The athlete's heart: allometric considerations on published papers and relation to cardiovascular variables.

To evaluate the morphology of the "athlete's heart", left ventricular (LV) wall thickness (WT) and end-diastolic internal diameter (LVIDd) at rest were addressed in publications on skiers, rowers, swimmers, cyclists, runners, weightlifters (n = 927), and untrained controls (n = 173) and related to the acute and maximal cardiovascular response to their respective disciplines. Dimensions of the heart at rest and functional variables established during the various sport disciplines were scaled to body weight for comparison among athletes independent of body mass. The two measures of LV were related (r = 0.8; P = 0.04) across athletic disciplines. With allometric scaling to body weight, LVIDd was similar between weightlifters and controls but 7%-15% larger in the other athletic groups, while WT was 9%-24% enlarged in all athletes. The LVIDd was related to stroke volume, oxygen pulse, maximal oxygen uptake, cardiac output, and blood volume (r = ~ 0.9, P < 0.05), while there was no relationship between WT and these variables (P > 0.05). In conclusion, while cardiac enlargement is, in part, essential for the generation of the cardiac output and thus stroke volume needed for competitive endurance exercise, an enlarged WT seems important for the development of the wall tension required for establishing normal arterial pressure in the enlarged LVIDd.

Fluctuations in cardiac stroke volume during rowing.

Preload to the heart may be limited during rowing because both blood pressure and central venous pressure increase when force is applied to the oar. Considering that only the recovery phase of the rowing stroke allows for unhindered venous return, rowing may induce large fluctuations in stroke volume (SV). Thus, the purpose of this study was to evaluate SV continuously during the rowing stroke. Eight nationally competitive oarsmen (mean ± standard deviation: age 21 ± 2 years, height 190 ± 9 cm, and weight 90 ± 10 kg) rowed on an ergometer at a targeted heart rate of 130 and 160 beats per minute. SV was derived from arterial pressure waveform by pulse contour analysis, while ventilation and force on the handle were measured. Mean arterial pressure was elevated during the stroke at both work rates (to 133 ± 10 [P < .001] and 145 ± 11 mm Hg [P = .024], respectively). Also, SV fluctuated markedly during the stroke with deviations being largest at the higher work rate. Thus, SV decreased by 27 ± 10% (31 ± 11 mL) at the beginning of the stroke and increased by 25 ± 9% (28 ± 10 mL) in the recovery (P = .013), while breathing was entrained with one breath during the drive of the stroke and one prior to the next stroke. These observations indicate that during rowing cardiac output depends critically on SV surges during the recovery phase of the stroke.

CO2 supplementation dissociates cerebral oxygenation and middle cerebral artery blood velocity during maximal cycling.

This study evaluated whether the reduction of prefrontal cortex oxygenation (ScO2 ) during maximal exercise depends on the hyperventilation-induced hypocapnic attenuation of middle cerebral artery blood velocity (MCA Vmean ). Twelve endurance-trained males (age: 25 ± 3 years, height: 183 ± 8 cm, weight: 75 ± 9 kg; mean ± SD) performed in three separate laboratory visits, a maximal oxygen uptake (VO2 max) test, an isocapnic (end-tidal CO2 tension (PetCO2 ) clamped at 40 ± 1 mmHg), and an ambient air controlled-pace constant load high-intensity ergometer cycling to exhaustion, while MCA Vmean (transcranial Doppler ultrasound) and ScO2 (near-infrared spectroscopy) were determined. Duration of exercise (12 min 25 s ± 1 min 18 s) was matched by performing the isocapnic trial first. Pulmonary VO2 was 90 ± 6% versus 93 ± 5% of the maximal value (P = .012) and PetCO2 40 ± 1 versus 34 ± 4 mmHg (P < .05) during the isocapnic and control trials, respectively. During the isocapnic trial MCA Vmean increased by 16 ± 13% until clamping was applied and continued to increase (by 14 ± 28%; P = .017) until the end of exercise, while there was no significant change during the control trial (P = .071). In contrast, ScO2 decreased similarly in both trials (-3.2 ± 5.1% and -4.1 ± 9.6%; P < .001, isocapnic and control, respectively) at exhaustion. The reduction in prefrontal cortex oxygenation during maximal exercise does not depend solely on lowered cerebral blood flow as indicated by middle cerebral blood velocity.

