Cardiovascular control during voluntary static exercise in humans with tetraplegia.

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C(6)-C(7)). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.     

Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans.

The purpose of the study was to examine the effect of 1) passive (assisted pedaling), 2) active (loadless pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), skin blood flow (SkBF), and sweating during recovery after 15 min of dynamic exercise. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, SkBF, and sweating during exercise recovery. Six male subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 15 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (T(sk)), esophageal temperature (T(es)), SkBF, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, and 15 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active and passive recovery modes, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining CO, SV, MAP, CVC, and sweat rate above inactive recovery. Sweat rate was different among all modes after 8 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the passive and inactive modes (P < 0.05). No differences in either T(es) or T(sk) were observed among conditions. Given that MAP was higher during passive and active recovery modes than during inactive recovery suggests differences in CVC may be due to differences in baroreceptor unloading and not factors attributed to central command. However, differences in sweat rate may be influenced by factors such as central command and mechanoreceptor stimulation.     

Gender differences in cardiovascular regulation during recovery from exercise.

Are women more susceptible to acute postexercise orthostatic hypotension compared with men? We hypothesized that decreases in arterial pressure during recovery from dynamic exercise are greater in women compared with men. We studied 8 men and 11 women during inactive and active recovery from cycling exercise. Heart rate, stroke volume (SV), cardiac output, mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured during and after 3 min of exercise at 60% of calculated maximum heart rate. At 1 min after exercise, MAP decreased less (P < 0.05) during inactive recovery in men (-18 +/- 2 mmHg) compared with women (-30 +/- 2 mmHg). This difference was due to greater decreases in SV and less increase in TPR during inactive recovery from exercise in women compared with men. These differences persisted for 5 min after exercise. MAP decreased less during active recovery in men compared with women. These findings suggest that women may have increased risk of postexercise orthostatic hypotension and that active recovery from exercise may reduce this risk.     

Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women.

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (Tsk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode (P < 0.05). No differences in either Tes or Tsk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.     

Oxygen-conserving effects of apnea in exercising men.

We sought to determine whether apnea-induced cardiovascular responses resulted in a biologically significant temporary O(2) conservation during exercise. Nine healthy men performing steady-state leg exercise carried out repeated apnea (A) and rebreathing (R) maneuvers starting with residual volume +3.5 liters of air. Heart rate (HR), mean arterial pressure (MAP), and arterial O(2) saturation (Sa(O(2)); pulse oximetry) were recorded continuously. Responses (DeltaHR, DeltaMAP) were determined as differences between HR and MAP at baseline before the maneuver and the average of values recorded between 25 and 30 s into each maneuver. The rate of O(2) desaturation (DeltaSa(O(2))/Deltat) was determined during the same time interval. During apnea, DeltaSaO(2)/Deltat had a significant negative correlation to the amplitudes of DeltaHR and DeltaMAP (r(2) = 0.88, P < 0.001); i.e., individuals with the most prominent cardiovascular responses had the slowest DeltaSa(O(2))/Deltat. DeltaHR and DeltaMAP were much larger during A (-44 +/- 8 beats/min, +49 +/- 4 mmHg, respectively) than during R maneuver (+3 +/- 3 beats/min, +30 +/- 5 mmHg, respectively). DeltaSa(O(2))/Deltat during A and R maneuvers was -1.1 +/- 0.1 and -2.2 +/- 0.2% units/s, respectively, and nadir Sa(O(2)) values were 58 +/- 4 and 42 +/- 3% units, respectively. We conclude that bradycardia and hypertension during apnea are associated with a significant temporary O(2) conservation and that respiratory arrest, rather than the associated hypoxia, is essential for these responses.     

