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Journal of Physiology (2001), 533.3, pp. 871-880
© Copyright 2001 The Physiological Society
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ABSTRACT |
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INTRODUCTION |
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During exercise, heart rate (HR) and mean arterial pressure (MAP) simultaneously increase in relation to the intensity of exercise. This finding has resulted in many investigators concluding that baroreflex function is either attenuated or not operable during static and dynamic exercise (McRitchie et al. 1976; Mancia et al. 1978). However, investigations with both animals and human subjects have identified that the arterial baroreflex maintains its sensitivity during exercise (Melcher & Donald, 1981) with its stimulus-response curve reset upward on the response arm and rightward on the operating arm (to the prevailing blood pressure) during dynamic (DiCarlo & Bishop, 1992; Potts et al. 1993) and static (Ebert, 1986) exercise. It has been hypothesized that this resetting allows for a simultaneous increase in HR and MAP (Potts et al. 1993). Rowell & O'Leary (1990) have suggested that two neural mechanisms are primarily involved in the resetting of the carotid baroreflex during exercise. First, a feed-forward mechanism, identified as central command, acts through central processes to regulate the cardiovascular and somatomotor systems in parallel (Goodwin et al. 1972; Waldrop et al. 1996). Secondly, mechanically and chemically sensitive afferent signals arising from skeletal muscle regulate cardiovascular responses through negative feedback to the brainstem (Coote et al. 1971; McCloskey & Mitchell, 1972; Mitchell & Schmidt, 1983; Kaufman et al. 1983). Collectively, these afferent signals arising from skeletal muscle have been termed the exercise pressor reflex (Mitchell & Schmidt, 1983).
Iellamo et al. (1997) have confirmed that in human subjects central command and the exercise pressor reflex together were involved in the resetting of the arterial baroreflex during exercise. In addition, we have demonstrated in humans that an increase in central command input actively resets the carotid baroreflex, shifting the stimulus-response curve upward and rightward during dynamic and static exercise without altering reflex sensitivity (Gallagher et al. 2001). However, the exact role of afferents from muscle remains unclear. Papelier et al. (1997) reported in human subjects that activation of chemically sensitive receptors using post-exercise occlusion altered the sensitivity and reflex characteristics of the carotid baroreflex MAP (carotid- vasomotor) stimulus-response curve. However, the sensitivity of the HR (carotid-cardiac) stimulus- response curve was unaffected. McWilliam et al. (1991) in decerebrate cats demonstrated that afferent stimulation reduced the sensitivity of the baroreflex curve. Alternatively, Eiken et al. (1992) demonstrated that activation of the exercise pressor reflex with lower-body positive pressure relocated the carotid-cardiac stimulus- response curve and increased its sensitivity when modelled using a neck pressure/neck suction technique that assessed changes in R-R interval in response to changes in carotid sinus pressure. In contrast, lower-body positive pressure has also been reported to decrease the sensitivity of the carotid baroreflex (Shi et al. 1993). Finally, animal studies (Coote & Dodds, 1976; McMahon & McWilliam, 1992; Potts & Mitchell, 1998) have demonstrated that activation of skeletal muscle afferents during exercise resets the threshold of the carotid baroreflex to higher arterial pressures. These findings have yet to be demonstrated in humans. Therefore previous work suggests that the exercise pressor reflex is capable of resetting the carotid baroreflex threshold to higher arterial pressures (i.e. a rightward shift). However, it remains to be determined what role the exercise pressor reflex has in the resetting of the entire carotid baroreflex function curve during exercise (Potts & Mitchell, 1998). In addition, the effect of activation of the exercise pressor reflex on the sensitivity of the carotid baroreflex remains unclear. In the present investigation, we attempted to stimulate the exercise pressor reflex in active skeletal muscle during steady-state dynamic and static exercise with the application of medical anti-shock (MAS) trousers. The investigation was designed to determine the role of the exercise pressor reflex in the resetting of the carotid baroreflex during static and dynamic exercise in humans.