The physiology of rowing with perspective on training and health.

PURPOSE: This review presents a perspective on the expansive literature on rowing. METHODS: The PubMed database was searched for the most relevant literature, while some information was obtained from books. RESULTS: Following the life span of former rowers paved the way to advocate exercise for health promotion. Rowing involves almost all muscles during the stroke and competition requires a large oxygen uptake, which is challenged by the pulmonary diffusion capacity and restriction in blood flow to the muscles. Unique training adaptations allow for simultaneous engagement of the legs in the relatively slow movement of the rowing stroke that, therefore, involves primarily slow-twitch muscle fibres. Like other sport activities, rowing is associated with adaptation not only of the heart, including both increased internal diameters and myocardial size, but also skeletal muscles with hypertrophy of especially slow-twitch muscle fibres. The high metabolic requirement of intense rowing reduces blood pH and, thereby, arterial oxygen saturation decreases as arterial oxygen tension becomes affected. CONCLUSION: Competitive rowing challenges most systems in the body including pulmonary function and circulatory control with implication for cerebral blood flow and neuromuscular activation. Thus, the physiology of rowing is complex, but it obviously favours large individuals with arms and legs that allow the development of a long stroke. Present inquiries include the development of an appropriately large cardiac output despite the Valsalva-like manoeuvre associated with the stroke, and the remarkable ability of the brain to maintain motor control and metabolism despite marked reductions in cerebral blood flow and oxygenation.

Cardiac output during exercise is related to plasma atrial natriuretic peptide but not to central venous pressure in humans.

NEW FINDINGS: What is the central question of this study? Is cardiac output during exercise dependent on central venous pressure? What is the main finding and its importance? The increase in cardiac output during both rowing and running is related to preload to the heart, as indicated by plasma atrial natriuretic peptide, but unrelated to central venous pressure. The results indicate that in upright humans, central venous pressure reflects the gravitational influence on central venous blood rather than preload to the heart. ABSTRACT: We evaluated the increase in cardiac output (CO) during exercise in relationship to central venous pressure (CVP) and plasma arterial natriuretic peptide (ANP) as expressions of preload to the heart. Seven healthy subjects (four men; mean ± SD: age 26 ± 3 years, height 181± 8 cm and weight 76 ± 11 kg;) rested in sitting and standing positions (in randomized order) and then rowed and ran at submaximal workloads. The CVP was recorded, CO (Modelflow) calculated and arterial plasma ANP determined by radioimmunoassay. While sitting, (mean ± SD) CO was 6.2 ± 1.6 l min-1 , plasma ANP 70 ± 10 pg ml-1 and CVP 1.8 ± 1.1 mmHg, and when standing decreased to 5.9 ± 1.0 l min-1 , 63 ± 10 pg ml-1 and -3.8 ± 1.2 mmHg, respectively (P < 0.05). Ergometer rowing elicited an increase in CO to 22.5 ± 5.5 l min-1 as plasma ANP increased to 156 ± 11 pg ml-1 and CVP to 3.8 ± 0.9 mmHg (P < 0.05). Likewise, CO increased to 23.5 ± 6.0 l min-1 during running, albeit with a smaller (P < 0.05) increase in plasma ANP, but with little change in CVP (-0.9 ± 0.4 mmHg). The increase in CO in response to exercise is related to preload to the heart, as indicated by plasma ANP, but unrelated to CVP. The results indicate that in upright humans, CVP reflects the gravitational influence on central venous blood rather than preload to the heart.

Elevated arterial lactate delays recovery of intracellular muscle pH after exercise.

