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J Appl Physiol 95: 43-48, 2003. First published January 24, 2003; doi:10.1152/japplphysiol.00895.2002
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Interaction between muscle metaboreflex and mechanoreflex modulation of arterial baroreflex sensitivity in exercise

C. A. Carrington, C. Ubolsakka, and M. J. White

School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom

Submitted 30 September 2002 ; accepted in final form 17 January 2003


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The effect of external calf compression on baroreflex sensitivity (BRS) during electrically evoked plantar flexion and postexercise circulatory occlusion (PECO) was studied. Subjects took part in two experimental trials: control and compression. In both trials, electrically evoked isometric plantarflexion (Stim) was performed at 30% maximum voluntary contraction force for 2 min. During compression, a cuff (inflated to 250 mmHg) was applied to the active calf during exercise and PECO. Sequence analysis carried out on the systolic blood pressure responses, and R-wave-R-wave intervals revealed a rightward shift of the regression line along the pressure axis during Stim in both trials. In the control experiment, BRS was significantly (P < 0.01) increased from 10.37 ± 1.87 ms/mmHg during Stim to 12.79 ± 1.62 ms/mmHg during PECO. With external compression, BRS was unaltered between Stim (10.84 ± 1.86 ms/mmHg) and PECO (11.40 ± 1.54 ms/mmHg). Because the metabolic conditions were the same in both experiments, the results may best be explained by reactivation of muscle mechanoreceptor activity by external compression during PECO.

cardiovascular control; muscle afferents; isometric exercise

AT REST, AN INCREASE IN BLOOD pressure elicits an arterial baroreflex-mediated reduction in heart rate, but, during exercise, both blood pressure and heart rate increase together. It was initially thought that, during exercise, the human arterial baroreflex was either suppressed or inoperable (2, 16); however, more recent studies suggest that the baroreflex is reset (4, 12, 13, 22, 24, 28). Central command was originally thought to modulate the human arterial baroreflex during exercise (8, 29), but it is now accepted that muscle afferent activation can also modify arterial baroreflexes (4, 12, 13, 25).

Skeletal muscle contraction activates both group III and IV muscle afferent fibers, which, in turn, mediate increases in blood pressure and heart rate (7). Broadly, group III muscle afferents are sensitive to mechanical stimuli, and group IV to chemical stimuli, although a proportion of both group III and IV muscle afferents is polymodal and responds to both forms of stimuli (14, 15, 20). To date, interest has focused mainly on the role of the chemoreflex (4, 12, 13, 25); therefore, comparatively little is known about the effects of the muscle mechanoreflex on the arterial baroreflex. In decerebrate cats, electrical stimulation of group III fibers of the peroneal nerve inhibited the cardiac vagal component of the arterial baroreflex (19), and, in another animal study on anesthetized dogs, stimulation of the mechanoreceptors by passive stretch reset the carotid baroreflex (27). In humans, there have been studies that set out to separate the influences of central command and muscle afferent inputs on the arterial baroreflex (10, 23). However, the volitional exercise used in these protocols makes the roles of muscle mechanoreceptor and chemoreceptor afferent feedback difficult to interpret, because the presence of central command may mask or modify their influence. This is of particular concern with regard to the muscle mechanoreflex effects on arterial baroreflex sensitivity (BRS), as was illustrated by the work of Iellamo et al. (13). They used low-level electrically evoked knee-extensor exercise to remove central command and separated the influence of muscle mechanoreflex activation from that of muscle chemoreceptor stimulation on BRS by performing the exercise with and without circulatory occlusion. In the absence of central command, during exercise with open circulation, when it was supposed that muscle mechanoreceptors alone were activated, albeit weakly, they reported a reduction in BRS. When the same exercise was performed volitionally, this effect was lost, as it was also when the electrically evoked exercise was performed with closed circulation, thereby causing muscle chemoreflex activation (13). Their conclusion was that both central command and muscle chemoreflex activation overwhelmed the inhibitory influence of the muscle mechanoreceptor stimulation. In a previous study, our laboratory (4) observed that BRS was increased during postexercise circulatory occlusion (PECO) after electrically evoked plantar flexion, when muscle chemosensitive afferents alone were stimulated. The question then arises: in the absence of central command, could mechanoreceptor activation override a strong preexisting metaboreflex-increased BRS? The present study was designed to investigate this question.

