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1 Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA
2 Copenhagen Muscle Research Center, Rigshospitalet, DK-2200, Copenhagen N, Denmark
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(Received 7 April 2004;
accepted after revision 25 June 2004;
first published online 2 July 2004)
Corresponding author D. W. Wray: Department of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0623, USA. Email: dwray{at}ucsd.edu
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Introduction |
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It is well known that the CBR is by nature a dynamic system with intrinsic nonlinearity (Eckberg, 1980; Iellamo, 2001; Zhang et al. 2001). As such, recent evidence suggests that alternative models may be more appropriate to evaluate the dynamic nature of the CBR, using more prolonged, dynamic stimuli such as oscillatory neck suction (Bernardi et al. 1997; Keyl et al. 2000; Zhang et al. 2001). First utilized by Bath et al. (1981), oscillatory CBR loading with neck suction has since been applied in studies investigating the role of the CBR in modulation of cutaneous blood flow (Bernardi et al. 1997) and muscle sympathetic outflow (Bath et al. 1981; Furlan et al. 2003). These studies have demonstrated an apparent ‘entrainment’ of R–R interval (RRI), MSNA and ABP corresponding to the oscillating frequency of the neck chamber pressure, providing direct evidence of dynamic CBR control on these measured variables. However, this dynamic model has never been utilized to assess CBR control of the peripheral circulation at rest or during exercise.
The vasculature of active skeletal muscle is influenced by the opposing effects of neural sympathetic input and locally produced vasodilatory metabolites during exercise (Laughlin et al. 1996). Remensnyder et al. (1962) coined the term ‘functional sympatholysis’ to describe the observation that sympathetic vasoconstriction in active skeletal muscles may be attenuated by local control factors. Many studies in animals (Thomas et al. 1998; Buckwalter et al. 2001, 2004) and humans (Hansen et al. 1999; Dinenno & Joyner, 2003; Rosenmeier et al. 2003; Wray et al. 2004) have considered the influence of metabolic factors on sympathetic control of the skeletal muscle vasculature during exercise. However, the interaction of this sympatholytic event with reflex arterial blood pressure control mechanisms remains unclear.
The importance of local metabolic events on ABP regulation is underscored by the fact that as blood flow in the exercising muscle increases, changes in vascular conductance in the skeletal muscle vascular bed produce more pronounced systemic effects (Buckwalter & Clifford, 2001; Collins et al. 2001). Thus, effective reflex control of the exercising muscle vasculature is crucial to ensure that adequate tissue perfusion is achieved without sacrificing systemic arterial pressure. Numerous studies have shown that CBR control of RRI (Eckberg, 1977; Iellamo et al. 1994) and ABP (Bevegard & Shepherd, 1966; Potts et al. 1993; Ogoh et al. 2003) is preserved from rest to exercise in humans. More recently, continued CBR control of MSNA (Fadel et al. 2001) and leg vascular conductance (Keller et al. 2003) during exercise have also been demonstrated. Using the variable pressure neck chamber, these studies have established the cardiac, neural and haemodynamic responsiveness to a single, static pulse of neck pressure (NP, CBR unloading) and neck suction (CBR loading). However, the extent of CBR control at the level of the skeletal muscle microcirculation in the face of exercise-induced local metabolic influences has not been investigated.
In the present study we sought to determine: (1) the simultaneous control of cardiac, neural and haemodynamic end-organ activity by the CBR; and (2) the relationship between CBR-mediated reflex control and local metabolic control of the skeletal muscle vasculature during dynamic exercise. Oscillatory NP was applied to assess CBR control over haemodynamic function at rest and during moderate-intensity knee-extension exercise. We hypothesized that dynamic CBR-mediated sympathoexcitation would produce similar changes in RRI, ABP and MSNA at rest and during exercise, but that metabolites from the exercising muscle would attenuate CBR control of peripheral haemodynamic measurements of femoral blood velocity and skeletal muscle tissue oxygenation.