PURPOSE: We evaluated muscle proton elimination following similar exercise in the same muscle group following two exercise modalities. METHODS: Seven rowers performed handgrip or rowing exercise for ~ 5 min. The intracellular response of the wrist flexor muscles was evaluated by 31P nuclear magnetic resonance spectroscopy, while arterial and venous forearm blood was collected. RESULTS: Rowing and handgrip reduced intracellular pH to 6.3 ± 0.2 and 6.5 ± 0.1, arterial pH to 7.09 ± 0.03 and 7.40 ± 0.03 and venous pH to 6.95 ± 0.06 and 7.20 ± 0.04 (P < 0.05), respectively. Arterial and venous lactate increased to 17.5 ± 1.6 and 20.0 ± 1.6 mM after rowing while only to 2.6 ± 0.8 and 6.8 ± 0.8 mM after handgrip exercise. Arterio-venous concentration difference of bicarbonate and phosphocreatine recovery kinetics (T50% rowing 1.5 ± 0.7 min; handgrip 1.4 ± 1.0 min) was similar following the two exercise modalities. Yet, intramuscular pH recovery in the forearm flexor muscles was 3.5-fold slower after rowing than after handgrip exercise (T50% rowing of 2 ± 0.1 vs. 7 ± 0.3 min for handgrip). CONCLUSION: Rowing delays intracellular-pH recovery compared with handgrip exercise most likely because rowing, as opposed to handgrip exercise, increases systemic lactate concentration. Thus the intra-to-extra-cellular lactate gradient is small after rowing. Since this lactate gradient is the main driving force for intracellular lactate removal in muscle and, since pHi normalization is closely related to intracellular lactate removal, rowing results in a slower pHi recovery compared to handgrip exercise.

Hepato-splanchnic fluxes during exercise in patients with cirrhosis-a pilot study.

In cirrhotic patients, compromised hepatocyte function combined with disturbed hepatic blood flow could affect hepato-splanchnic substrate and metabolite fluxes and exacerbate fatigue during exercise. Eight cirrhotic patients performed incremental cycling trials (3 × 10 min; at light (28 [19-37] W; median with range), moderate (55 [41-69] W), and vigorous (76 [50-102] W) intensity). Heart rate increased from 68 (62-74) at rest to 95 (90-100), 114 (108-120), and 140 (134-146) beats/min (P < 0.05), respectively. The hepatic blood flow, as determined by constant infusion of indocyanine green with arterial and hepatic venous sampling, declined from 1.01 (0.75-1.27) to 0.69 (0.47-0.91) L/min (P < 0.05). Hepatic glucose output increased from 0.6 (0.5-0.7) to 1.5 (1.3-1.7) mmol/min, while arterial lactate increased from 0.8 (0.7-0.9) to 9.0 (8.1-9.9) mmol/L (P < 0.05) despite a rise in hepatic lactate uptake. Arterial ammonia increased in parallel to lactate from 47.3 (40.1-54.5) to 144.4 (120.5-168.3) µmol/L (P < 0.05), although hepatic ammonia uptake increased from 19.5 (12.4-26.6) to 69.5 (46.5-92.5) µmol/min (P < 0.05). Among the 14 amino acids measured, glutamate was released in the liver, while the uptake of free fatty acids decreased. During exercise at relatively low workloads, arterial lactate and ammonia levels were comparable to those seen in healthy subjects at higher workloads, while euglycemia was maintained due to sufficient hepatic glucose production. The accumulation of lactate and ammonia may contribute to exercise intolerance in patients with cirrhosis.

Renal lactate elimination is maintained during moderate exercise in humans.

Reduced hepatic lactate elimination initiates blood lactate accumulation during incremental exercise. In this study, we wished to determine whether renal lactate elimination contributes to the initiation of blood lactate accumulation. The renal arterial-to-venous (a-v) lactate difference was determined in nine men during sodium lactate infusion to enhance the evaluation (0.5 mol x L(-1) at 16 ± 1 mL x min(-1); mean ± s) both at rest and during cycling exercise (heart rate 139 ± 5 beats x min(-1)). The renal release of erythropoietin was used to detect kidney tissue ischaemia. At rest, the a-v O(2) (CaO(2)-CvO(2)) and lactate concentration differences were 0.8 ± 0.2 and 0.02 ± 0.02 mmol x L(-1), respectively. During exercise, arterial lactate and CaO(2)-CvO(2) increased to 7.1 ± 1.1 and 2.6 ± 0.8 mmol x L(-1), respectively (P < 0.05), indicating a -70% reduction of renal blood flow with no significant change in the renal venous erythropoietin concentration (0.8 ± 1.4 U x L(-1)). The a-v lactate concentration difference increased to 0.5 ± 0.8 mmol x L(-1), indicating similar lactate elimination as at rest. In conclusion, a -70% reduction in renal blood flow does not provoke critical renal ischaemia, and renal lactate elimination is maintained. Thus, kidney lactate elimination is unlikely to contribute to the initial blood lactate accumulation during progressive exercise.