If external compression is applied to isometrically contracting muscle and maintained during a phase of PECO, cardiovascular responses seen during PECO are accentuated, and these increased responses have been attributed to the additional muscle mechanoreceptor stimulation (17, 32). Therefore, we used external compression after isometric exercise to reactivate the muscle mechanoreceptors during PECO to examine further the interaction of muscle mechanoreceptor and chemoreceptor afferent activation on BRS. Our hypothesis was that, during PECO, when central command is absent and muscle is quiescent, mechanoreceptor activation by external compression would alter the existing exercise-induced metaboreflex increase in BRS.


   METHODS
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 METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Data were collected from 15 healthy, normotensive subjects (9 men) with a mean (±SE) age of 29 ± 2 yr. Subjects were recruited from the student population of the University of Birmingham and were recreationally active. All subjects provided written, informed consent before their participation in the study, which had local ethics committee approval.

Subjects were habituated to all procedures before definitive measurement, and none of the procedures elicited pain. Maximum voluntary contraction (MVC) and evoked pressor responses at 30% MVC were measured by well-established methods (3, 9). There were two trials: 1) control and 2) compression. Each trial followed the same protocol, which consisted of four continuous 2-min phases. A 2-min rest period, to obtain baseline measures, was followed by a 2-min electrically evoked isometric contraction (Stim), produced by submaximal tetanic stimulation at a frequency of 20 Hz, and maintained at 30% maximum voluntary strength. During Stim, circulation was occluded to the lower leg by inflation of a thigh cuff to >200 mmHg, and, after Stim, the inflated thigh cuff remained in place for a further 2 min (PECO). A 2-min recovery period followed. However, during compression, which was performed on a separate day, a cuff (inflated to 250 mmHg) was applied to the active calf during Stim and PECO.

Continuous blood pressure responses and R-wave-R-wave (R-R) intervals were recorded throughout the 8-min protocol. The R-R interval was recorded by using a three-lead ECG and heart rate monitor (Cardiorater CR7, Cardiac Records). A 2300 Finapres (Ohmeda) was used to record beat-to-beat blood pressure from the middle finger of the left hand, which was supported at heart level throughout the experiment by means of an adjustable stand. Analog blood pressure and ECG signals were transmitted to an analog-to-digital converter (Cambridge Electronic Design 1401 plus). The sampling frequency of analog-to-digital conversion was 1,000 Hz for each signal. Blood pressure and ECG data were displayed and analyzed on a personal computer (Vale Platinum).

BRS was calculated by the spontaneous sequence analysis technique (see Ref. 26 for review). Beat-to-beat systolic blood pressure (SBP) and R-R intervals were searched, by purpose-written software, for sequences of three or more consecutive beats in which SBP increased progressively and the subsequent R-R interval lengthened or vice versa. The minimum change was 1 mmHg for SBP and 1 ms for R-R interval, and a lag of one beat was used. Linear regressions relating SBP to R-R interval were plotted for each sequence, and only those with linear r values >0.92 were used. Slopes derived from all sequences within each of the four 2-min phases were pooled so that one measure of BRS was obtained for each subject for each phase (rest, Stim, PECO, recovery) of the protocol.

Statistics. Data are reported as group means (±SE), unless otherwise stated. Comparison of the measured variables during the four phases of the protocol was made by using a repeated-measures multivariate analysis of variance. A post hoc Student's paired t-test was performed, if a significant effect was indicated. The criterion for statistical significance was P < 0.05.


   RESULTS
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 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
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Cardiovascular responses. Resting SBP, diastolic blood pressure, and heart rate were 132 ± 3 mmHg, 77 ± 2 mmHg, and 72 ± 3 beats/min, respectively, during the control experiment and 131 ± 4 mmHg, 75 ± 3 mmHg, and 72 ± 3 beats/min, respectively, during the compression experiment. Under both control and compression conditions, electrically evoked plantar flexion produced a rise in blood pressure and heart rate; when the contraction ceased at the start of the PECO phase, blood pressure fell immediately, but to a level that was significantly higher than that at rest and was maintained until the thigh cuff was released (Fig. 1). In both conditions, heart rate fell rapidly during PECO to precontraction levels (Fig. 1). Mean average SBP changes during Stim were 24.8 ± 2.6 and 25.9 ± 2.9 mmHg and during PECO were 17.8 ± 3.4 and 22.1 ± 2.8 mmHg for control and compression, respectively (Fig. 1).



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  		Fig. 1. Mean (±SE) changes in systolic blood pressure (SBP; A) and heart rate (HR; B) during the control ({circ}) and the compression ({blacksquare}) trials.