Effects of airflow and work load on cardiovascular drift and skin blood flow

Cardiovascular drift (CVD) can be defined as a progressive increase in heart rate (HR), decreases in stroke volume (SV) and mean arterial pressure (MAP), and a maintained cardiac output (Q) during prolonged exercise. To test the hypothesis that the magnitude of CVD would be related to changes in skin blood flow ( SkBF ), eight healthy, moderately trained males performed 70-min bouts of cycle ergometry in a 2 X 2 assortment of airflows (less than 0.2 and 4.3 m X s-1) and relative work loads (43.4% and 62.2% maximal O2 uptake). Ambient temperature and relative humidity were controlled to mean values of 24.2 +/- 0.8 degrees C and 39.5 +/- 2.4%, respectively. Q, HR, MAP, SkBF , skin and rectal temperatures, and pulmonary gas exchange were measured at 10-min intervals during exercise. Between the 10th and 70th min during exercise at the higher work load with negligible airflow, HR and SkBF increased by 21.6 beats X min-1 and 14.0 ml X 100 ml-1 X min-1, respectively, while SV and MAP decreased by 16.4 ml and 11.3 mmHg. The same work load in the presence of 4.3 m X s-1 airflow resulted in nonsignificant changes of 7.6 beats X min-1, 4.0 ml X (100 ml-1 X min)-1, -2.7 ml, and -1.7 mmHg for HR, SkBF , SV, and MAP. Since nonsignificant changes in HR, SkBF , SV, and MAP were observed at the lower work load in both airflow conditions, the results emphasize that CVD occurs only in conditions which combine high metabolic and thermal circulatory demands.(ABSTRACT TRUNCATED AT 250 WORDS)     

Spontaneous beat-by-beat fluctuations of total peripheral and cerebrovascular resistance in response to tilt

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-->HR), MAP to total peripheral resistance (TPR) and cerebrovascular resistance index (CVRi) (MAP-->TPR and MAP-->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-->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-->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-->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-->CVRi. The SV-->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.     

Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs.

There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 +/- 25%, P < 0.05), systemic vascular resistance (SVR; +33 +/- 16%, P < 0.0005), and heart rate (HR; +5 +/- 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; -16 +/- 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater ( approximately 14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes.     

Use of the Frank-Starling mechanism during exercise is linked to exercise-induced changes in arterial load

Effective arterial elastance(E(A)) is a measure of the net arterial load imposed on the heart that integrates the effects of heart rate(HR), peripheral vascular resistance(PVR), and total arterial compliance(TAC) and is a modulator of cardiac performance. To what extent the change in E(A) during exercise impacts on cardiac performance and aerobic capacity is unknown. We examined E(A) and its relationship with cardiovascular performance in 352 healthy subjects. Subjects underwent rest and exercise gated scans to measure cardiac volumes and to derive E(A)[end-systolic pressure/stroke volume index(SV)], PVR[MAP/(SV*HR)], and TAC(SV/pulse pressure). E(A) varied with exercise intensity: the ΔE(A) between rest and peak exercise along with its determinants, differed among individuals and ranged from -44% to +149%, and was independent of age and sex. Individuals were separated into 3 groups based on their ΔE(A)I. Individuals with the largest increase in ΔE(A)(group 3;ΔE(A)≥0.98 mmHg.m(2)/ml) had the smallest reduction in PVR, the greatest reduction in TAC and a similar increase in HR vs. group 1(ΔE(A)<0.22 mmHg.m(2)/ml). Furthermore, group 3 had a reduction in end-diastolic volume, and a blunted increase in SV(80%), and cardiac output(27%), during exercise vs. group 1. Despite limitations in the Frank-Starling mechanism and cardiac function, peak aerobic capacity did not differ by group because arterial-venous oxygen difference was greater in group 3 vs. 1. Thus the change in arterial load during exercise has important effects on the Frank-Starling mechanism and cardiac performance but not on exercise capacity. These findings provide interesting insights into the dynamic cardiovascular alterations during exercise.     

Cardiovascular, metabolic and plasma catecholamine responses to passive and active exercises.

