Cardiovascular and splenic responses to exercise in humans.

To investigate splenic erythrocyte volume after exercise and the effect on hematocrit- and hemoglobin-based plasma volume equations, nine men cycled at an intensity of 60% maximal O(2) uptake for 5-, 10-, or 15-min duration, followed by an incremental ride to exhaustion. The reduction in spleen volume, calculated using (99m)Tc-labeled erythrocytes, was not significantly different among the three submaximal rides (5 min = 28%, 10 min = 30%, 15 min = 36%; P = 0.26). The incremental ride to exhaustion resulted in a 56% reduction in spleen volume, which recovered to baseline levels within 20 min. Plasma catecholamines were inversely related to spleen volume after exercise (r = 0.70-0.84; P < 0.0001). There were no differences in red cell or total blood volume pre- to postexercise; however, a significant reduction in plasma volume was observed (18.9%; P < 0.01). There was no difference between the iodinated albumin and the hematocrit and hemoglobin methods of assessing plasma volume changes. These results suggest that the spleen regulates its volume in response to an intensity-dependent signal, and plasma catecholamines appear partially responsible. Splenic release of erythrocytes has no effect on indirect measures of plasma volume.     

Cardiovascular responses to apneic facial immersion during altered cardiac filling.

The hypothesis that reduced cardiac filling, as a result of lower body negative pressure (LBNP) and postexercise hypotension (PEH), would attenuate the reflex changes to heart rate (HR), skin blood flow (SkBF), and mean arterial pressure (MAP) normally induced by facial immersion was tested. The purpose of this study was to investigate the cardiovascular control mechanisms associated with apneic facial immersion during different cardiovascular challenges. Six subjects randomly performed 30-s apneic facial immersions in 6.0 +/- 1.2 degrees C water under the following conditions: 1) -20 mmHg LBNP, 2) +40 mmHg lower body positive pressure (LBPP), 3) during a period of PEH, and 4) normal resting (control). Measurements included SkBF at one acral (distal phalanx of the thumb) and one nonacral region of skin (ventral forearm), HR, and MAP. Facial immersion reduced HR and SkBF at both sites and increased MAP under all conditions (P < 0.05). Reduced cardiac filling during LBNP and PEH significantly attenuated the absolute HR nadir observed during the control immersion (P < 0.05). The LBPP condition did not result in a lower HR nadir than control but did result in a nadir significantly lower than that of the LBNP and PEH conditions (P < 0.05). No differences were observed in either SkBF or MAP between conditions; however, the magnitude of SkBF reduction was greater at the acral site than at the nonacral site for all conditions (P < 0.05). These results suggest that the cardiac parasympathetic response during facial immersion can be attenuated when cardiac filling is compromised.     

Heart rate variability in exercising humans: effect of water immersion

Power spectrum analysis of heart-rate variability was made in seven men [mean age 22 (SEM 1) years] in head-out water immersion (W) and in air (A, control) at rest and during steady-state cycling to maximal intensity (maximum oxygen uptake, V˙O_2max). At rest W resulted in a trebled increase in the total power (P < 0.05), coupled with minimal changes in the power (as a percentage of the total) of the high frequency peak (HF, centred at 0.26 Hz; 18% vs 28%) and of the low frequency peak (LF, 0.1 Hz; 24% vs 32%). A third peak at about 0.03 Hz (very low frequency, VLF) represented the remaining power both in W and A. These changes as a whole indicated that immersion caused a vagal dominance in cardiac autonomic interaction, due to the central pooling of blood and/or the pressure of water on the trunk. Exercise caused a decrease in the total power in W and A. The LF% did not change up to about 50% V˙O_2max, thereafter decreasing towards nil in both conditions. The HF% decreased in similar ways in W and A to about half at 55%–60% V˙O_2max and then increased to reach 1.5 times the resting values at V˙O_2max. The central frequency of HF increased linearly with oxygen uptake, showing a tendency to be higher in W than in A at medium to high intensities. The VLF% remained unchanged. The lack of differences in the LF peak between W and A during exercise would suggest that blood distribution had no effect on the readjustments in control mechanisms of arterial pressure. On the other hand, the findings of similar HF powers and the very similar values for ventilation in W and A confirmed the direct effect of the respiratory activity in heart rate modulation during exercise. Accepted: 25 August 1997     

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.     