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Methods |
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Twelve young (18- to 35-year-old) volunteer subjects free from obvious cardiopulmonary and neuromuscular disease participated in the study. Written informed consent was obtained from all participants, and experiments were approved by the local Institutional Review Board at the University of North Texas Health Science Center and performed in accordance with the Declaration of Helsinki. All subjects were familiarized with the procedures before the experimental day, which included evaluation of CBR responsiveness to ensure that the variable pressure neck chamber technique could adequately alter carotid sinus transmural pressure (Querry et al. 2001). All studies were performed in a quiet, thermoneutral environment, with subjects in a semirecumbent position (approximately 30 deg reclined).
Continuous measurements of HR, ABP (finger photoplethysmography), femoral blood velocity (ultrasound Doppler) and tissue oxygenation (near-infrared spectroscopy) were collected concurrently. The peroneal nerve of the nonexercising leg was instrumented for continuous recordings of muscle sympathetic nerve activity (MSNA). MSNA recordings were attempted in all subjects during exercise. However, inevitable movement of the instrumented leg caused a shift in needle placement and loss of signal fidelity in some subjects, so MSNA measurements were obtained throughout the protocol in only six subjects. Following all instrumentation, 5 min data segments were collected before and during 5 s pulses of neck pressure (NP) at +40 mmHg applied in a oscillating sinusoidal manner (0.1 Hz, i.e. 5 s on, 5 s off for 5 min) using a traditional neck collar. After resting measurements, unilateral knee-extension exercise was performed at 30 kicks per minute (7 W) with a modified cycle ergometer, as previously described (Andersen et al. 1985; Keller et al. 2003). After 5 min of exercise to achieve steady-state conditions, sinusoidal NP was again applied for 5 min, followed by 5 min of steady-state exercise measurements.
Techniques of measurement
Sinusoidal neck pressure technique. The traditional neck collar technique alters neck chamber pressure using either a pulsatile (R-wave gated) or static stimulus, producing a sigmoid curve relating R–R interval or ABP to carotid sinus pressure (Eckberg & Sleight, 1992). However, recent studies analysing the dynamic relationship of the CBR suggest that a more sophisticated, nonlinear mathematical model may be better suited to describe the intrinsic nature of the system (Iellamo, 2001; Zhang et al. 2001). Complex modelling restricts the traditional techniques which can be used to provide CBR loading and unloading, and in the case of spectral analysis a relatively long, steady-state stimulus is required. To meet these criteria, we utilized a sinusoidal NP technique that was applied in an oscillating manner over several minutes. This sympathoexcitatory stimulus created fluctuations in carotid sinus transmural pressure at a predetermined frequency, and the modifications in end-organ CBR activity were evaluated using measurements of RRI, ABP, MSNA, femoral blood velocity and skeletal muscle tissue oxygenation. We reasoned that the degree of end-organ activity may be assessed by analysing the variability of the above-mentioned cardiovascular variables in response to sinusoidal NP stimuli, as previously described (Bath et al. 1981; Bernardi et al. 1997; Furlan et al. 2003).
Ultrasound Doppler. Leg blood flow was evaluated using the well-established ultrasound Doppler technique (Shoemaker et al. 1994; Radegran, 1997; Keller et al. 2003; Wray et al. 2004). Femoral blood velocity was determined at the common femoral artery distal to the inguinal ligament but above the bifurcation into the superficial and profundus femoral branches. The probe position was held at a constant insonation angle with the use of a custom-built aluminium cradle, which rested on the leg and held the probe at a constant 45 deg angle. Femoral blood velocity was measured with a bidirectional Doppler transducer operating at 5 MHz (model MD6, D. E. Hokanson, Inc., Bellevue, WA, USA) and calculated according to the formula: fa = 64.9VcosØ Hz, where fa is the audio frequency, Ø is the angle of insonation, and V is the blood velocity (cm s–1). This procedure of blood velocity measurement has previously been shown to produce accurate absolute values of flow when combined with femoral artery diameter measurements (Radegran, 1997; Wray et al. 2004). It has been demonstrated that common femoral artery diameter does not change significantly in response to +40 mmHg neck pressure (Keller et al. 2003) or during 7 W knee-extensor exercise (Wray et al. 2004), and in the present study we confirmed these findings. Thus, femoral blood flow was not calculated, and power spectral analysis was performed using the raw femoral blood velocity signal.
