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Themed Issue Papers |
Departments of 1 Internal Medicine2 Health Care Sciences3 Physical Therapy, University of Texas Southwestern Medical Center, Dallas, TX, USA4 Department of Anaesthesia, Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark 5 Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX, USA
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(Received 2 September 2005;
accepted after revision 27 October 2005; first published online 1 November 2005)
Corresponding author K. M. Gallagher: Department of Internal Medicine, Division of Cardiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9034, USA. Email: kevin.gallagher{at}utsouthwestern.edu
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Introduction |
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In humans, Iellamo et al. (1997) have presented evidence to suggest that central command and the exercise pressor reflex together are involved in the resetting of the baroreflex during exercise. More recently, using stimulus–response relationships to quantify baroreflex function, our laboratory demonstrated that increasing central command activity resets the carotid–cardiac (i.e. heart rate) and carotid–vasomotor (i.e. blood pressure) stimulus–response curves upward-vertically on the response arm and rightward-laterally to higher arterial pressures during dynamic and static exercise without altering the maximal gain of the reflex (Gallagher et al. 2001a; Querry et al. 2001; Ogoh et al. 2002). Complementing these findings, reductions in central command activity attenuate CBR resetting (Ogoh et al. 2002). Additionally, we have demonstrated that activation of the exercise pressor reflex resets the carotid–vasomotor baroreflex in a manner similar to that of central command (i.e. an upward-vertical and rightward-lateral relocation of the stimulus–response curve) during dynamic and static exercise without altering the maximal gain of the reflex (Gallagher et al. 2001b). In contrast, the exercise pressor reflex only resets the carotid–cardiac stimulus–response relationship rightward-laterally to operate at the higher arterial pressures established by exercise (Gallagher et al. 2001b). By inhibiting the afferent arm of the exercise pressor reflex with epidural anaesthesia during dynamic and static exercise, similar results have been demonstrated with respect to both the carotid–vasomotor and carotid–cardiac baroreflexes but in the opposite direction (Smith et al. 2003c). Therefore, both central command and the exercise pressor reflex are capable of independently resetting the CBR during exercise. However, no data exist in humans to demonstrate how these neural inputs interact to induce this resetting.
In this investigation, we sought to assess the interactive relationship between central command and the exercise pressor reflex in mediating baroreflex resetting during exercise. Our approach was to simultaneously augment the activity of both inputs during static exercise and to compare these responses to the enhancement of each input alone. We hypothesized that the combined potentiation of central command and exercise pressor reflex activity during exercise would reset baroreflex function to a greater extent than when either input was activated alone.
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Methods |
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Six men, with a mean age of 27 ± 2 years, height of 185 ± 3 cm and weight of 79 ± 1 kg, volunteered to participate in this investigation. Each subject was informed of all risks and aspects of the study and signed an informed consent approved by the Municipal Ethical Committee of Copenhagen, Denmark. Experiments were performed in accordance with the Declaration of Helsinki. All subjects were non-smokers, were not taking medication and were asymptomatic for cardiovascular and respiratory disease. The subjects were asked to abstain from alcoholic beverages and exercise for 24 h and from caffeinated beverages for 12 h prior to any scheduled session. Additional subjects were recruited and participated in the study. However, owing to the technical and physical demands of the protocols implemented, several subjects were unable to complete all phases of the investigation successfully. As a result, only the six subjects who finished each experimental protocol were included in the data analyses.
Exercise protocols
Subjects performed static leg exercise at 20% maximal voluntary contraction (MVC) under four conditions: control, no perturbation; neuromuscular blockade (NMB) induced by administration of the neuromuscular blocking agent Norcuron (central command activation; Leonard et al. 1985; Gallagher et al. 2001a); MAST, application of medical antishock trousers inflated to 100 mmHg (exercise pressor reflex activation; Williamson et al. 1994; Gallagher et al. 2001b); and Combo, NMB plus MAST (concomitant central command and exercise pressor reflex activation). For all protocols, the subjects were seated in a semirecumbent position on a hospital bed which supported the upper body. The bed was modified to allow the subjects to perform one-legged static knee extension from a 90 deg knee angle. Preceding any exercise, the subjects attempted three static knee extensions to determine MVC. Control static knee extension at 20% of MVC was performed for 3.5 min, after which exercise was repeated at the same absolute (20% of control MVC) workloads after the administration of whole-body NMB or the application of medical antishock trousers, or both simultaneously. All exercise bouts were randomized and separated by a minimum of 30 min. Each exercise bout was preceded by a 5 min data collection period for resting baseline measurements.