Eight healthy male volunteers (aged 19.6+/-3.0 years) were submitted to the unloaded active (AE) and passive (PE) cycling exercise-tests performed on an adapted cycle ergometer at a pedalling rate of 50 rpm. Intensity of active exercise was about 10% of VO2 max. In the PE exercise test the ergometer was moved electrically. During both tests the systolic time intervals (STI), stroke volume (SV), heart rate (HR), blood pressure (BP), oxygen uptake (VO2), rating of perceived exertion (RPE), electrical muscle activity (EMG), plasma adrenaline (A), noradrenaline (NE) and blood lactate (LA) concentrations were measured. Exercise induced changes in VO2, RPE and EMG were significantly higher during AE than PE. Shortening of the pre-ejection period (PEP) and diminishing of the PEP to ejection time (ET) ratio were similar in both types of exercise, whereas HR increased only during AE. A significant increase in cardiac output (p<0.01) resulted from increased SV (p<0.01) during PE and from increased HR (p <0.01) during AE. MAP increased only during PE and it was higher than at rest and during AE (p<0.01). Absence of changes in SV and MAP during AE may be considered as a secondary effect of the decrease in TPR. Plasma catecholamines did not increase above resting values in either type of exercise. Blood LA concentration increased during both PE and AE but it reached higher values (p<0.01) after the latter test. The present data suggest that the inotropic state depends on the mechanoreflexes originated in skeletal muscles. However, contribution of changes in preload to shortening of PEP can not be excluded.     

Cardiovascular responses to voluntary and nonvoluntary static exercise in humans.

We have measured the cardiovascular responses during voluntary and nonvoluntary (electrically induced) one-leg static exercise in humans. Eight normal subjects were studied at rest and during 5 min of static leg extension at 20% of maximal voluntary contraction performed voluntarily and nonvoluntarily in random order. Heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were determined, and peripheral vascular resistance (PVR) and stroke volume (SV) were calculated. HR increased from approximately 65 +/- 3 beats/min at rest to 80 +/- 4 and 78 +/- 6 beats/min (P < 0.05), and MAP increased from 83 +/- 6 to 103 +/- 6 and 105 +/- 6 mmHg (P < 0.05) during voluntary and nonvoluntary contractions, respectively. CO increased from 5.1 +/- 0.7 to 6.0 +/- 0.8 and 6.2 +/- 0.8 l/min (P < 0.05) during voluntary and nonvoluntary contractions, respectively. PVR and SV did not change significantly during voluntary or nonvoluntary contractions. Thus the cardiovascular responses were not different between voluntary and electrically induced contractions. These results suggest that the increases in CO, HR, SV, MAP, and PVR during 5 min of static contractions can be elicited without any contribution from a central neural mechanism (central command). However, central command could still have an important role during voluntary static exercise.     

Ventilatory baroreflex sensitivity in humans is not modulated by chemoreflex activation

Increasing arterial blood pressure (AP) decreases ventilation, whereas decreasing AP increases ventilation in experimental animals. To determine whether a "ventilatory baroreflex" exists in humans, we studied 12 healthy subjects aged 18-26 yr. Subjects underwent baroreflex unloading and reloading using intravenous bolus sodium nitroprusside (SNP) followed by phenylephrine ("Oxford maneuver") during the following "gas conditions:" room air, hypoxia (10% oxygen)-eucapnia, and 30% oxygen-hypercapnia to 55-60 Torr. Mean AP (MAP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), expiratory minute ventilation (V(E)), respiratory rate (RR), and tidal volume were measured. After achieving a stable baseline for gas conditions, we performed the Oxford maneuver. V(E) increased from 8.8 ± 1.3 l/min in room air to 14.6 ± 0.8 l/min during hypoxia and to 20.1 ± 2.4 l/min during hypercapnia, primarily by increasing tidal volume. V(E) doubled during SNP. CO increased from 4.9 ± .3 l/min in room air to 6.1 ± .6 l/min during hypoxia and 6.4 ± .4 l/min during hypercapnia with decreased TPR. HR increased for hypoxia and hypercapnia. Sigmoidal ventilatory baroreflex curves of V(E) versus MAP were prepared for each subject and each gas condition. Averaged curves for a given gas condition were obtained by averaging fits over all subjects. There were no significant differences in the average fitted slopes for different gas conditions, although the operating point varied with gas conditions. We conclude that rapid baroreflex unloading during the Oxford maneuver is a potent ventilatory stimulus in healthy volunteers. Tidal volume is primarily increased. Ventilatory baroreflex sensitivity is unaffected by chemoreflex activation, although the operating point is shifted with hypoxia and hypercapnia.     