Near-infrared spectroscopy. Near-infrared spectroscopy is based upon the relative ease with which infrared light (700–1000 nm) passes through biological tissue, and on the O2-dependent absorption changes of haemoglobin and myoglobin. Tissue oxygenation measurements are limited to the skeletal muscle microcirculation owing to the low probability that photons of light will emerge from arteries and veins (Beer's law), and therefore provide a beat-to-beat index of skeletal muscle tissue oxygen delivery relative to its use. For the present study, two fibre optical bundles with an optode separation of 4 cm were placed on the skin over the vastus lateralis muscles of both legs, 15–20 cm above the knee along the major axis of the muscle. The probe was secured with adhesive tape and covered with an elastic bandage to shield ambient light and minimize movement artifact. The near-infrared signals at four different wavelengths were sampled concurrently at a rate of 1 Hz, converted to optical densities by using known algorithms and stored digitally for analysis (NIRO 300, Hamamatsu Photonics, Hamamatsu City, Japan). The near-infrared HbO2 signal (expressed in arbitrary units, a.u.) was used as an index of skeletal muscle tissue oxygenation and as an indirect indication of microcirculatory blood flow (Hansen et al. 1996; Sander et al. 2000; Fadel et al. 2004).
Muscle sympathetic nerve recordings. Postganglionic muscle sympathetic nerve activity (MSNA) was recorded with standard microneurographic techniques as previously described (Wallin & Eckberg, 1982). Briefly, a tungsten microelectrode was inserted into the peroneal nerve near the fibular head. The nerve signal was processed by a preamplifier and an amplifier (model 662C-3, Nerve Traffic Analyser; University of Iowa Bioengineering, Iowa City, IA, USA) with a total gain of 90 000. Amplified signals were bandpass filtered (700–2000 Hz), rectified and integrated by a resistance–capacitance circuit with a time constant of 0.1 s. MSNA recordings display a pulse-synchronous burst pattern and an increase in burst frequency with end-expiratory breath holds and Valsalva manoeuvres. However, there is no response to arousal or skin stroking. These characteristics were used to determine proper electrode placement for the MSNA recordings. For baseline comparisons, MSNA was expressed as burst frequency.
Data analysis
To evaluate the influence of the CBR on haemodynamic variables, sinusoidal neck pressure (NP) at +40 mmHg was produced to evoke sinusoidal oscillations in carotid sinus transmural pressure at a frequency of 0.1 Hz. This dynamic input to the CBR at a constant period was presumably transduced to all end organs influenced by the CBR, effectively forcing entrainment of these cardiovascular, neural and haemodynamic variables. Such CBR entrainment is quantified at the end organ via the degree of change, i.e. ‘variability’, in the measured signal. End-organ variability associated with CBR entrainment was analysed using power spectral analysis, which provides a sensitive measure of variability in the frequency domain, creating a discrete spectral peak at the frequency with which sinusoidal NP was applied. Coherence testing was applied to verify that the observed end-organ entrainment was evoked by the NP stimulus (Saul et al. 1991; Pagani et al. 1997).
Fast Fourier transformation was performed to calculate spectral power of the R–R interval, ABP, MSNA, femoral blood velocity and skeletal muscle tissue oxygenation time series, as previously described (Cooke et al. 1999). Briefly, beat-to-beat changes in RRI, ABP, MSNA, femoral blood velocity and skeletal muscle tissue oxygenation were linearly interpolated and resampled at 5 Hz to convert the unequally spaced beat-to-beat time series to a uniformly spaced time series. Five minute data sets (1500 samples) were evaluated using a 60 s window sliding every 10 s. These data were detrended, Hanning filtered and fast-Fourier transformed to their respective frequency representations. The area under the low-frequency (LF, 0.085–0.115 Hz) peak was integrated and averaged for all subjects.