 

Baroreflex responses. In both control and compression experiments, there was a rightward shift of the regression line along the pressure axis during Stim, indicated by a decrease in intercept along the R-wave-R-wave interval axis, which reached significance (P < 0.05) during the compression experiment (Table 1). In the control experiment, BRS was significantly (P < 0.01) increased from 10.37 ± 1.87 ms/mmHg during Stim to 12.79 ± 1.62 ms/mmHg during PECO (Fig. 2). However, in the external compression experiment, BRS did not increase between Stim (10.84 ± 1.86 ms/mmHg) and PECO (11.40 ± 1.54 ms/mmHg).


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  		Table 1. Intercept values for baroreflex regression lines for each phase during both control and external compression experiments

 


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  		Fig. 2. Mean regression lines calculated from spontaneous baroreflex sequences for each phase during control (A) and external compression (B) experiments. Lines are as follows: A, rest; B, electrically evoked isometric exercise; C, postexercise circulatory occlusion; D, recovery.

 


   DISCUSSION
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This experiment set out to examine whether manipulation of muscle mechanoreceptor activation could influence a muscle chemoreflex-induced increase in BRS. To this end, external muscle compression was used in an attempt to reactivate muscle mechanoreflex activity during a phase when muscle chemoreflex activity was controlled by PECO, an established method for selective activation of muscle chemoreceptive afferents (1). The first question that must be answered is whether external compression applied to a human muscle activates muscle mechanoreceptors. There is no direct evidence for this from human studies, as to date only experiments on animals have made direct recordings of muscle mechanoreceptor afferent discharge during external muscle compression (14). However, there are a limited number of human studies that have examined the effects of external limb compression on cardiovascular control. These provide a body of indirect evidence supporting activation of muscle mechanoreceptor afferents by compression of active or resting limbs, evinced by blood pressure rises (21, 33) or muscle sympathetic nerve activity increases (17). Williamson et al. (33) demonstrated a reflex increase in blood pressure during external unilateral or bilateral leg compression, which was abolished by spinal anesthesia. However, their conclusion that this effect was mediated by mechanoreceptor stimulation may be questioned, because the response to external compression was abolished when local arterial flow to the resting limb was restored. This implies that muscle metaboreceptor stimulation was an important part of the response that they observed. More recently, Nishiyasu et al. (21) demonstrated a very clear effect on blood pressure of pulsed or static external limb compression applied to a limb with occluded circulation. This was effective both at rest and during exercise. Occlusion of limb blood flow alone during rest had no effect on cardiovascular variables, suggesting that the muscle chemoreflex was unlikely to be active during the compression protocols applied under the same conditions. McClain et al. (17) found that, during sustained isometric handgrip exercise, external compression of the forearm caused muscle sympathetic nerve activity and blood pressure to rise significantly above levels measured during control contractions. Because all experiments were carried out with local circulatory arrest, there can not have been any differences in metabolite accumulation between trials; therefore, the increases with compression were likely to have been due to stimulation of mechanosensitive afferents. It is unlikely that skin afferents could account for the cardiovascular response to limb compression, because, in other experiments, we have shown that skin anesthesia does not affect the cardiovascular response to calf compression (31). Finally, none of the subjects reported pain during the experimental protocols. Therefore, on the basis of this evidence, we believe that, in the present experiments, we are likely to have stimulated muscle mechanoreceptor afferents by the application of external compression.

During PECO, central command and muscle mechanoreceptor activation are absent, and, therefore, muscle chemosensitive afferents alone are stimulated. We (4) have shown that, during PECO, after electrically evoked plantar flexion, BRS was increased above that seen during evoked exercise, where both muscle mechanoreceptor and chemoreceptor afferents would be active, but not central command. The control experiment of the present study confirms a significant increase in BRS during PECO from that seen during evoked exercise. The novel finding is that the likely restoration of mechanoreceptor activation by the application of external compression during PECO prevented the BRS increase seen in the control experiment, even though blood pressure was further elevated during compression. Gallagher et al. (10) reported a reset baroreflex with unaltered sensitivity during volitional exercise, with further resetting and unaltered sensitivity when attempting to manipulate muscle afferent input with medical antishock trousers (10). However, the background of central command in this study may act to override muscle afferent effects on BRS. Additionally, the vascular obstruction caused by medical antishock trouser inflation to 100 mmHg may also increase muscle chemoreceptor afferent discharge, together with that of the intended muscle mechanoreceptor afferents.