Static knee extension was accomplished by placing a padded strap around the ankle of the dominant leg. Force was recorded by a strain gauge dynamometer (model 540 DNH, Holland). Visual feedback of force was provided by a monitor in order for the subject to maintain the desired force. Since NMB weakens eye muscles, however, verbal feedback was used to maintain force during the NMB condition. Subjects were instructed to keep their upper body relaxed during all testing.
Whole-body neuromuscular blockade (Norcuron, 1 mg ml–1, a newer analogue in the same class as curare) was administered through venous access in the back of the hand. Prior to NMB administration, static handgrip MVC was determined. A bolus dose of Norcuron was injected, followed by 10 ml of saline. Supplemental doses were administered until handgrip strength was reduced to approximately 50% of control values. After the desired reduction in strength was achieved, the 5 min rest collection period was initiated, followed by the exercise bout. The injections were repeated as required in order to maintain the targeted reduction in muscle strength. At all times an Ambu-E resuscitator apparatus, neostigmine and atropine were available if necessary to obviate any complications caused by curare administration.
Medical antishock trousers were applied to both lower extremities of the subject and inflated to 100 mmHg. The medical antishock trousers were designed without inflation bladders around the knees and ankles, which allowed the subjects to exercise. The abdomen section of the medical antishock trousers was not applied to the subjects to eliminate abdominal and bladder reflexes. Subjects did not report any discomfort associated with the MAST trousers during exercise.
Measurements
During each test, heart rate (HR) was monitored by a standard lead II electrocardiogram. Arterial blood pressure (ABP) was monitored by a Teflon catheter (20 gauge) placed in the brachial artery of the non-dominant arm. The ABP catheter was connected to a sterile disposable pressure transducer (Baxter, Uden, Holland) interfaced with a pressure monitor (Dialogue 2000, Danico Electronic, Denmark). The zero reference pressure was set at heart level. During each experiment, HR and ABP (i.e. mean (MAP), systolic (SBP) and diastolic blood pressures (DBP)) were acquired using a beat-to-beat customized software data acquisition system interfaced with a personnel computer. Additionally, measurements of ratings of perceived exertion (RPE) were determined during the last 10 s of each exercise bout (Borg, 1982).
Carotid baroreflex control of HR and MAP was assessed using a neck pressure/neck suction (NP/NS) technique in which variable pressure stimuli were applied through a cushioned malleable collar placed around the anterior two-thirds of the neck (Pawelczyk & Raven, 1989). Owing to the brevity of the exercise protocols, a rapid ramping of pressure was used (Eckberg et al. 1975). Computer-controlled pulsatile pressures ranging from +40 to –80 mmHg were generated by a variable pressure source and delivered to the neck collar through large-bore two-way solenoid valves (model 8215B, Asco, Florham Park, NJ, USA; Fadel et al. 2003). Between each pressure pulse, the neck chamber pressure was vented to atmospheric pressure. The generated level of neck collar pressure was measured by a transducer (model DP45, Validyne Engineering, Northridge, CA, USA). The computer software gated the pulses of pressure to occur 50 ms after initiation of the R-wave detected by ECG. The 50 ms delay allowed the artificial NP/NS to coincide with the arterial pressure wave at the carotid sinus. Each pulse was 500 ms in duration. The NP/NS pulse train was conducted at end-expiratory breath hold to eliminate the confounding effects of respiratory sinus arrhythmia. The total duration of breath hold varied between 10 and 12 s. During static exercise, two CBR trains were obtained after the second minute of exercise. A minimum of 45 s of recovery time were allotted between rapid pulse trains of NP/NS. Rapid pulse trains of NP/NS were also performed at rest before all exercise bouts.