Statistical analysis
Because the power spectrum of some measured signals exhibited a skewed distribution, natural logarithm (ln) transformation was performed before statistical testing, as previously described (Bernardi et al. 1997; Cevese et al. 2001). The effect of sinusoidal NP was evaluated after data was natural log transformed, resulting in an estimate of spectral power based on the raw signal variability. For the absolute power spectral values less than 1, ln transformation produced a negative value. Since exercise produced an increase in signal variability and thus a new baseline, comparisons were made between baseline and sinusoidal NP at rest and during exercise separately. Student's paired t test was performed to test for a significant difference between baseline and sinusoidal NP conditions for low-frequency power of RRI, ABP, MSNA, femoral blood velocity and skeletal muscle tissue oxygenation at rest and during exercise. Coherence function testing in the low-frequency range was used to confirm significant linearity between neck chamber pressure and end-organ measurements, with coherence values >0.50 considered significant. All results are expressed as means ± S.E.M. and statistical significance was set at P < 0.05.
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Results |
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Spectral analysis was performed to identify changes in the variability of each signal in the low-frequency (LF, 0.085–0.115 Hz) band during baseline and 0.1 Hz sinusoidal NP conditions. During sinusoidal NP, the sympathoexcitation due to positive neck chamber pressure evoked an increase in end-organ activity as measured by changes in RRI, ABP, MSNA, femoral blood velocity and skeletal muscle tissue oxygenation. Figure 1 presents the visible entrainment of raw signals and the power spectra for one subject during sinusoidal NP at rest and during exercise.
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Cardiovascular measurements
During the resting condition, sinusoidal NP significantly increased HR (from 60 ± 2 to 67 ± 2 beats min–1), mean arterial pressure (from 91 ± 2 to 101 ± 3 mmHg), femoral blood velocity (from 6.3 ± 0.5 to 7.6 ± 0.5 cm s–1) and skeletal muscle tissue oxygenation (from 0.102 ± 0.03 to 0.176 ± 0.05 a.u.) with no significant change in MSNA burst frequency. Exercise alone significantly increased baseline HR (from 61 ± 2 to 73 ± 3 beats min–1), mean arterial pressure (from 91 ± 2 to 101 ± 4 mmHg) and femoral blood velocity (from 6.3 ± 0.5 to 22.7 ± 1.1 cm s–1), with no significant change in MSNA. Absolute skeletal muscle tissue oxygenation did not significantly change in the exercising or nonexercising leg. Sinusoidal NP applied during exercise significantly increased HR (from 73 ± 3 to 77 ± 3 beats min–1) and mean arterial pressure (from 101 ± 4 to 110 ± 2 mmHg), with no significant change in femoral blood velocity or MSNA burst frequency. Exercising sinusoidal NP did not significantly change skeletal muscle tissue oxygenation of the exercising leg, but significantly decreased oxygenation in the nonexercising leg (from 0.21 ± 0.06 to 0.15 ± 0.06 a.u.).
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Discussion |
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While it is well established that the CBR remains effective during exercise (Bevegard & Shepherd, 1966; DiCarlo & Bishop, 1992; Potts et al. 1993; Fadel et al. 2001; Keller et al. 2003; Ogoh et al. 2003), we believe several aspects of the present study add significant new insight into reflex cardiovascular control. Using prolonged, oscillating NP stimuli rather than a single static pulse of NP, we have further characterized the dynamic nature of CBR control during exercise. Moreover, inclusion of peripheral haemodynamic measurements extends previous findings by evaluating the influence of exercise-induced metabolites on CBR control of skeletal muscle blood flow and tissue oxygenation. Finally, the use of spectral analysis techniques has provided a novel approach for quantifying the magnitude of CBR control.
Most CBR studies in animals and humans have utilized static changes in carotid sinus transmural pressure, which produce a sigmoid-shaped curve relating R–R interval or ABP to carotid sinus transmural pressure. Using this technique, an upward and rightward resetting of the curve during exercise has been identified, with no change in CBR–ABP maximal gain (DiCarlo & Bishop, 1992; Potts et al. 1993). Others have evaluated the individual efferent neural and end-organ components of the CBR, demonstrating that control of RRI (O'Leary & Seamans, 1993; Iellamo et al. 1994), ABP (Strange et al. 1990; Ogoh et al. 2003) and MSNA (Fadel et al. 2001; Ogoh et al. 2003) is unchanged from rest to exercise. However, during exercise the carotid baroreceptors are exposed to perpetual fluctuations in ABP and so must provide adequate changes in efferent activity on a very dynamic, beat-to-beat basis. As such, we presumed that the carotid baroreceptors might respond differently to an oscillating NP stimulus than to a single pulse of static NP and that this stimulus might thus more appropriately reproduce the intrinsic physiological conditions of exercise. We believe that significant additional information regarding the dynamic nature of CBR control during exercise becomes apparent when an extended period of oscillating input is applied and the average response across several minutes is considered.
