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The purpose of the experiments was to examine the role of central command in the exercise-induced resetting of the carotid baroreflex. Eight subjects performed 30 % maximal voluntary contraction (MVC) static knee extension and flexion with manipulation of central command (CC) by patellar tendon vibration (PTV). The same subjects also performed static knee extension and flexion exercise without PTV at a force development that elicited the same ratings of perceived exertion (RPE) as those observed during exercise with PTV in order to assess involvement of the exercise pressor reflex. Carotid baroreflex (CBR) function curves were modelled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid changes in neck pressure and suction during steady state static exercise. Knee extension exercise with PTV (decreased CC activation) reset the CBR-HR and CBR-MAP to a lower operating pressure (P < 0.05) and knee flexion exercise with PTV (increased CC activation) reset the CBR-HR and CBR-MAP to a higher operating pressure (P < 0.05). Comparison between knee extension and flexion exercise at the same RPE with and without PTV found no difference in the resetting of the CBR-HR function curves (P > 0.05) suggesting the response was determined primarily by CC activation. However, the CBR-MAP function curves were reset to operating pressures determined by both exercise pressor reflex (EPR) and central command activation. Thus the physiological response to exercise requires CC activation to reset the carotid-cardiac reflex but requires either CC or EPR to reset the carotid-vasomotor reflex.
Recently, we selectively augmented the influence of central command during steady state static and dynamic leg exercise using partial neuromuscular blockade (norcuron; Gallagher et al. 2001b). In addition, Querry et al. (2001) reduced exercise pressor reflex input while augmenting central command activation during static and dynamic arm exercise by inducing partial axillary neural blockade (lidocaine). Augmentations in central command in both studies resulted in increases in heart rate (HR) and mean arterial blood pressure (MAP) as well as rightward and upward (i.e. parallel) resetting of the carotid baroreflex function curves for both heart rate (CBR-HR) and mean arterial blood pressure (CBR-MAP). However, within these investigations, it remains unclear whether neuromuscular blockade activated undefined central neural pathways associated with increased subject anxiety. Activation of such neural circuitry could contribute to the physiological responses elicited.
In cats, Potts & Mitchell (1998) demonstrated that activation of metabolically and mechanically sensitive skeletal muscle afferent fibres resets the carotid baroreflex. Likewise, McIlveen et al. (2001) demonstrated that selectively stimulating: (i) the mesencephalic locomotor region (a site potentially involved in central command signalling); (ii) statically contracting the triceps surae muscle (activation of the exercise pressor reflex); or (iii) stretching the hindlimb muscle (activation of the skeletal muscle mechanoreflex) reset the carotid baroreflex to higher operating pressures in cats. These findings in animals complement those recently described in humans (Gallagher et al. 2001a,b; Querry et al. 2001).
By using tendon vibration to assist or to oppose an exercising muscle group while developing a given force one can decrease (agonist activation) or increase (antagonist inhibition) the influence of central command without inducing nociceptor afferent input or augmenting normal exercise pressor reflex activation (Goodwin et al. 1972). Using this technique in combination with non-invasive baroreflex testing (i.e. neck pressure/suction), we investigated the role of central command in the resetting of the carotid baroreflex.
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The data of the present investigation independently verify previous reports in animals (McIlveen et al. 2001) and humans (Gallagher et al. 2001b) that central command actively contributes to carotid baroreflex resetting during exercise. By using the uniquely selective tendon vibration paradigm, we were able to demonstrate that the carotid baroreflex was further reset upwards on the response arm and rightwards to higher operating arterial pressures during knee flexion exercise with antagonist patellar tendon vibration (i.e. increased central command). In contrast, but of equal importance, the data obtained during knee extension exercise with agonist patellar tendon vibration (i.e. decreased central command) demonstrated that the carotid baroreflex was reset lower on the response arm and leftwards to lower operating arterial pressures. Further, this resetting occurred in the absence of the increased subject anxiety and/or nociceptive input often caused during neural blockade experiments.
In an effort to determine the selectivity of the tendon vibration technique in activating central command, seven of the subjects were asked to repeat the knee extension and knee flexion exercise at the same RPE. Williamson et al. (2001) have demonstrated that the individual's RPE or ‘effort sense’ during physical activity, independent of the force production, appears to dictate the magnitude of central command (Asmussen, 1965; Hobbs & Gandevia, 1985; Leonard et al. 1985; Gandevia & Hobbs, 1990). Hence, by comparing exercise with vibration to the exercise without vibration (Study 2, Fig. 1) at the same RPE (or effort sense) we expected to account for activation of the exercise pressor reflex (Potts & Mitchell, 1998; Gallagher et al. 2001a) in the resetting of the carotid baroreflex.
Although, the same amount of central command was reflected by there being no significant difference in RPE and HR between 30 % MVC with agonist vibration exercise and the smaller 22.6 % MVC force without vibration (Fig. 5), the MAP responses were decreased significantly during static knee extension with the smaller force development. Therefore, it was apparent that the smaller force effectively reduced the input of the exercise pressor reflex at the same amount of central command activation during knee extension. This reduction in exercise pressor reflex afferent input resulted in the carotid-HR response curves being unaltered by the decreased muscle tension when performed using the same amount of central command. However, the carotid-MAP reflex curves were reset downwards during decreased muscle contraction performed at the same central command. These data suggest a predominant effect of central command on the HR responses to exercise and its effect on the resetting of the carotid-HR baroreflex function curve. However, the data also suggest that the resetting of the carotid-vasomotor (CBR-MAP) baroreflex function curve was accomplished by a redundant activation of both central command and the exercise pressor reflex.