Cardiovascular responses to military antishock trouser inflation during standing arm exercise

Military antishock trousers (MAST) inflated to 50 mmHg were used with 12 healthy males (mean age 28 +/- 1 yr) to determine the effects of lower-body positive pressure on cardiac output (Q), stroke volume (SV), heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MABP), total peripheral resistance (TPR), and O2 uptake (VO2) during graded arm-cranking exercise. Subjects were studied while standing at rest and at 25, 50, and 75% of maximal arm-cranking VO2. At each level, rest or work was continued for 6 min with MAST inflated and for 6 min with MAST deflated. Order of inflation and deflation was alternated at each experimental rest or exercise level. Measurements were obtained during the last 2 min at each level. Repeated-measures analysis of variance revealed significant increases (P less than 0.001) in Q, SV, and MABP and a consistent decrease in HR with MAST inflation. There was no apparent change in Q/VO2 between inflated and control conditions. There was no effect of MAST inflation on VO2 or TPR. MAST inflation counteracts the gravitational effect of venous return in upright exercise, restoring central blood volume and thereby increasing Q and MABP from control. HR is decreased consequent to increased MABP through arterial baroreflexes. The associated decrease in TPR is not observed, being offset by the mechanical compression of leg vasculature with MAST inflation.     

WISE 2005: stroke volume changes contribute to the pressor response during ischemic handgrip exercise in women.

The mechanism of the pressor response to small muscle mass (e.g., forearm) exercise and during metaboreflex activation may include elevations in cardiac output (Q) or total peripheral resistance (TPR). Increases in Q must be supported by reductions in visceral venous volume to sustain venous return as heart rate (HR) increases. Therefore, this study tested the hypothesis that increases in Q, supported by reductions in splanchnic volume (portal vein constriction), explain the pressor response during handgrip exercise and metaboreflex activation. Seventeen healthy women performed 2 min of static ischemic handgrip exercise and 2 min of postexercise circulatory occlusion (PECO) while HR, stroke volume and superficial femoral artery flow (Doppler), blood pressure (Finometer), portal vein diameter (ultrasound imaging), and muscle sympathetic nerve activity (MSNA; microneurography) were measured followed by the calculation of Q, TPR, and leg vascular resistance (LVR). Compared with baseline, mean arterial blood pressure (MAP) (P < 0.001) and Q (P < 0.001) both increased in each minute of exercise accompanied by a approximately 5% reduction in portal vein diameter (P < 0.05). MAP remained elevated during PECO, whereas Q decreased below exercise levels. MSNA was elevated above baseline during the second minute of exercise and through the PECO period (P < 0.05). Neither TPR nor LVR was changed from baseline during exercise and PECO. The data indicate that the majority of the blood pressure response to isometric handgrip exercise in women was due to mobilization of central blood volume and elevated stroke volume and Q rather than elevations in TVR or LVR resistance.     

Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans.

The effect of the diving response on alveolar gas exchange was investigated in 15 subjects. During steady-state exercise (80 W) on a cycle ergometer, the subjects performed 40-s apneas in air and 40-s apneas with face immersion in cold (10 degrees C) water. Heart rate decreased and blood pressure increased during apneas, and the responses were augmented by face immersion. Oxygen uptake from the lungs decreased during apnea in air (-22% compared with eupneic control) and was further reduced during apnea with face immersion (-25% compared with eupneic control). The plasma lactate concentration increased from control (11%) after apnea in air and even more after apnea with face immersion (20%), suggesting an increased anaerobic metabolism during apneas. The lung oxygen store was depleted more slowly during apnea with face immersion because of the augmented diving response, probably including a decrease in cardiac output. Venous oxygen stores were probably reduced by the cardiovascular responses. The turnover times of these gas stores would have been prolonged, reducing their effect on the oxygen uptake in the lungs. Thus the human diving response has an oxygen-conserving effect.     