Cardiovascular and neuroendocrine responses to water immersion in compensated heart failure

The hypothesis was tested that cardiovascular and neuroendocrine (norepinephrine, renin, and vasopressin) responses to central blood volume expansion are blunted in compensated heart failure (HF). Nine HF patients [New York Heart Association class II-III, ejection fraction = 0.28 +/- 0.02 (SE)] and 10 age-matched controls (ejection fraction = 0.68 +/- 0.03) underwent 30 min of thermoneutral (34.7 +/- 0.02 degrees C) water immersion (WI) to the xiphoid process. WI increased (P < 0.05) central venous pressure by 3.7 +/- 0.6 and 3.2 +/- 0.4 mmHg and stroke volume index by 12.2 +/- 2.1 and 7.2 +/- 2.1 ml. beat(-1). m(-2) in controls and HF patients, respectively. During WI, systemic vascular resistance decreased (P < 0.05) similarly by 365 +/- 66 and 582 +/- 227 dyn. s. cm(-5) in controls and HF patients, respectively. Forearm subcutaneous vascular resistance decreased by 19 +/- 7% (P < 0.05) in controls but did not change in HF patients. Heart rate decreased less during WI in HF patients, whereas release of norepinephrine, renin, and vasopressin was suppressed similarly in the two groups. We suggest that reflex control of forearm vascular beds and heart rate is blunted in compensated HF but that baroreflex-mediated systemic vasodilatation and neuroendocrine responses to central blood volume expansion are preserved.     

Comparison of acute cardiovascular responses to water immersion and head-down tilt in humans.

The hypothesis was tested that acute water immersion to the neck (WI) compared with 6 degrees head-down tilt (HDT) induces a more pronounced distension of the heart and lower plasma levels of vasoconstrictor hormones. Ten healthy males underwent 30 min of HDT, WI, and a seated control (randomized). During WI, left atrial diameter and stroke volume increased to the same extent as during HDT. Cardiac output increased by 1 l/min more during WI than during HDT. (P < 0.05). Plasma atrial natriuretic peptide increased during WI (P < 0.05) but not during HDT, whereas plasma norepinephrine, vasopressin, and renin activity were suppressed similarly. Mean arterial pressure decreased by 9 mmHg (P < 0.05) during HDT and was unchanged during WI, and heart rate decreased more during HDT (P < 0.05). Arterial pulse pressure increased considerably more during HDT than during WI. In conclusion, the hypothesis was not confirmed because the cardiac atria were similarly distended by acute HDT and WI and the release of vasoconstrictor hormones were suppressed to the same extent.     

Habituation of the metabolic and ventilatory responses to cold-water immersion in humans

An experiment was undertaken to answer long-standing questions concerning the nature of metabolic habituation in repeatedly cooled humans. It was hypothesised that repeated skin and deep-body cooling would produce such a habituation that would be specific to the magnitude of the cooling experienced, and that skin cooling alone would dampen the cold-shock but not the metabolic response to cold-water immersion. Twenty-one male participants were divided into three groups, each of which completed two experimental immersions in 12 °C water, lasting until either rectal temperature fell to 35 °C or 90 min had elapsed. Between these two immersions, the control group avoided cold exposures, whilst two experimental groups completed five additional immersions (12 °C). One experimental group repeatedly immersed for 45 min in average, resulting in deep-body (1.18 °C) and skin temperature reductions. The immersions in the second experimental group were designed to result only in skin temperature reductions, and lasted only 5 min. Only the deep-body cooling group displayed a significantly blunted metabolic response during the second experimental immersion until rectal temperature decreased by 1.18 °C, but no habituation was observed when they were cooled further. The skin cooling group showed a significant habituation in the ventilatory response during the initial 5 min of the second experimental immersion, but no alteration in the metabolic response. It is concluded that repeated falls of skin and deep-body temperature can habituate the metabolic response, which shows tissue temperature specificity. However, skin temperature cooling only will lower the cold-shock response, but appears not to elicit an alteration in the metabolic response.     