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METHODS |
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Subjects
Eight men and two women, with a mean age of 27.7 ± 1.1 years (± S.E.M.), height of 179.6 ± 2.0 cm, weight of 74.0 ± 1.5 kg and maximal oxygen uptake (
O2,max) of 3.52 ± 0.3 l min-1, volunteered to participate in this investigation. Each subject was informed of all aspects of the study and signed an informed consent approved by the Municipal Ethical Committee of Copenhagen, Denmark. All experiments were performed in accordance with the Declaration of Helsinki. All subjects were non-smokers and were not using prescribed or over-the-counter medications. The subjects were asymptomatic for cardiovascular and respiratory disease. The subjects were asked to abstain from alcoholic beverages and exercise for 24 h and caffeinated beverages for 12 h prior to any experimental or testing session.
Exercise
Each subject performed preliminary incremental work rate (30 W min-1) exercise on a cycle ergometer (modified Krogh) to volitional fatigue for the determination of O2,max. After the maximal exercise test, the subject was familiarized with the protocols for baroreflex testing and static exercise. On a separate day, the subjects performed static and dynamic exercise with and without the application of MAS trousers inflated to a pressure of 100 mmHg in order to activate the exercise pressor reflex via stimulation of the mechano- and metaboreflex (Williamson et al. 1994). For both protocols the subjects were seated in a semi-recumbent 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) and two-legged cycling. Preceding any exercise, the subjects attempted three static knee extensions to determine maximal voluntary contraction (MVC). Two bouts of control static knee extension at 20 % of MVC were performed for 3.5 min. In addition, the subjects performed 7 min of cycling at 20 % O2,max. The static and dynamic exercise bouts were repeated with the application of MAS trousers. All exercise bouts were randomized and separated by a minimum of 30 min. Each exercise bout was preceded by a 5 min collection period for resting baseline measurements.
Static knee extension was accomplished by placing a padded strap around the ankle of the subject's dominant leg. Force was recorded by a strain gauge dynamometer calibrated prior to each trial with accurate sensitivity (model 540 DNH, The Netherlands). In order for the subject to maintain the desired force, visual feedback of force produced was provided to the subject on a monitor. For dynamic exercise, the cycle ergometer was adjusted for each subject so that the knee angle at maximal leg extension was consistent for both tests. Subjects were requested to maintain a pedal cadence of 60 r.p.m. dictated by a metronome and they were instructed to keep their entire upper body relaxed.
Medical anti-shock trousers were applied to both lower extremities of the subject and inflated to 100 mmHg. The MAS trousers were designed without inflation bladders around the knees and ankles which allowed the subjects to exercise. The abdomen section of the MAS trousers was not applied to the subjects to eliminate abdominal and bladder reflexes. The subjects reported no discomfort with MAS trousers inflation.
Measurements
Heart rate was monitored by a standard lead II electrocardiogram. Mean arterial blood pressure (MAP) was directly measured with a Teflon catheter (20 gauge) placed in the brachial artery of the non-dominant arm. The MAP catheter was connected to a sterile disposable pressure transducer (Baxter, Uden, The Netherlands) interfaced with a pressure monitor (Danico Electronic-Dialogue 2000, Denmark). The zero reference pressure was set at heart level. During each experiment HR and arterial blood pressure (ABP; i.e. mean, systolic (SBP) and diastolic (DBP) blood pressures) were acquired using a beat-to-beat customized software data acquisition system interfaced with a personnel computer. In addition, ratings of perceived exertion (RPE) were obtained during the last 30 s of static exercise and at the 4th and 7th minute of dynamic exercise using the Borg scale (range 6-20) (Borg, 1982).
The subjects respired through a mouthpiece attached to a low-resistance turbine volume transducer (Pneumotach, MedGraphic) for measurements of breath volumes while gases were continuously sampled from the mouthpiece for analysis of fractional concentrations of O2, CO2 and N2 to determine oxygen uptake (mass spectrometer model 2001; Medical Graphics Corporation, St Paul, MN, USA). The system was calibrated before each test using known high-precision standard gases. Device input signals underwent analog-to-digital conversion for on-line breath-by-breath determination. Standardized calculations of metabolic data were corrected for ambient conditions.