Dose of Bicarbonate to Maintain Plasma pH During Maximal Ergometer Rowing and Consequence for Plasma Volume.

Rowing performance may be enhanced by attenuated metabolic acidosis following bicarbonate (BIC) supplementation. This study evaluated the dose of BIC needed to eliminate the decrease in plasma pH during maximal ergometer rowing and assessed the consequence for change in plasma volume. Six oarsmen performed "2,000-m" maximal ergometer rowing trials with BIC (1 M; 100-325 ml) and control (CON; the same volume of isotonic saline). During CON, pH decreased from 7.42 ± 0.01 to 7.17 ± 0.04 (mean and SD; p < 0.05), while during BIC, pH was maintained until the sixth minute where it dropped to 7.32 ± 0.08 and was thus higher than during CON (p < 0.05). The buffering effect of BIC on metabolic acidosis was dose dependent and 300-325 mmol required to maintain plasma pH. Compared to CON, BIC increased plasma sodium by 4 mmol/L, bicarbonate was maintained, and lactate increased to 25 ± 7 vs. 18 ± 3 mmol/L (p < 0.05). Plasma volume was estimated to decrease by 24 ± 4% in CON, while with BIC the estimate was by only 7 ± 6% (p < 0.05) and yet BIC had no significant effect on performance [median 6 min 27 s (range 6 min 09 s to 6 min 57 s) vs. 6 min 33 s (6 min 14 s to 6 min 55 s)]. Bicarbonate administration attenuates acidosis during maximal rowing in a dose-dependent manner and the reduction in plasma volume is attenuated with little consequence for performance.

The Effect of Hyperoxia on Central and Peripheral Factors of Arm Flexor Muscles Fatigue Following Maximal Ergometer Rowing in Men.

PURPOSE: This study evaluates the effect of hyperoxia on cerebral oxygenation and neuromuscular fatigue mechanisms of the elbow flexor muscles following ergometer rowing. METHODS: In 11 competitive male rowers (age, 30 ± 4 years), we measured near-infrared spectroscopy determined frontal lobe oxygenation (ScO2) and transcranial Doppler ultrasound determined middle cerebral artery mean flow velocity (MCA V mean) combined with maximal voluntary force (MVC), peak resting twitch force (P tw) and cortical voluntary activation (VATMS) of the elbow flexor muscles using electrical motor point and magnetic motor cortex stimulation, respectively, before, during, and immediately after 2,000 m all-out effort on rowing ergometer with normoxia and hyperoxia (30% O2). RESULTS: Arterial hemoglobin O2 saturation was reduced to 92.5 ± 0.2% during exercise with normoxia but maintained at 98.9 ± 0.2% with hyperoxia. The MCA V mean increased by 38% (p < 0.05) with hyperoxia, while only marginally increased with normoxia. Similarly, ScO2 was not affected with hyperoxia but decreased by 7.0 ± 4.8% from rest (p = 0.04) with normoxia. The MVC and P tw were reduced (7 ± 3% and 31 ± 9%, respectively, p = 0.014), while VATMS was not affected by the rowing effort in normoxia. With hyperoxia, the deficit in MVC and P tw was attenuated, while VATMS was unchanged. CONCLUSION: These data indicate that even though hyperoxia restores frontal lobe oxygenation the resultant attenuation of arm muscle fatigue following maximal rowing is peripherally rather than centrally mediated.

The intracellular to extracellular proton gradient following maximal whole body exercise and its implication for anaerobic energy production.