Cardiovascular and humoral responses to sustained muscle metaboreflex activation in humans

Nishiyasu, Takeshi, Nobusuke Tan, Keiko Morimoto, RyokoSone, and Naotoshi Murakami. Cardiovascular and humoral responses to sustained muscle metaboreflex activation in humans.J. Appl. Physiol. 84(1): 116-122, 1998.The cardiovascular and humoral responses to sustained musclemetaboreflex activation were examined in eight male volunteers whilethey performed two 24-min exercise protocols. Each of these consistedof six 1-min bouts of isometric handgrip exercise (the left and righthands being used alternately) at 50% of maximal voluntary contraction;after each bout, there was either 3-min postexercise occlusion(occlusion protocol) or 3-min rest (control protocol). In the occlusionprotocol, mean arterial blood pressure was ~25 mmHg higher thanduring the control protocol, indicating that the muscle metaboreflexwas activated during occlusion. During the control protocol, plasmarenin activity, plasma vasopressin, and adrenocorticotropic hormonevalues were not significantly different from the values at rest. Duringthe occlusion protocol, however, plasma renin activity, plasmavasopressin, and adrenocorticotropic hormone were all significantlyincreased at 25 min. These data demonstrate that, in humans, thesustained activation of the muscle metaboreflex causes the secretion of several hormones originating from different regions.

     

Cardiovascular and cerebrovascular responses to acute isocapnic and poikilocapnic hypoxia in humans

We examined the cardiovascular and cerebrovascular responses to acute isocapnic (IH) and poikilocapnic hypoxia (PH) in 10 men (25.7 +/- 4.2 yr, mean +/- SD). Heart rate (HR), mean arterial pressure (MAP), and mean peak middle cerebral artery blood flow velocity (Vp) were measured continuously during two randomized protocols of 20 min of step IH and PH (45 Torr). HR was elevated during both IH (P < 0.01) and PH (P < 0.01), with no differences observed between conditions. MAP was modestly elevated across all time points during IH but only became elevated after 5 min during PH. During IH, Vp was elevated from baseline throughout the exposure with a consistent hypoxic sensitivity of approximately 0.34 cm x s(-1).%desaturation(-1) (P < 0.05). The Vp response to PH was biphasic with an initial decrease from baseline occurring at 79 +/- 23 s, followed by a subsequent elevation, becoming equivalent to the IH response by 10 min. The nadir of the PH response exhibited a hypoxic sensitivity of -0.24 cm x s(-1) x % desaturation(-1). When expressed in relation to end-tidal Pco2, a sensitivity of -1.08 cm x s(-1).Torr(-1) was calculated, similar to previously reported sensitivities to euoxic hypocapnia. Cerebrovascular resistance (CVR) was not changed during IH. During PH, an initial increase in CVR was observed. However, CVR returned to baseline by 20 min of PH. These data show the cerebrovascular response to PH consists of an early hypocapnia-mediated response, followed by a secondary increase, mediated predominantly by hypoxia.     

Cardiovascular responses to nonrespiratory and respiratory arousals in a porcine model

Spontaneous and provoked nonrespiratoryarousals can be accompanied by a patterned hemodynamic response. Toinvestigate whether a patterned response is also elicited byrespiratory arousals, we compared nonrespiratory arousals (NRA) torespiratory arousals (RA) induced by airway occlusion during non-rapideye movement sleep. We monitored mean arterial blood pressure (MAP),heart rate, iliac and renal blood flow, and sleep stage in 7 pigsduring natural sleep. Iliac and renal vascular resistance werecalculated. Airway occlusions were obtained by manually inflating achronically implanted tracheal balloon during sleep. The balloon wasquickly deflated as soon as electroencephalogram arousal occurred. As previously reported, NRA generally elicited iliac vasodilation, renalvasoconstriction, little change in MAP, and tachycardia. In contrast,RA generally elicited iliac and renal vasoconstriction, an increase inMAP and tachycardia. The frequent occurrence of iliac vasoconstrictionand arterial pressure elevation following RA but not NRA suggests thatsleep state change alone does not account for the hemodynamic responseto airway occlusion during sleep.