Our finding is compatible with that of Iellamo and coworkers (13), who, using the same sequence analysis technique, reported a decreased BRS during low-level (~15% MVC) electrically evoked rhythmic dynamic exercise. It was assumed that, at this low level of involuntary exercise under local free blood flow conditions, only mechanoreceptors would be activated. However, it is unclear whether this activation was caused by the concentric exercise or, as recently demonstrated (11), the passive muscle stretch, which would occur during recovery of the limb. The reduction in BRS was abolished when the same exercise was repeated under ischemic conditions, which would lead to activation of muscle chemoreceptors. This prompted Iellamo and coworkers to conclude that any influence exerted by muscle mechanoreceptor stimulation was overwhelmed by the rising level of muscle chemoreflex activation, which would occur during their 3- to 3.5-min dynamic exercise protocol when it was performed with occluded limb blood flow. Our data show that the influence of existing muscle chemoreflex activation on BRS can be overcome by the addition of external compression, which may activate muscle mechanoreceptive afferents. Taken together with our earlier findings and those of Iellamo et al., the data suggest that the primacy of muscle mechano- or chemoreflex activation is unimportant in determining the resultant BRS. Clearly, further studies that manipulate the relative magnitudes of these reflexes are required to fully describe their relationship and central integration and indeed to study their influence on BRS when central command is present at different levels.

The sequence technique has some advantages over other methods (see Refs. 5, 26 for review), and, in many respects, it is an ideal tool for this work because it is noninvasive and reflects spontaneous changes in BRS within the normal working range of blood pressure. However, it does not give a full description of the baroreflex curve, and this restricts interpretation of BRS change, because it must be assumed that any such change occurs within the linear portion of the baroreflex range. Although an alternate explanation of our data could be a shift of the baroreflex to a less sensitive portion of a reset but normally shaped baroreflex curve, the assumption that the BRS changes seen in this study occur within the linear portion of the baroreflex range does not seem unreasonable in healthy individuals performing exercise at this level. Most importantly, the sequence technique reveals baroreflex-driven changes in heart period that are mediated via changes in vagal tone (26). The findings of the present study, that muscle mechanoreflex activation seems capable of reducing BRS against a background of muscle chemoreflex activation, add further support to a model put forward to explain muscle afferent modulation of BRS (4) (Fig. 3). Briefly, it is suggested that, during electrically evoked isometric exercise, blood pressure rise excites baroreflex afferents, and this provides an excitatory input to cardiac vagal motoneurons in the nucleus tractus solitarius. This offsets the inhibitory effect of muscle mechanoreceptor activation (18) on these same motoneurons (30). The net result of mechanoreflex, chemoreflex, and baroreflex activation is an unchanged BRS about a higher arterial pressure during exercise. In the absence of central command, cessation of evoked exercise leads to the abrupt loss of mechanoreceptor activation and the inhibitory effect of the muscle mechanoreflex on cardiac vagal motoneurons. Continued muscle chemoreflex-induced sympathoexcitation during PECO prevents the complete restoration of blood pressure to resting levels and, therefore, maintains an increased stimulus to baroreflex firing. The result of the withdrawal of the muscle mechanoreceptor inhibition and the maintenance of the baroreflex excitation at above resting levels would be an increased firing of the cardiac vagal motoneurons during spontaneous blood pressure fluctuations. The outcome is an increased BRS (4, 13). Our previous finding (4) of increased BRS during PECO after electrically evoked isometric plantar flexion, replicated in the present study, fits well with this model, which can also be used to explain our present findings. When external compression is applied to the active muscle during PECO, some mechanoreceptor activation is restored, and the inhibitory effect of these afferents on cardiac vagal motoneuron excitability results in the suppression of the increased BRS seen with pure muscle chemoreflex activation in the control experiment.



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  		Fig. 3. Schematic diagram of the model put forward to explain muscle afferent modulation of baroreflex sensitivity (BRS) during electrically evoked isometric exercise (A) and during postexercise circulatory occlusion (B) with and without (shaded boxes) external compression. +, Excitation; -, inhibition; CVS, cardiovascular system; NTS, nucleus tractus solitarius; ABP, arterial blood pressure.

 

In conclusion, we have shown that external lower leg compression prevents the rise in BRS expected during a phase of local circulatory occlusion after calf muscle exercise. This result is compatible with muscle mechanoreceptor activation by calf muscle compression and supports the idea that this additional mechanoreceptor afferent activity can modify baroreflex-driven excitation of cardiac vagal motoneurons.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This work is supported by the British Heart Foundation (PG/99148).


   FOOTNOTES
 

Address for reprint requests and other correspondence: C. A. Carrington, School of Sport and Exercise Sciences, Univ. of Birmingham, Edgbaston, Birmingham B15 2TT, UK (E-mail: C.A.Carrington{at}bham.ac.uk).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
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 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

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