Maximal exercise elicits systemic acidosis where venous pH can drop to 6.74 and here we assessed how much lower the intracellular value (pH(i)) might be. The wrist flexor muscles are intensively involved in rowing and (31)P-magnetic resonance spectroscopy allows for calculation of forearm pH(i) and energy metabolites at high time resolution. Arm venous blood was collected in seven competitive rowers (4 males; 72 +/- 5 kg; mean +/- SD) at rest and immediately after a "2,000 m" maximal rowing ergometer effort when hemoglobin O(2) saturation decreased from 51 +/- 4 to 29 +/- 9% and lactate rose from 1.0 +/- 0.1 to 16.8 +/- 3.6 mM. Venous pH and pH(i) decreased from 7.43 +/- 0.01 to 6.90 +/- 0.01 and from 7.05 +/- 0.02 to 6.32 +/- 0.19 (P < 0.05), respectively, while the ratio of inorganic phosphate to phosphocreatine increased from 0.12 +/- 0.03 to 1.50 +/- 0.49 (P < 0.05). The implication of the recorded intravascular and intracellular acidosis and the decrease in PCr is that the anaerobic contribution to energy metabolism during maximal rowing corresponds to 4.47 +/- 1.8 L O(2), a value similar to that defined as the "accumulated oxygen deficit". In conclusion, during maximal rowing the intracellular acidosis, expressed as proton concentration, surpasses approximately 4-fold the intravascular acidosis, while the resting gradient is approximately 2.

Are the arms and legs in competition for cardiac output?

Oxygen transport to working skeletal muscles is challenged during whole-body exercise. In general, arm-cranking exercise elicits a maximal oxygen uptake (VO2max) corresponding to approximately 70% of the value reached during leg exercise. However, in arm-trained subjects such as rowers, cross-country skiers, and swimmers, the arm VO2max approaches or surpasses the leg value. Despite this similarity between arm and leg VO2max, when arm exercise is added to leg exercise, VO2max is not markedly elevated, which suggests a central or cardiac limitation. In fact, when intense arm exercise is added to leg exercise, leg blood flow at a given work rate is approximately 10% less than during leg exercise alone. Similarly, when intense leg exercise is added to arm exercise, arm blood flow and muscle oxygenation are reduced by approximately 10%. Such reductions in regional blood flow are mainly attributed to peripheral vasoconstriction induced by the arterial baroreflex to support the prevailing blood pressure. This putative mechanism is also demonstrated when the ability to increase cardiac output is compromised; during exercise, the prevailing blood pressure is established primarily by an increase in cardiac output, but if the contribution of the cardiac output is not sufficient to maintain the preset blood pressure, the arterial baroreflex increases peripheral resistance by augmenting sympathetic activity and restricting blood flow to working skeletal muscles.

Cardiovascular control during whole body exercise.

It has been considered whether during whole body exercise the increase in cardiac output is large enough to support skeletal muscle blood flow. This review addresses four lines of evidence for a flow limitation to skeletal muscles during whole body exercise. First, even though during exercise the blood flow achieved by the arms is lower than that achieved by the legs (∼160 vs. ∼385 ml·min(-1)·100 g(-1)), the muscle mass that can be perfused with such flow is limited by the capacity to increase cardiac output (42 l/min, highest recorded value). Secondly, activation of the exercise pressor reflex during fatiguing work with one muscle group limits flow to other muscle groups. Another line of evidence comes from evaluation of regional blood flow during exercise where there is a discrepancy between flow to a muscle group when it is working exclusively and when it works together with other muscles. Finally, regulation of peripheral resistance by sympathetic vasoconstriction in active muscles by the arterial baroreflex is critical for blood pressure regulation during exercise. Together, these findings indicate that during whole body exercise muscle blood flow is subordinate to the control of blood pressure.

Effects of hyperthermia on cerebral blood flow and metabolism during prolonged exercise in humans.