In the present study, frequency-domain spectral analysis provided a unique method for quantifying the degree of CBR control over each measured variable. When sinusoidal NP was applied, we observed a similar degree of entrainment between rest and exercise for the efferent neural and end-organ measurements of MSNA and RRI, indicating preservation of CBR control for these measurements. However, during exercise the application of sinusoidal NP evoked a smaller change in LF spectral power of ABP, femoral blood velocity and skeletal muscle tissue oxygenation compared to rest, indicating a diminished entrainment of these variables. These findings are consistent with the concept of an altered end-organ responsiveness caused by metabolic byproducts emanating from the exercising muscle, i.e. functional sympatholysis (Remensnyder et al. 1962).
Several studies have sought to evaluate the reduced end-organ responsiveness to sympathetic stimuli using various reflex and pharmacological interventions, with varied results. Using an exercise mode and intensity similar to the present study, we have recently reported an exercise-induced attenuation in 
-adrenoreceptor responsiveness (Wray et al. 2004). Attenuation of -adrenoreceptor responsiveness has also been reported from studies using the selective ‘exogenous’ agonists in the rat (Anderson & Faber, 1991; Thomas et al. 1994) and dog hindlimb (Buckwalter et al. 2001) and human forearm (Rosenmeier et al. 2003) during exercise. In addition, recent studies in humans have demonstrated an attenuated response to tyramine during exercise, a pharmacological approach which utilizes exogenous drug application to provoke endogenous noradrenaline release from the nerve terminals (Tschakovsky et al. 2002; Rosenmeier et al. 2003). Since sympathoexcitation from sinusoidal NP is transduced to the vascular smooth muscle via postjunctional -adrenoreceptors, we believe these findings extend previous observations of attenuated end-organ responsiveness. Importantly, in the present study the stimulus was not pharmacological, but rather utilized reflex CBR-mediated sympathoexcitation and subsequent release of noradrenaline from the sympathetic nerve terminals. We believe this methodology may provide a more physiological stimulus to the vasculature of the exercising muscle.
Studies in animals (Collins et al. 2001) and humans (Keller et al. 2003) have also utilized reflex manoeuvres to evaluate CBR control of skeletal muscle blood flow, with differing results. Collins et al. (2001) evaluated the change in vascular conductance of the dog hindlimb and renal vascular bed following carotid sinus hypotension at rest and during ramped treadmill exercise, and reported an increased CBR-mediated change in vascular conductance in the exercising hindlimb compared to rest and the renal vascular bed. Using single bouts of NP and neck suction, Keller et al. (2003) identified attenuation of CBR-mediated changes in vascular conductance during unilateral knee-extension exercise. Taken together, these studies confirm the importance of the active muscle vasculature in the maintenance of systemic arterial blood pressure during exercise hyperaemia. Data from the present study extend these findings with the additional measurements of MSNA and skeletal muscle tissue oxygenation, providing a comprehensive assessment of CBR control, ranging from central reflex autonomic effects to peripheral changes at the level of the skeletal muscle microcirculation.
CBR entrainment of ABP was reduced during exercise, which appears inconsistent with previous findings of preserved CBR control of ABP from rest to exercise (Bevegard & Shepherd, 1966; Potts et al. 1993; Ogoh et al. 2003). This disparity may be explained by considering differences in the technique of CBR perturbation and in the methods of data analysis. Previous studies using the variable pressure neck chamber have applied a static, single NP pulse for 5 s and measured the peak change in HR and ABP. This technique allows the full range of the CBR response to be characterized with a sigmoid-shaped curve using a logistic fit model (Kent et al. 1972), including points of threshold, saturation and gain. Using this technique, we have shown that as the operating point approaches threshold during exercise, the change in ABP during hypotensive stimuli (i.e. NP) is attenuated (Potts et al. 1993). Data from the present study support these findings, since CBR control of ABP is attenuated, but not abolished. In addition, it should be noted that, unlike previous studies using the variable pressure neck chamber, the oscillatory NP technique alters carotid sinus transmural pressure in a dynamic manner, so that both ‘on’ and ‘off’ responses to the CBR unloading across several minutes are measured simultaneously.