Data and statistical analysis
The dependent variables HR or MAP were used to create either the carotid–cardiac (HR) or carotid–vasomotor (MAP) function curves when plotted against the independent variable of estimated carotid sinus pressure (CSP). These curves were individually fitted for each subject to a four parameter logistic function (Kent et al. 1972). This function incorporates the following equation:
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Several characteristic parameters are derived from the resulting model, including the estimated threshold, saturation and maximal gain of the carotid–cardiac and carotid–vasomotor reflexes. Baroreceptor threshold and saturation were described as the minimum and maximum CSP, respectively, that elicit a reflex change in HR or MAP. The calculation of threshold and saturation utilized the following equations: Threshold = –2.0/A2 + A3 and Saturation = –2.0/A2 + A3. These calculations have been found to be the CSP at which MAP or HR was within 5% of its maximal or minimal response (Chen & Chang, 1991). The gain of the carotid–cardiac and carotid–vasomotor reflexes was derived from the first derivative of the Kent logistic function, and the maximal gain was defined as the gain value located at the centring point of the reflex stimulus–response curve. In addition, the operating point was defined as the prestimulus MAP. Parameters for all subjects within an experimental condition were averaged to provide group mean responses.
Analysis of variance (ANOVA) with repeated measures was employed to determine significant differences. Student–Newman–Keuls post hoc pairwise comparisons were used to establish significant group mean differences. Data are presented as means ± S.E.M. The alpha level was set at P < 0.05. All analyses were conducted using Sigma Stat (Jandell Corp.)
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Results |
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Baseline HR and MAP were not altered by NMB, MAST or Combo conditions. From control baseline, static exercise evoked significant increases in HR (from 56 ± 2 to 68 ± 1 beats min–1) and MAP (from 86 ± 2 to 100 ± 3 mmHg). As expected, compared to control exercise, the increase in heart rate was similar during MAST (to 67 ± 4 beats min–1) and further enhanced by NMB (to 73 ± 3 beats min–1). However, the greatest elevation in HR occurred during the Combo condition (to 78 ± 3 beats min–1). Similarly, the largest increase in MAP during exercise occurred with the Combo condition (to 125 ± 5 mmHg). However, both NMB and MAST also elevated MAP (to 113 ± 4 and to 112 ± 3 mmHg, respectively) in comparison to control exercise. The RPE was 12.9 ± 0.6 during control static exercise and was not affected by MAST (12.9 ± 0.3). However, NMB and Combo significantly increased RPE (14.7 ± 0.7 and 15.0 ± 0.5, respectively) compared to control exercise. There was no significant difference between RPE during NMB and Combo.
Carotid–cardiac stimulus–response curves
The logistic parameters and calculated variables describing CBR control of HR are presented in Table 1. The stimulus–response curves for the carotid–cardiac reflex at rest and during static exercise under control, NMB, MAST and Combo conditions are shown in Fig. 1. Static exercise resulted in a significant resetting of the CBR from rest under all conditions. Compared to control exercise, the resetting of the carotid–cardiac stimulus–response curve was largely unaffected by MAST. In contrast, both NMB and Combo conditions resulted in a further resetting of the CBR–HR curve in comparison to control exercise. Moreover, the extent of CBR resetting was greater during the Combo condition than during either the NMB or MAST conditions.
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The logistic parameters and calculated variables describing CBR control of MAP are presented in Table 2. The stimulus–response curves for the carotid–vasomotor reflex at rest and during static exercise under control, NMB, MAST and Combo conditions are shown in Fig. 2. Static exercise resulted in a significant resetting of the CBR from rest under all conditions. The resetting of the carotid–vasomotor stimulus–response curve was equally augmented during NMB and MAST conditions compared to control exercise. Furthermore, this potentiated resetting of the CBR–MAP curve was greater with the Combo condition than during either the NMB or MAST conditions.