Samples of arterial blood were obtained at rest and during the last 30 s of exercise for determination of plasma catecholamine concentration (nmol l-1) and lactate concentration (mmol l-1). Blood was placed in tubes kept on ice containing reduced glutathione and EGTA and centrifuged at 3000 g for 5 min at 3 °C. The plasma fraction was stored at -20 °C for blind analysis of noradrenaline and adrenaline. Samples were assayed by a single isotope radioenzymatic method (Knigge et al. 1990). Remaining syringe blood samples were immediately used for lactate determination (Lac TSI 2300; Yellow Springs Instrument Co., Inc., OH, USA).
Carotid baroreflex (CBR) control of HR and MAP was assessed using a rapid neck pressure/neck suction (NP/NS) technique (Potts et al. 1993). Pressure stimuli were applied through a cushioned malleable lead collar placed around the anterior 2/3 of the neck. The neck collar was modified from a design described by Sprenkle et al. (1986). Due to the brevity of the exercise protocols, a NP/NS technique with a rapid ramping of pressure was used. Twelve computer controlled pulsatile pressures ranging from +40 to -80 mmHg (40, 40, 40, 40, 20, 10, 0, -10, -20, -40, -60, -80) 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). Between each pressure pulse the neck chamber pressure was vented to atmospheric pressure. The generated level of neck collar pressure was measured by a pressure 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 pressure or suction to coincide with the arterial pressure wave at the carotid sinus. Each pulse of pressure or suction 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. Four subjects were unable to maintain the end-expiratory breath hold throughout the entire NP/NS pulse train during dynamic exercise. Therefore only six subjects were included in data describing responses to dynamic exercise. Three to four NP/NS pressure-response curves were obtained during dynamic exercise after the 4th minute of exercise. During static exercise, two CBR NP/NS pressure-response curves were obtained after the second minute of exercise. A minimum of 45 s of recovery was allotted between rapid pulse trains of NP/NS. Rapid pulse trains of NP/NS were also obtained at rest before all exercise bouts.
Data and statistical analysis
The dependent variables HR and MAP were used to create either the carotid-cardiac (HR) or carotid-vasomotor (MAP) stimulus- response 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 described by Kent et al. (1972). This function incorporates the following equation:
HR or MAP = A1{1 + exp[A2(CSP - A3)]}-1 + A4.
Carotid sinus pressure was calculated by subtracting the chamber pressure from the pre-stimulus MAP. Parameter A1 was the range of response of the dependent variable (maximum-minimum), A2 was the gain coefficient, A3 was the CSP required to elicit equal pressor and depressor responses (centring point) and A4 was the minimum response of HR or MAP. Individual data were applied to this model by a non-linear least-squares regression that predicted a curve of 'best fit' for the data and minimized the sum of squares error.
Several characteristic parameters were derived from the resulting model, including the estimated threshold (CSPthr), saturation (CSPsat) and maximal gain (Gmax) of the carotid-cardiac and carotid- vasomotor reflexes. Baroreceptor CSPthr and CSPsat were described as the minimum and maximum CSPs, respectively, that elicited a reflex change in HR or MAP. For calculation of CSPthr and CSPsat, we applied equations described by Chen & Chang (1991): CSPthr = -2.0/A2 + A3 and CSPsat = 2.0/A2 + A3. These calculations of CSPthr and CSPsat have been found to be the CSP at which MAP or HR are within 5 % of their maximal or minimal responses. The gains of the carotid-cardiac and the carotid-vasomotor reflexes were derived from the first derivative of the Kent logistic function, with the maximal gain defined as the gain value located at the centring point (CP) of the reflex. In addition, the operating point (OP) was defined as the intersection of the pre-stimulus (PS) HR or MAP and CSP (i.e. resting MAP). In order to quantify repositioning of the OP to a different carotid sinus pressure on the reflex curve, which may occur during exercise (Potts et al. 1993), the OP is subtracted from the fixed CP (i.e. A3). Parameters for all subjects within an experimental condition were averaged to provide group mean responses.