Conversely, during static knee flexion the subjects performed at a greater force (41.0 ± 2.4 % MVC) to achieve the same RPE as that obtained during the knee flexion exercise at 30 % MVC with vibration. Thus, the subjects required the same central effort with increased activation of the exercise pressor reflex to achieve the greater absolute force (41.0 % MVC) compared to the static knee flexion of 30 % MVC plus patellar tendon vibration. Surprisingly, the MAP responses were not increased significantly during static knee flexion at the 41.0 % MVC force compared with the 30 % MVC plus vibration flexion exercise. During knee flexion carotid-HR and carotid-MAP had the same responses during the 41.0 % MVC flexion exercise performed without vibration compared with the 30 % MVC flexion exercise performed with vibration (Fig. 7). We suggest that because the amplitude of the EMG in the hamstrings during flexion with the patellar tendon vibration was greater than the control flexion exercise in some subjects (Fig. 8), it was possible that the technique was unable to selectively isolate central command by utilizing the patellar tendon vibration technique during knee flexion. It was likely that the increased exercise pressor reflex activity of the 41.0 % MVC force without vibration (Fig. 1, Trial III) was not much different from the exercise pressor reflex activation that occurred during the 30 % MVC flexion plus patellar tendon vibration trial. In summary, the patellar tendon vibration technique appeared to jointly activate both the central command and the exercise pressor reflex in the control of the carotid-vasomotor (CBR-MAP) reflex and suggests that the resetting of the carotid-vasomotor reflex during exercise functions through both central command and the exercise pressor reflex. Because of technical difficulties in consistently maintaining the vibrator at the same position on the patellar tendon during dynamic exercise, we are currently unable to verify similar findings using this exercise modality. However, based upon the similarity of responses to both static and dynamic exercise obtained during muscle weakness experiments (Gallagher et al. 2001b) and activated exercise pressor reflex experiments (Gallagher et al. 2001a) we would expect similar findings to be obtained from patellar tendon vibration studies during dynamic exercise.
Previously, Strange et al. (1993) evaluated the role of central command and the exercise pressor reflex in the control of the cardiovascular response to exercise. In nine subjects exercise was performed under three conditions: (i) voluntarily; (ii) during electrically stimulated (E-S) muscle contraction (i.e. no central command); and (iii) during E-S muscle contraction with epidural anaesthesia (i.e. no central command and no exercise pressor reflex). During voluntary exercise, arterial blood pressure was increased. During E-S exercise, the increase in blood pressure was augmented. However, during E-S muscle contraction under epidural anaesthesia the increase in arterial blood pressure was abolished. In a separate study, Winchester et al. (2000) demonstrated the contribution of central command and the exercise pressor reflex to cardiovascular control during static exercise in patients with Brown-Sequard syndrome (i.e. spinal cord hemi-section). Their data indicated that the magnitude of the HR and blood pressure responses in these patients was affected by the level of central command activity. In addition, the cardiovascular response was determined to be mediated by the exercise pressor reflex in the absence of central command in these individuals. Importantly, these studies also suggested that activation of either central command or the exercise pressor reflex was requisite for the parallel resetting of the arterial baroreflex. These investigations along with the data of the present study provide evidence of the redundancy of the two major neural control mechanisms involved in the control of the cardiovascular system during exercise.
Although the relative intensity during knee extension was the same as for knee flexion (30 % MVC), the RPE, HR and MAP responses to knee extension were larger than during the knee flexion exercise (Fig. 2). Petrofsky et al. (1981) indicated the importance of muscle fibre composition in determining the blood pressure response for isometric contractions. In addition, Silva et al. (1999) found that the HR increase or EMG activity was significantly higher in isometric knee extension than flexion. Therefore, it is likely that the predominant mechanism responsible for the larger increase in these responses to knee extension as compared to flexion was dependent on qualitative and quantitative differences in the fibre type composition found in each muscle group.
The neural pathways involved in the activation of central command remain an area of intense investigation. Anatomical and physiological investigations in animals (Yasui et al. 1991; Waldrop et al. 1996) have identified the insular cortex and the locomotor regions of the hypothalamus and mesencephalon as potential sites for the generation of central command (Waldrop et al. 1996). In addition, the dorsolateral, ventrolateral, periventricular and commissural regions of the nucleus tractus solitarius have been identified as possible sites of integration of inputs from sites generating central command with the afferent input from the arterial baroreflexes and the exercise pressor reflex (Yasui et al. 1991; Potts & Mitchell, 1998). In humans, the use of Single Photon Emission Computerized Tomography (SPECT) or Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI) for measures of the anatomical location of active metabolic brain activity used in conjunction with hypnotic manipulation of effort sense (Fink et al. 1995; Williamson et al. 2001) and imagined exercise (Thornton et al. 2001; Williamson et al. 2002) have anatomically identified sites where motor and cardiovascular activities vary in relation to perception of effort (Williamson et al. 2001, 2002). Most recently, Thornton et al. (Thornton et al. 2002) demonstrated that electrical stimulation of the thalamus and basal ganglia of the midbrain in humans evoked increases in heart rate and arterial blood pressure. These findings suggest that activation of the insular and cingulate cortices and the midbrain may play a major role in the central activation of the cardiovascular responses to exercise.
In conclusion, the present investigation supports the hypothesis that central command actively contributes to baroreflex resetting during static exercise. The data further suggest that central command plays a predominant role in the resetting of the carotid-cardiac reflex. In contrast, both central command and exercise pressor reflex activation are requisite for carotid-vasomotor resetting.