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Discussion |
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A role for central command and the exercise pressor reflex in baroreflex resetting during exercise
Several studies in animals have established a functional and neuroanatomical basis for the interaction between central command and the exercise pressor reflex in adjusting baroreflex function during exercise. Functionally, potentiation of central command activity by electrically stimulating the mesencephalic locomotor region of paralysed cats displaces the linear relationship between carotid sinus pressure and HR or blood pressure in an upward direction (McIlveen et al. 2001). In both anaesthetized and decerebrate cats, electrically induced static muscle contraction and passive muscle stretch (manoeuvres which preferentially activate the exercise pressor reflex) induce a rapid resetting of the baroreflex (Coote & Dodds, 1976; Potts & Mitchell, 1998; McIlveen et al. 2001). Anatomically, afferent neurones from skeletal muscle and the carotid sinus that constitute the sensory components of the exercise pressor reflex and carotid baroreflex, respectively, have been shown to project to similar nuclei (e.g. nucleus tractus solitarius) within the cardiovascular centres of the brainstem (Kalia et al. 1981; Dean & Seagard, 1995; Li et al. 1998; Potts et al. 2002). In addition, input from cortical and subcortical regions of the brain associated with central command have been shown to synapse in these same brainstem nuclei (Waldrop et al. 1996). Collectively, this functional and anatomical evidence provides a basis for the interaction of the exercise pressor reflex, central command and the arterial baroreflex in animals.
Establishing similar evidence in humans has been an area of intense investigation. As stated, it was originally hypothesized that both central command and the exercise pressor reflex contributed significantly to baroreflex resetting during exercise (Rowell & O'Leary, 1990). Raven and colleagues have recently completed a series of studies to test this hypothesis in humans, culminating with the present investigation. The results of these experiments have established that central command (Norton et al. 1999b; Gallagher et al. 2001a; Querry et al. 2001; Ogoh et al. 2002) and the exercise pressor reflex (Gallagher et al. 2001b; Smith et al. 2003c) maintain the ability to reset baroreflex function independently during static and dynamic exercise. However, these studies did not attempt to address how these inputs interact to achieve this resetting, which was the purpose of this investigation.
Carotid baroreflex control of heart rate during exercise
In this study, enhancing central command input during exercise elicited a rightward lateral relocation of the carotid–cardiac stimulus–response curve such that the reflex operated around higher arterial pressures. In contrast, potentiated activation of the exercise pressor reflex had no appreciable effect on the baroreflex control of HR during static leg exercise. Concurrent enhancement of both central command and exercise pressor reflex activity induced a bi-directional relocation of the carotid–cardiac stimulus–response curve (i.e. a rightward lateral shift to operate at higher arterial pressures and an upward vertical shift on the response arm of the curve). This finding suggests that the interaction between these two inputs serves to accentuate the magnitude to which the carotid baroreflex control of HR is reset during exercise. However, given that potentiated activation of central command alone had a greater effect on the baroreflex than isolated enhancement of exercise pressor reflex activity, it is concluded that central command is the primary regulator of carotid–cardiac baroreflex resetting during exercise, with the exercise pressor reflex subserving a modulatory role in this process.
Carotid baroreflex control of blood pressure during exercise
In agreement with previous reports (Gallagher et al. 2001a; Querry et al. 2001; Ogoh et al. 2002), inducing central command overactivity during exercise evoked not only a rightward lateral relocation of the carotid–vasomotor stimulus–response curve to higher arterial pressures but shifted the curve in an upward vertical direction on the response arm. Enhanced activation of the exercise pressor reflex induced a resetting of the carotid–vasomotor stimulus–response curve in the same direction and to the same magnitude as that elicited by central command overactivity. More importantly, the combined supra-stimulation of these inputs further shifted the curve rightward-laterally and upward-vertically to a greater extent than when either input was activated alone. This finding suggests that a facilitatory interaction exists between central command and the exercise pressor reflex that functionally resets the carotid baroreflex control of blood pressure during static exercise. Given that the magnitude of baroreflex resetting was essentially the same when enhanced input from either central command or the exercise pressor reflex was isolated, it is concluded that both inputs contribute significantly to the resetting of the carotid–vasomotor baroreflex during exercise.