A two-way analysis of variance (ANOVA) with repeated measures was employed to determine significant differences at rest and exercise between either static or dynamic exercise with or without MAS trousers. Student-Newman-Keuls post hoc pairwise comparisons were used to establish significant group mean differences. In addition, Student's paired t test was used for individual comparisons. Data are presented as mean values with standard errors (mean ± S.E.M.). Significance was set at P < 0.05. All analyses were conducted using SigmaStat (Jandell Corp.)
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RESULTS |
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Selected physiological responses
Ratings of perceived exertion (RPE) during static exercise were not affected by the application of MAS trousers. However, RPE was elevated from control during dynamic exercise with MAS trouser inflation (P < 0.05) (Table 1). The subjects did not report any discomfort or increased difficulty performing the dynamic exercise with MAS trousers. Heart rate increased with static exercise but was unaffected by the application of MAS trousers at rest and during exercise when compared to control. However, MAP was significantly increased above control by the inflation of MAS trousers during steady-state dynamic exercise and static exercise (Fig. 1 and Fig. 2). HR and MAP reached steady state at the second minute of static exercise and at the fourth minute of dynamic exercise during control and MAS conditions. Oxygen uptake was increased from rest during dynamic and static exercise under control and MAS conditions (P < 0.05). However, oxygen uptake at the same absolute work rates was unaltered by the MAS condition when compared to control (Table 1).
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Figure 1. HR and MAP responses during 3 min of static exercise Heart rate and mean arterial pressure responses at rest and during 3 min one-legged static exercise (20 % maximal voluntary contraction) with ( | ||
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Figure 2. HR and MAP responses during 7 min of dynamic cycling exercise Heart rate and mean arterial pressure responses at rest and during 7 min of dynamic cycling exercise (20 % maximum oxygen uptake) with ( | ||
Plasma noradrenaline concentrations demonstrated significant increases from rest during dynamic and static exercise under control and MAS conditions (Table 1). Furthermore, the MAS condition elevated noradrenaline above the control condition during dynamic exercise (P < 0.05). This increase was not seen during static exercise. Plasma adrenaline and lactate concentrations were unaffected by the MAS condition when compared to control (Table 1).
Logistic parameters of carotid baroreflex
The four logistic parameters describing CBR control of HR (carotid-cardiac) and MAP (carotid-vasomotor) during static and dynamic exercise are presented in Table 2. The range of HR and MAP responses (A1) and gain coefficient (A2) were unaltered during exercise under control and MAS conditions. The centring point of the reflex (A3) demonstrated a progressive increase from rest during control exercise and was increased from control during exercise under the MAS condition (P < 0.05). The A1, A2 and A3 responses were the same for static and dynamic exercise. The minimal HR response (A4) was increased during control static and dynamic exercise and was unaffected by exercise under the MAS condition (P < 0.05). The minimal MAP response (A4) was increased from rest by control static exercise. In addition, the MAS condition significantly increased the minimal MAP response (A4) from control during static and dynamic exercise.
Carotid-cardiac (CSP-HR) stimulus-response curves during static exercise
The stimulus-response relationships for carotid-cardiac (CSP-HR) and carotid-vasomotor (CSP-MAP) reflexes at rest and during static exercise with or without the application of MAS trousers are shown in Fig. 3. The calculated variables describing the CSP-HR and CSP-MAP stimulus-response curves are shown in Tables 3 and 4. The maximal gain (i.e. sensitivity) of the CSP-HR stimulus-response curve was unaltered by static exercise under control and MAS conditions. Threshold carotid sinus pressure (CSPthr) and saturation carotid sinus pressure (CSPsat) for the CSP-HR stimulus-response curve demonstrated an increase from rest during control exercise. Further, CSPsat was significantly elevated from control exercise during static exercise under the MAS conditon. The pre-stimulus (PS) and centring point (CP) CSP-HR responses were significantly increased from rest by static exercise but no difference existed between control and MAS conditions. However, the relationship between OP (pre-stimulus CSP) and CP for the CSP-HR stimulus-response curve was unaffected by static exercise with or without MAS trousers (Table 4). The resetting of the CSP-HR stimulus-response curve evident during control exercise was further relocated rightward to a higher operating pressure by activation of the exercise pressor reflex during the MAS condition (Fig. 3).