Implication for functional sympatholysis
We have recently reported that alterations in systemic vascular conductance are the primary means by which the carotid baroreflex regulates ABP both at rest (Ogoh et al. 2002) and during exercise (Ogoh et al. 2003), despite a reduced vascular responsiveness in the exercising muscle (Keller et al. 2003; Wray et al. 2004). Data from the present study extend these findings by addressing aspects of both systemic and local CBR control. We found that the degree of CBR-mediated entrainment of ABP, femoral blood velocity and skeletal muscle tissue oxygenation was reduced during exercise, yet a discreet spectral peak was clearly evident for all measurements. This observed preservation of some degree of peripheral haemodynamic control is consistent with the traditional definition of sympatholysis, which suggests a reduced but not ablated responsiveness of the active skeletal muscle vasculature to sympathoexcitation (Remensnyder, 1962; Buckwalter & Clifford, 2001; Joyner & Thomas, 2003). This is a significant observation when considering the functional importance of local blood flow control, since any change in vascular conductance will alter systemic ABP more profoundly as blood flow increases, in accordance with Ohm's law. As such, the observed reduction in CBR-mediated entrainment of ABP, femoral blood velocity and skeletal muscle tissue oxygenation does not necessarily have a negative impact on cardiovascular homeostasis during exercise. On the contrary, the attenuation in end-organ responsiveness may serve to prevent robust CBR-mediated vasoconstriction of the skeletal muscle vasculature that could jeopardize oxygen delivery to the exercising muscle and also preclude excessive increases in ABP. Thus, the observed attenuation in CBR control at the end organ may in fact serve a protective role, modulating sympathetic input to ensure adequate tissue perfusion while at the same time maintaining ABP during exercise.
Potential limitations
One of the potential limitations of the present study is the use of near-infrared spectroscopy as an index of microcirculatory blood flow. Near-infrared spectroscopy does not directly measure tissue blood flow, but instead provides a qualitative index of tissue oxygenation. However, recent studies have demonstrated a close correlation between blood flow values measured by plethysmography, the Fick method, and near-infrared spectroscopy (Edwards et al. 1993; Van Beekvelt et al. 2001). In addition, validation studies have reported a high correlation between changes in muscle tissue oxygenation and conventional ultrasound Doppler measurements to reflex sympathetic activation in the human forearm (Fadel et al. 2004). Together, these studies support the use of skeletal muscle tissue oxygenation as an indirect index of microcirculatory blood flow.
The relatively light exercise intensity used in the present study was necessary to minimize movement artifact that would prevent continuous MSNA recording in the nonexercising leg. This exercise caused only a modest increase in HR with no increase in MSNA burst frequency, though blood flow increased approximately 4-fold to the exercising leg. In a recent study we have identified profound reduction in vascular responsiveness during very light exercise (Wray et al. 2004), while others have observed attenuated vascular responses even during the first few contractions of an exercise bout (DeLorey et al. 2002). These previous findings led us to conclude that the exercise intensity employed was sufficient to allow adequate evaluation of the influence of metabolic factors on CBR-mediated control of the peripheral circulation. However, care should be taken in extrapolating these findings to exercise of greater intensities and/or exercise engaging a larger muscle mass.
Conclusion
Using a reflex sympathoexcitatory stimulus, the present study has demonstrated simultaneous entrainment of all CBR end-organ measurements, ranging from cardiac chronotropic effects to alterations at the level of the skeletal muscle microcirculation. Furthermore, during exercise an attenuated degree of CBR entrainment for all measurements of the peripheral circulation was observed, suggesting a diminution in end-organ responsiveness. Collectively, these data have identified a significant and specific attenuation of end-organ responsiveness to CBR-mediated sympathoexcitation in the vasculature of the exercising muscle, suggesting a shift from reflex control towards more predominant local control of blood flow. Despite these changes in CBR control, systemic ABP is well preserved throughout exercise.
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