Although our primary findings suggest that central command and the exercise pressor reflex interact such that signals from one input facilitate signals from the other, resulting in an accentuated resetting of the baroreflex during exercise, differences between the CBR–HR and CBR–MAP curve should be considered. A facilitatory interaction between central command and the exercise pressor reflex seems more obvious in the resetting of the CBR–HR curve, in that the resetting during Combo was clearly greater than the effect of NMB alone plus the effect of MAST alone, since the latter had no major effect. However, in the resetting of the CBR–MAP curve, a facilitatory interaction cannot be proved merely by the enhanced resetting of CBR in the Combo condition because both the NMB and MAST conditions caused significant resetting of the CBR–MAP curve from the control exercise condition. In this case, the resetting of the CBR–MAP curve in the Combo condition may be caused by the summation of resetting in NMB alone and MAST alone, and therefore the interaction between central command and the exercise pressor reflex may have characteristics of a linear summation rather than facilitation. Clearly, the interaction of these two neural inputs in the central nervous system is quite complex. As such, since we were unable to quantify resetting in absolute terms, care should be taken in the interpretation of these data. Nevertheless, our findings are the first to demonstrate a true interaction between central command and the exercise pressor reflex in baroreflex resetting during exercise in humans.
Clinical perspectives
The cardiorespiratory response to exercise is altered in a number of pathological conditions. For example, exaggerated increases in sympathetic nerve activity, blood pressure, HR, vascular resistance and ventilation during exercise have been reported in patients and animals with heart failure and hypertension (Pickering, 1987; Kazatani et al. 1995; Piepoli et al. 1996; Legramante et al. 1999; Hammond et al. 2000; Middlekauff et al. 2000). The abnormal cardiorespiratory response that accompanies exercise, in combination with other disease-induced physiological disorders, may reduce exercise capacity and increase the risk for cardiac arrhythmia, acute myocardial infarction and stroke during physical activity (Mittleman et al. 1993; Ponikowski et al. 2001; Kokkinos et al. 2002). Clearly, the arterial baroreflex, central command and the exercise pressor reflex are the primary regulators of the cardiovascular response to exercise (Strange et al. 1993; Winchester et al. 2000; Fadel et al. 2004). As such, it is likely that the abnormal circulatory responses to physical activity characteristic of diseases such as heart failure and hypertension are mediated by changes in the individual functions or interactive relationships of these inputs. In support of this contention, reductions in baroreflex sensitivity are commonly denoted with the advent of ventricular dysfunction or hypertension and in some cases can be used as a predictor of cardiac mortality or incidence of cardiac arrhythmia (La Rovere et al. 2001; Minami et al. 2003; Kim et al. 2004). Likewise, increasing evidence suggests that exercise pressor reflex dysfunction develops in both heart failure and hypertension that maintains the potential to drive the exaggerated cardiovascular responses to exercise associated with each disease (Middlekauff et al. 2001; Smith et al. 2003a, b, 2005; Li et al. 2004). Given the consequences of such alterations in reflex regulation, identification of the neural mechanisms of autonomic dysfunction is paramount. Additionally, dissection of the pathophysiology of exercise may lead to the development of novel therapeutic strategies targeted at improving circulatory haemodynamics during physical activity and thereby reducing the cardiovascular risks associated with exercise in disease.
Conclusion
In summary, the resetting of the carotid baroreflex control of HR and blood pressure during exercise is mediated by the combined interactions of central command and the exercise pressor reflex. Importantly, the interaction between these two inputs serves to accentuate the magnitude of this resetting. With respect to the baroreflex control of HR during exercise, the findings suggest that the magnitude of baroreflex resetting is primarily regulated by central command, with the exercise pressor reflex providing more of a modulatory role. In contrast, both central command and the exercise pressor reflex maintain the potential to reset the carotid–vasomotor baroreflex independently to the same magnitude during exercise. Regardless of the end-organ system controlled, signals from central command and the exercise pressor reflex are likely to be requisite for the normal ‘physiological’ resetting of the baroreflex during exercise, given the interactive relationship between these neural inputs.
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Acknowledgements |
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Author's present address
P. J. Fadel: University of Missouri School of Medicine, Department of Medical Pharmacology and Physiology, One Hospital Drive, M 516, Columbia, MO 65212, USA.
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