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Figure 3. Reflex responses in HR and MAP during static exercise Reflex responses in HR (carotid-cardiac) and MAP (carotid-vasomotor) after perturbations to carotid sinus baroreceptors at rest ( | ||
Carotid-vasomotor (CSP-MAP) stimulus-response curves during static exercise
The maximal gain of the CSP-MAP stimulus-response curve was unaltered by static exercise under control and MAS conditions. Threshold (CSPthr) and saturation (CSPsat) carotid sinus pressure for the CSP-MAP stimulus- response curve demonstrated an increase from rest during control exercise and was significantly elevated from control rest during static exercise under the MAS condition. The PS and CP of the CSP-MAP response was significantly increased from rest by static exercise and augmented further from control exercise by the MAS condition. However, the relationship between OP and CP for the CSP-MAP stimulus-response curve was unaffected by static exercise with or without MAS trousers (Table 4). Differences between the PS and CP of the CSP-MAP response produced during exercise under control and MAS conditions were obtained using an a priori paired t test. The CSP-MAP stimulus-response curve was reset upward on the response arm and rightward to a higher operating pressure which was further augmented upward and rightward by the MAS condition (activation of the exercise pressor reflex) (Fig. 3).
Carotid-cardiac (CSP-HR) stimulus-response curves during dynamic exercise
The stimulus-response relationships for CSP-HR and CSP-MAP at rest and during dynamic exercise with or without the application of MAS trousers are shown in Fig. 4. The calculated variables describing stimulus- response curves are shown in Tables 3 and 4. The maximal gain of the CSP-HR stimulus-response curve was unaltered from resting conditions by dynamic exercise during control and MAS conditions. Threshold (CSPthr) and saturation (CSPsat) carotid sinus pressures for the CSP-HR stimulus- response curve demonstrated an increase from rest during exercise. In addition, CSPthr and CSPsat for the CSP-HR stimulus- response curve were significantly increased from control exercise by MAS trouser application. The PS and CP of the CSP-HR responses were significantly increased from rest by dynamic exercise but were unaltered from control exercise under the MAS condition. The OP was shifted away from the CP for the CSP-HR stimulus- response curve at rest during dynamic exercise but was unaffected by exercise with MAS trousers (Table 4). The upward and rightward resetting of the CSP-HR stimulus- response curve during control exercise was further relocated rightward to higher operating pressures by exercise pressor reflex activation during the MAS condition (Fig. 4).
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Figure 4. Reflex responses in HR and MAP during dynamic exercise Reflex responses in HR (carotid-cardiac) and MAP (carotid-vasomotor) after perturbations to carotid sinus baroreceptors at rest ( | ||
Carotid-vasomotor (CSP-MAP) stimulus-response curves during dynamic exercise
The maximal gain of the CSP-MAP stimulus-response curve was unaltered from rest by dynamic exercise during control and MAS conditions. Threshold carotid sinus pressure and CSPsat for the CSP-MAP stimulus- response curve were significantly increased from control exercise by the application of MAS trousers. The PS and CP for CSP-MAP responses were not altered from rest by control dynamic exercise, but were significantly increased from rest and control exercise during the MAS condition. The relationship between OP and CP for the CSP-MAP stimulus-response curve was unaffected by exercise with or without MAS trousers (Table 4). Collectively, this relocation upward on the response arm and rightward to higher operating pressures of the CSP-MAP stimulus- response curve suggests resetting of the CBR during control dynamic exercise which was further augmented by the MAS condition (activation of the exercise pressor reflex) (Fig. 4).