Relationships between the extent of apnea-induced bradycardia and the vascular response in the arm and leg during dynamic two-legged knee extension exercise

Our aim was to test the hypothesis that apnea-induced hemodynamic responses during dynamic exercise in humans differ between those who show strong bradycardia and those who show only mild bradycardia. After apnea-induced changes in heart rate (HR) were evaluated during dynamic exercise, 23 healthy subjects were selected and divided into a large response group (L group; n = 11) and a small response group (S group; n = 12). While subjects performed a two-legged dynamic knee extension exercise at a work load that increased HR by 30 beats/min, apnea-induced changes in HR, cardiac output (CO), mean arterial pressure (MAP), arterial O(2) saturation (Sa(O(2))), forearm blood flow (FBF), and leg blood flow (LBF) were measured. During apnea, HR in the L group (54 ± 2 beats/min) was lower than in the S group (92 ± 3 beats/min, P < 0.05). CO, Sa(O(2)), FBF, LBF, forearm vascular conductance (FVC), leg vascular conductance (LVC), and total vascular conductance (TVC) were all reduced, and MAP was increased in both groups, although the changes in CO, TVC, LBF, LVC, and MAP were larger in the L group than in the S group (P < 0.05). Moreover, there were significant positive linear relationships between the reduction in HR and the reductions in TVC, LVC, and FVC. We conclude that individuals who show greater apnea-induced bradycardia during exercise also show greater vasoconstriction in both active and inactive muscle regions.     

Hypoxemia alone does not explain blood pressure elevations after obstructive apneas

In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (SaO2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (SaO2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (SaO2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (SaO2 nadir 79-82%): 18.8 +/- 7.1 vs. 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P less than 0.01); and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.     

Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers.

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10 degrees C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial PO(2) and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.     

Cardiovascular responses to an orthostatic challenge and electrical-stimulation-induced leg muscle contractions in individuals with paraplegia

The purpose of this study was to investigate the cardiovascular and haemodynamic responses that occur during moderate orthostatic challenge in people with paraplegia, and the effect of electrical stimulation (ES)-induced leg muscle contractions on their responses to orthostatic challenge. Eight males with complete spinal lesions between the 5th and 12th thoracic vertebrae (PARA) and eight able-bodied individuals (AB) volunteered for this study. Changes in heart rate (fc), stroke volume (SV), cardiac output (Qc), mean arterial pressure (MAP), total peripheral resistance (TPR), limb volumes and indices of neural modulation of fc, [parasympathetic (PNS) and sympathetic (SNS) nervous system indicators] were assessed during: (1) supine rest (REST), (2) REST with lower-body negative pressure at -30 torr (LBNP -30, where 1 torr = 133.32 N/m2), and (3) for PARA only, LBNP -30 with ES-induced leg muscle contractions (LBNP + ES). LBNP -30 elicited a decrease in SV (by 23% and 22%), Qc (by 15% and 18%) and the PNS indicator, but an increase in fc (by 10% and 9%), TPR (by 23% and 17%) and calf volume (by 1.51% and 4.04%) in both PARA and AB subjects, respectively. The SNS indicator was increased in the AB group only. Compared to LBNP -30, LBNP + ES increased SV (by 20%) and Qc (by 16%), and decreased TPR (by 12%) in the PARA group. MAP was unchanged from REST during all trials, for both groups. The orthostatic challenge induced by LBNP -30 elicited similar cardiovascular adaptations in PARA and AB subjects. ES-induced muscle contractions during LBNP -30 augmented the cardiovascular responses exhibited by the PARA group, probably via reactivation of the skeletal muscle pump and improved venous return.     

Beat-to-beat cardiovascular responses to rapid, low-level LBNP in humans

The hypothesis tested was that there are significant transient changes in the cardiovascular variables after rapid onset and release of mild lower body negative pressure (LBNP, -20 mmHg), even in experimental situations where there is no detectable change in steady-state values. Twelve subjects participated in the study. Heart rate, stroke volume (SV), cardiac output, mean arterial pressure (MAP), total peripheral resistance (TPR), acral and nonacral skin blood flow, and blood flow velocity in the brachial artery were continuously recorded during the pre-LBNP period (0-120 s), during LBNP (120-420 s), and during the post-LBNP period (420-600 s). The main finding was that MAP is transiently but strongly affected by rapid changes in LBNP as small as -20 mmHg. There was also a characteristic asymmetry in cardiovascular responses to the onset and release of LBNP, particularly in the responses in SV. The transient changes in MAP indicate that the neural responses that affect TPR are not fast enough to compensate for the rapid changes in LBNP. In this case, the arterial baroreceptors will be activated as well as the low-pressure baroreceptors that sense central venous pressure. This must be taken into consideration in future discussions of the results of LBNP protocols.