high frequency (HF; 0.15-0.40 Hz) spectral components of HR variability, and systolic blood pressure variability were analyzed at baseline, during NE infusion, and during NE infusion after Phe administration. The NE infusion increased the mean blood pressure and decreased the average HR (P < 0.01 for both). MSNA (10 [+ or -] 2 vs. 2 [+ or -] 1 bursts/min, P < 0.01), LF oscillations of HR (43 [+ or -] 13 vs. 35 [+ or -] 13 normalized units, P < 0.05), and systolic blood pressure (3.1 [+ or -] 2.3 vs. 2.0 [+ or -] 1.1 mm[Hg.sup.2], P < 0.05) decreased significantly during the NE infusion. During the NE infusion after PHE, average HR and mean blood pressure returned to baseline levels. However, MSNA (4 [+ or -] 2 bursts/ min), LF power of HR (33 [+ or -] 9 normalized units), and systolic blood pressure variability (1.7 [+ or -] 1.1 mm[Hg.sup.2]) remained significantly (P < 0.05 for all) below baseline values. Baroreflex gain did not change significantly during the interventions. Elevated levels of circulating NE cause a feedback inhibition on sympathetic outflow in healthy subjects. These inhibitory effects do not seem to be mediated by pressor effects on the baroreflex loop but perhaps by a presynaptic autoregulatory feedback mechanism or some other mechanism that is not prevented by a nonselective [alpha]-adrenergic blockade. heart rate dynamics; catecholamines; blood pressure oscillation

Beat-by-beat estimates of total peripheral resistance (TPR) can be obtained from continuous measurements of cardiac output by using Doppler ultrasound and noninvasive mean arterial blood pressure (MAP). We employed transfer function analysis to study the heart rate (HR) and vascular response to spontaneous changes in blood pressure from the relationships of systolic blood pressure (SBP) to HR (SBP[right arrow]HR), MAP to total peripheral resistance (TPR) and cerebrovascular resistance index (CVRi) (MAP[right arrow]TPR and MAP[right arrow]CVRi), as well as stroke volume (SV) to TPR in nine healthy subjects in supine and 45[degrees] head-up tilt positions. The gain of the SBP[right arrow]HR transfer function was reduced with tilt in both the low- (0.03-0.15 Hz) and high-frequency (0.15-0.35 Hz) regions. In contrast, MAP[right arrow]TPR transfer function gain was not affected by head-up tilt, but it did increase from low- to high-frequency regions. The phase relationships between MAP[right arrow] TPR were unaffected by head-up tilt, but, consistent with an autoregulatory system, changes in MAP were followed by directionally similar changes in TPR, just as observed for the MAP[right arrow]CVRi. The SV[right arrow]TPR had high coherence with a constant phase of 150-160[degrees]. Together, these data that showed changes in MAP preceded changes in TPR, as well as a possible link between SV and TPR, are consistent with complex interactions between the vascular component of the arterial and cardiopulmonary baroreflexes and intrinsic properties such as the myogenic response of the resistance arteries. baroreflex; power spectral analysis; Doppler ultrasound; cardiac output; myogenic; autoregulation

The new two-breath C[O.sub.2] method was employed to test the hypotheses that small alterations in arterial PC[O.sub.2] had an impact on the magnitude and dynamic response time of the C[O.sub.2] effect on cerebrovascular resistance (CVRi) and the dynamic autoregulatory response to fluctuations in arterial pressure. During a 10-min protocol, eight subjects inspired two breaths from a bag with elevated PC[O.sub.2], four different times, while end-tidal PC[O.sub.2] was maintained at three levels: hypocapnia (LoC[O.sub.2], 8 mmHg below resting values), normocapnia, and hypercapnia (HiC[O.sub.2], 8 mmHg above resting values). Continuous measurements were made of mean blood pressure corrected to the level of the middle cerebral artery (B[P.sub.MCA]), PC[O.sub.2] (estimated from expired C[O.sub.2]), and mean flow velocity (MFV, of the middle cerebral artery by Doppler ultrasound), with CVRi = B[P.sub.MCA]/MFV. Data were processed by a system identification technique (autoregressive moving average analysis) with gain and dynamic response time of adaptation estimated from the theoretical step responses. Consistent with our hypotheses, the magnitude of the PC[O.sub.2]-CVRi response was reduced from LoC[O.sub.2] to HiC[O.sub.2] [from -0.04 (SD 0.02) to -0.01 (SD 0.01) (mmHg*[cm.sup.-1]*s)*mmHg [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]] and the time to reach 95% of the step plateau increased from 12.0 [+ or -] 4.9 to 20.5 [+ orR -] 10.6 s. Dynamic autoregulation was impaired with elevated PC[O.sub.2], as indicated by a reduction in gain from LoC[O.sub.2] to HiC[O.sub.2] [from 0.021 [+ or -] 0.012 to 0.007 [+ or -] 0.004 (mmHg*[cm.sup.-1]*s)*mmHg [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]], and time to reach 95% increased from 3.7 [+ or -] 2.8 to 20.0 [+ or -] 9.6 s. The two-breath technique detected dependence of the cerebrovascular C[O.sub.2] response on PC[O.sub.2] and changes in dynamic autoregulation with only small deviations in estimated arterial PC[O.sub.2]. Doppler ultrasound; brain blood flow; autoregressive moving average; carbon dioxide

Different magnitudes and durations of postocchision reactive hyperemia were achieved by occluding different volumes of tissue with and without ischemic exercise to test the hypotheses that flow-mediated dilation (FMD) of the brachial artery would depend on the increase in peak flow rate or shear stress and that the position of the occlusion cuff would affect the response. The brachial artery FMD response was observed by high-frequency ultrasound imaging with curve fitting to minimize the effects of random measurement error in eight healthy, young, nonsmoking men. Reactive hyperemia was graded by 5-min occlusion distal to the measurement site at the wrist and the forearm and proximal to the site in the upper arm. Flow was further increased by exercise during occlusion at the wrist and forearm positions. For the two wrist occlusion conditions, flow increased eightfold and FMD was only 1 to 2% (P > 0.05). After the forearm and upper arm occlusions, blood flow was almost identical hut FMD after forearm occlusions was 3.4% (P < 0.05), whereas it was significantly greater (6.6%, P < 0.05) and more prolonged after proximal occlusion. Forearm occlusion plus exercise caused a greater and more prolonged increase in blood flow, yet FMD (7.0%) was qualitatively and quantitatively similar to that after proximal occlusion. Overall, the magnitude of FMD was significantly correlated with peak forearm blood flow (r = 0.59, P < 0.001), peak shear rate (r = 0.49, P < 0.002), and total 5-min reactive hyperemia (r = 0.52, P < 0.001). The prolonged FMD after upper arm occlusion suggests that the mechanism for FMD differs with occlusion cuff position. hyperemia; endothelium; shear stress; ischemic exercise; blood flow