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DISCUSSION |
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The major new finding from this study was that activation of skeletal muscle receptors (exercise pressor reflex) by medical anti-shock trousers during both static and dynamic exercise reset the carotid-vasomotor stimulus-response curve upward on the response arm and rightward to a higher operating pressure. Further, the carotid-cardiac stimulus-response curve was also relocated, albeit exhibiting a rightward shift only. Sensitivity of the carotid-vasomotor and carotid-cardiac stimulus-response curves was unaltered by exercise pressor reflex activation. In addition, stimulation of skeletal muscle somatosensory afferents with MAS trousers during exercise failed to relocate the OP of the carotid- vasomotor and carotid-cardiac stimulus- response curves away from the CP. The hypothesis originally advanced by Rowell & O'Leary (1990) suggested that the exercise pressor reflex relocates the CBR stimulus-response curve upward on the response arm. However, these data suggest that the exercise pressor reflex is capable of actively resetting the carotid-vasomotor stimulus-response curve in both the upward and rightward directions during dynamic and static exercise, while appearing only to modulate the carotid-cardiac stimulus-response curve rightward to a higher operating pressure.
Melcher & Donald (1981) determined that the carotid baroreflex maintained its ability to regulate arterial pressure during exercise. Subsequently, DiCarlo & Bishop (1992) demonstrated in rabbits that the arterial baroreflex was shifted to function at higher pressures at the initiation of exercise. Augmented renal sympathetic and HR responses occurred during exercise when the normal pressure response was reduced by nitroglycerine. Potts et al. (1993) artificially stimulated the carotid baroreceptors using NP/NS during rest and dynamic exercise in humans. They reported that the stimulus- response relastionship describing the carotid baroreflex was reset upward on the response arm and rightward to higher operating pressures (classical resetting); these alterations were in direct relation to the intensity of exercise and exhibited no alterations in gain (i.e. sensitivity). In addition, they determined that the pre-stimulus HR or MAP (i.e. operating point) of the response curve was relocated away from the centring point and closer to threshold. They suggested that relocation of the operating point permits the carotid baroreflex to respond to a wider range of carotid sinus hypertension (Potts et al. 1993). This resetting of the carotid baroreflex has been confirmed to occur not only during dynamic exercise but also during static exercise (Ebert, 1986), being directly related to the intensity of exercise up to maximum levels (Papelier et al. 1994; Norton et al. 1999).
Rowell & O'Leary (1990) have hypothesized that two neural inputs, central command and the exercise pressor reflex, are involved in the resetting of the carotid baroreflex during exercise. Central command is a 'feed-forward' controller involved in the regulation of somatomotor and cardiovascular responses (Waldrop et al. 1996). From its putative location in the hypothalamic locomotor region, it provides regulatory synaptic input to medullary neurons that comprise the central baroreceptor pathways (Waldrop et al. 1996). We increased the influence of central command on the circulation during dynamic and static exercise using partial neuromuscular blockade (Gallagher et al. 2001) and found that elevated central command further resets the carotid-vasomotor and carotid-cardiac stimulus-response curves upward and rightward from control exercise without alterations in gain. In addition, neuromuscular blockade augmented the relocation of the operating point away from the centring point and closer to the threshold. Therefore central command actively regulates the resetting of the carotid baroreflex during exercise.
We applied MAS trousers inflated to 100 mmHg to the lower limbs to activate muscle mechanoreceptors and chemoreceptors during static and dynamic exercise. Williamson et al. (1994) demonstrated augmented blood pressure responses with the application of MAS trousers. They eliminated this response by blocking afferent feedback from the compressed muscle by epidural blockade. Similarly, we found an augmented MAP response during exercise with the application of MAS trousers, with no effect on HR. We did demonstrate an increase in plasma noradrenaline levels and perceived exertion response during dynamic exercise with inflated MAS trousers. The subjects did not report any discomfort with the MAS trousers. However, because the inflated bladders in the trousers were located at the inner thigh, the subjects were required to displace their legs laterally in order to perform dynamic cycling. This could explain why perceived exertion was elevated only during dynamic exercise with MAS trousers. The increase in perceived exertion does imply central command activation during dynamic cycling with MAS trousers, which might confound interpretation of the results. However, since HR was not affected by MAS trousers and the overall results were similar between static and dynamic exercise, we suggest that any increase in central command during dynamic exercise was minimal.