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known whether the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose, and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, either when subjects remained normothermic (core temperature = 37.9 degrees C; control) or when severe hyperthermia had developed (core temperature = 39.5 degrees C; hyperthermia). The gCBF was similar after 15 min in the two trials, and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18% and was therefore lower in hyperthermia compared with control at the end of exercise (43 +/- 4 vs. 51 +/- 4 ml. 100 g(-1). min(-1); P < 0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arteriovenous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise cerebral blood flow seems to relate to a concomitant 18% lowering of arterial carbon dioxide tension, whereas the higher cerebral metabolic rate of oxygen may be ascribed to a Q(10) (temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.

Bicarbonate attenuates arterial desaturation during maximal exercise in humans.

The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200-350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a "2,000-m" maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 +/- 0.3 to 38.9 +/- 0.1 degrees C (P < 0.05; means +/- SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 +/- 0.01 at rest to 7.07 +/- 0.02 but only to 7.34 +/- 0.02 (P < 0.05) during the Bic trial. Arterial PO2 was reduced from 103.1 +/- 0.7 to 88.2 +/- 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 +/- 0.2% at rest and decreased to 89.0 +/- 0.7% during Sal exercise but only to 94.1 +/- 1% with Bic (P < 0.05). Arterial PCO2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 +/- 0.5 to 45.9 +/- 2.0 Torr (P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 +/- 14 vs. 142 +/- 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial PO2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.

Cerebral metabolism during upper and lower body exercise.

When continuation of exercise calls for a "will," the cerebral metabolic ratio of O2 to (glucose + lactate) decreases, with the largest reduction (30-50%) at exhaustion. Because a larger effort is required to exercise with the arms than with the legs, we tested the hypothesis that the reduction in the cerebral metabolic ratio would become more pronounced during arm cranking than during leg exercise. The cerebral arterial-venous differences for blood-gas variables, glucose, and lactate were evaluated in two groups of eight subjects during exhaustive arm cranking and leg exercise. During leg exercise, exhaustion was elicited after 25 +/- 6 (SE) min, and the cerebral metabolic ratio was reduced from 5.6 +/- 0.2 to 3.5 +/- 0.2 after 10 min and to 3.3 +/- 0.3 at exhaustion (P < 0.05). Arm cranking lasted for 35 +/- 4 min and likewise decreased the cerebral metabolic ratio after 10 min (from 6.7 +/- 0.4 to 5.0 +/- 0.3), but the nadir at exhaustion was only 4.7 +/- 0.4, i.e., higher than during leg exercise (P < 0.05). The results demonstrate that exercise decreases the cerebral metabolic ratio when a conscious effort is required, irrespective of the muscle groups engaged. However, the comparatively small reduction in the cerebral metabolic ratio during arm cranking suggests that it is influenced by the exercise paradigm.

Rowing, the ultimate challenge to the human body - implications for physiological variables.

Clinical diagnoses depend on a variety of physiological variables but the full range of these variables is seldom known. With the load placed on the human body during competitive rowing, the physiological range for several variables is illustrated. The extreme work produced during rowing is explained by the seated position and the associated ability to increase venous return and, thus, cardiac output. This review highlights experimental work on Olympic rowing that presents a unique challenge to the human capacities, including cerebral metabolism, to unprecedented limits, and provides a unique opportunity to reveal the extreme range of many physiological variables.

Carotid baroreflex function ceases during vasovagal syncope.

Despite the arterial baroreflex control of heart rate and blood pressure, vasovagal syncope is a common cause of loss of consciousness in people exposed to stimuli that reduce the central blood volume, such as head-up tilt. Carotid baroreflex function was evaluated using a rapid pulse train of neck pressure and neck suction in three conscious volunteers who developed a vasovagal episode during head-up tilt. The maximal gain of the carotid-heart rate and carotid-blood pressure baroreflex function curves were identified as measures of carotid baroreceptor responsiveness. When presyncopal symptoms developed, one further baroreflex assessment was obtained before the subjects were returned to the supine position. The bradycardia and hypotension exhibited during pre-syncope and syncope reflected a leftward and downward relocation of both the cardiac and vasomotor stimulus response curves. In addition, during the vasovagal syncope, baroreflex control was suppressed as blood pressure remained low during neck pressure stimuli. In conclusion, arterial baroreflex function ceases during vasovagal syncope.