     

Cardiovascular responses to static and dynamic contraction during comparable workloads in humans

Previous studies suggest that the blood pressure response to static contraction is greater than that caused by dynamic exercise. In anesthetized cats, however, pressor responses to electrically induced static and dynamic contraction of the same muscle group are similar during equivalent workloads and peak tension development [i.e., similar tension-time index (TTI)]. To determine if the same relationship exists in humans, where contraction is voluntary and central command is present, dynamic (180 s; 1/s) and static (90 s) contractions at 30% of maximal voluntary contraction (MVC) were performed. Dynamic contraction also was repeated at the same TTI for 90 s at 60% MVC. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), MAP during postexercise arterial occlusion (an index of the metaboreceptor-induced activation of the exercise pressor reflex), and relative perceived exertion (RPE) (an index of central command) were assessed. No differences in these variables were found between static and dynamic contraction at a tension of 30% MVC. During dynamic contraction at 60% MVC, changes in MAP (16 +/- 3 vs. 19 +/- 4 mmHg) and absolute HR (92 +/- 6 vs. 69 +/- 5 beats/min), CO (7.9 +/- 0.4 vs. 6.3 +/- 0.3 l/min), RPE (16 +/- 1 vs. 13 +/- 1), and MAP during postexercise arterial occlusion (115 +/- 3 vs. 100 +/- 4 mmHg) were greater than during static contraction (P < 0.05). Thus increases in MAP and HR, activation of central command, and muscle metabolite-induced stimulation of the exercise pressor reflex during static and dynamic contraction in humans seem to be similar when peak tension and TTI are equal. Augmented responses to dynamic contraction at 60% MVC are likely related to greater activation of these two mechanisms.     

Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 +/- 1 mmHg, P < 0.05) and less during WI + NS (4 +/- 1 mmHg) and NS (3 +/- 1 mmHg). The decrease in heart rate (HR) by 13 +/- 1 beats/min (P < 0.05) and the increase in arterial pulse pressure (PP) by 17 +/- 4 mmHg (P < 0.05) during supine was more pronounced (P < 0.05) than during WI + NS (10 +/- 2 beats/min and 7 +/- 2 mmHg, respectively) and WI (8 +/- 2 beats/min and 6 +/- 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS (P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change.     

Effects of hyperoxia on thermoregulatory responses during feet immersion to hot water in humans

This study examined effects of hyperoxia on thermoregulatory responses. Eight healthy male students (23.5+/-1.8 yrs) were involved in this study. They immersed their legs in a hot water bath (42 degrees C) for 60 minutes in a climate chamber. The conditions of oxygen concentration of a chamber were set at 21% (control), 25% (25%O(2)), and 30% (30%O(2)). Ambient temperature and relative humidity was maintained at 25 degrees C and 50% in every condition, respectively. Measurements included rectal temperature (Tre), skin temperature at 7 sites, laser Doppler flowmeter (LDF) on the back and forearm as an index of skin blood flow, heart rate, local sweat rate (Msw) on the back and forearm, and total body weight loss (BWL). Increases of Tre at 25%O(2) and 30%O(2) tended to be lower during the immersion than in the control. Mean skin temperature (Tsk) of the control increased gradually after the onset of sweating, while the Tsks at 25%O(2) and 30%O(2) maintained a constant level during sweating. LDFs on the forearm at 25%O(2) and 30%O(2) showed lower increases compared with the control. No significant differences in Msw on the back and the forearm and BWL were seen among the conditions. These results suggested that hyperoxia could not affect sweating responses but elicit an inhibitory effect on thermoregulatory skin blood flow.     

Cardiovascular responses to metabolic and respiratory acidosis and anesthesia in larval Ambystoma tigrinum

Larval Ambystoma tigrinum were examined to determine their cardiovascular responses to three types of acidosis: metabolic acidosis via NH₄Cl gavage; respiratory acidosis via hypercapnia; and anesthetic-induced acidosis, via triacine methanesulphonate. In addition, another group of (metabolic acidosis) animals were tested to determine the role of -mediated catecholamine control on cardiovascular and acid-base regulation. The metabolic and respiratory acidoses produced typical amphibian responses. Anesthesia produced a significant mixed acidosis with respiratory and metabolic components. The cardiovascular responses to metabolic and respiratory acidosis were increased heart rate and pulse pressure. There were no significant changes in diastolic pressure, however, systolic pressure increased as a result of the increased pulse pressure. Animals subjected to metabolic acidosis via -blockade with propranolol did not display the increased heart rate and pulse pressure and the acidosis was deepened and prolonged. Anesthesia resulted in a cardiac slowing and increased pulse pressure, probably explained by the Frank-Starling relationship. There was no change in diastolic pressure. Anesthetized animals had depressed blood O₂ tension and elevated blood lactate.Abbreviations HR heart rate - RBC red blood cell(s) - TMS triacine methanesulphonate