The data of the present investigation coincide with a recent report from Raymond et al. (2000). They artificially induced dynamic leg cycling (eliminating central command) in able-bodied subjects and in paraplegics (no afferent feedback from the skeletal muscle receptors). When central command was eliminated during non-voluntary exercise in able-bodied subjects, they found an upward and rightward resetting of the carotid-vasomotor and carotid-cardiac stimulus-response curves, while in paraplegics during electrically stimulated cycling (no central command or exercise pressor feedback) the carotid-vasomotor stimulus-response curve was not reset and the carotid-cardiac curve was only reset upward. In the paraplegics, the upward resetting of the carotid-cardiac stimulus-response curve must have been the result of a mechanism other than central command or the exercise pressor reflex because both mechanisms were effectively eliminated.
Afferent fibres from baroreceptors and skeletal muscle receptors synapse in the nucleus tractus solitarii (NTS) (Kalia et al. 1981; Nyberg & Blomqvist, 1984; McMahon et al. 1992; Waldrop et al. 1996; Potts et al. 1998). In addition, the central baroreceptor pathway consists of excitatory projections from the NTS to the caudal ventrolateral medulla (cVLM) (Waldrop et al. 1996). McMahon et al. (1992) reported that somatosensory input from peroneal nerve stimulation resulted in inhibition of barosensitive neurons in the NTS. Potts & Mitchell (1998) suggested that activation of skeletal muscle afferents would inhibit the barosensitive neurons in the NTS and would require a greater input stimulus to activate the baroreflex. This would result in a reflex that operates at a higher pressure range without a change in sensitivity. Additionally, central cortical (central command) neural inputs also synapse with the above-described baroreceptor neural pathways (Waldrop et al. 1996). Thus, both central command and the exercise pressure reflex are involved in regulation of the carotid baroreflex during exercise. However, since central command is a feedforward mechanism and resets the carotid baroreflex (Gallagher et al. 2001), central command would act more as the primary regulator of carotid baroreflex resetting. Furthermore, the results in the present investigation lend credence more to the exercise pressor reflex being a negative feedback modulator of carotid baroreflex resetting, using sympathetic neural activation as previously hypothesized by Rowell & O'Leary (1990).
We confirmed that the stimulus-response relationship of the carotid baroreflex was reset during dynamic and static exercise to the prevailing systemic pressure. We also demonstrated that activation of the exercise pressor reflex further resets the carotid-vasomotor baroreflex curve upward on the response arm and rightward to higher operating pressures (classical resetting) in the same manner during dynamic and static exercise without alterations in gain. However, exercise pressor reflex activation resets the carotid-cardiac baroreflex curve rightward only to higher operating pressures. In addition, the exercise pressor reflex does not appear to have an active role in relocating the pre-stimulus HR and MAP, i.e. the operating point, away from the centring point and closer to the threshold during exercise. We conclude that the exercise pressor reflex is capable of resetting the carotid-vasomotor response and modulating the carotid-cardiac response during exercise. However, due to the negative feedback nature of the exercise pressor reflex, it seems reasonable to conclude that the exercise pressor acts more as a modulator of carotid baroreflex resetting in response to the demands of the skeletal muscle.
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Acknowledgements
The authors would like to thank Kasper Horn for his technical support and Lisa Marquez for secretarial support during the preparation of the manuscript. This study was supported in part by the Danish National Research Foundation Grant (504-14) from the Copenhagen Muscle Research Center, Copenhagen, Denmark, by the National Aeronautics and Space Administration Grant (NAG5-4668) and by the National Institutes of Health of the United States of America under NIH Grant (45547). This paper was submitted by K. M. Gallagher to the University of North Texas Health Science Center at Fort Worth in partial fulfillment of the requirements for the degree of Doctor of Philosophy.
Corresponding author
P. B. Raven: Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699, USA.
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) and without (
) application of medical anti-shock trousers (MAS). Values are means ± S.E.M. * Significant difference between control and MAS (P < 0.05).
) and during static exercise after application of medical anti-shock trousers (MAS) (
). Data points represent means ± S.E.M. Arrows indicate operating points. Lines represent mean fits of data from individual subjects. MAS trouser rest curves were not significantly different from control rest curves and have been omitted for clarity.