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1 School of Sport and Exercise Sciences, University of Birmingham, Birmingham B15 2TT, UK
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Abstract |
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(Received 31 March 2005;
accepted after revision 7 July 2005; first published online 27 July 2005)
Corresponding author J. P. Fisher: School of Sport and Exercise Science, University of Birmingham B15 2TT, UK. Email: j.p.fisher{at}bham.ac.uk
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Introduction |
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When muscle mechanoreceptors are stimulated in isolation in an animal model, using muscle stretch, they have been shown to produce a decrease in cardiac vagal activity and an increase in cardiac and renal sympathetic nerve activity and blood pressure (Stebbins et al. 1988; Matsukawa et al. 1994; Wilson et al. 1994; Murata & Matsukawa, 2001). In human studies the cardiovascular responses to passive muscle stretch have been found to be more equivocal. Baum et al. (1995) demonstrated a progressive blood pressure increase but no heart rate change during sustained calf stretch. However, Gladwell & Coote (2002) and Gladwell et al. (2005) provided strong evidence for a vagally mediated increase in heart rate in the absence of a change in blood pressure at the onset of calf stretch.
More recent research using an animal model which closely mimics dynamic exercise suggests that metabo- and mechanoreceptors have polymodal properties (Adreani et al. 1997; Adreani & Kaufman, 1998) and that muscle ischaemia potentiates the firing of group III and IV afferents during muscle contraction (Mense & Stahnke, 1983; Adreani & Kaufman, 1998). Furthermore, intra-arterial injection of arachidonic acid increases the firing rate of group III, but not group IV, muscle afferents in response to evoked muscle contraction (Kaufman & Rybicki, 1987; Rotto et al. 1990). Recently, in human subjects we demonstrated that the cardiovascular response to calf compression was augmented in proportion to the level of muscle metaboreflex activation maintained during a period of postexercise circulatory occlusion (Bell & White, 2005). This is clear evidence for the sensitization of muscle mechanoreceptive afferents in man, where there is no potential for contamination by the presence of central command (Sterns et al. 1991; Herr et al. 1999). However, Leshnower et al. (2001) found no evidence for metabolic sensitization of mechanoreceptive muscle afferents in cat muscle, since they were unable to demonstrate that there was an augmented cardiovascular response during concurrent evoked muscle contraction and passive stretch.
The purpose of the present study was to investigate whether the cardiovascular response to a standard muscle stretch was altered by varying the metabolic conditions within the muscle. The muscle metaboreflex was manipulated by occluding the circulation to the calf muscles following exercise at varying levels of intensity (Alam & Smirk, 1937). The advantage of our experimental model is that the interaction between a standard mechanical stimulus and a controlled metabolic stimulus can be investigated in the absence of central command in humans. On the basis of our previous study (Bell & White, 2005) we hypothesized that the cardiovascular response to passive muscle stretch would be progressively greater when imposed upon a muscle with progressively elevated muscle metaboreflex activation.
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Methods |
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Experimental protocol
Subjects were seated in a semisupine position in the Biodex System 3 Pro (Biodex Medical Systems, Shirley, NY, USA) with the right knee flexed by 30 deg and the foot firmly strapped to the ankle plantar/dorsiflexion attachment. Velcro straps were placed across the top of the foot and a three-piece strap was positioned around the ankle to minimize heel lift (Harridge & White, 1993). The maximum voluntary contraction (MVC) of the calf plantar flexors was assessed by taking the highest torque produced in three maximal efforts. Calf muscle stretch was assessed by manually dorsiflexing the foot to the end of the comfortable range of motion. Throughout the experimental protocols subjects breathed in time to a metronome set to maintain a respiratory rate that was comfortable for each individual.
The experimental protocol is illustrated in Fig. 1. After subjects had been seated quietly for 15 min a 2 min baseline period was conducted. After 115 s of rest a cuff was inflated around the thigh of the right leg to 200 mmHg using a rapid inflation unit (E20, Hokanson, Bellevue, WA, USA; Bell & White, 2005). Five seconds later subjects were then instructed to contract their calf muscles to elicit a torque equivalent to the predetermined level (0, 30, 50 or 70% MVC), which was displayed on a computer screen directly in front of them. After 90 s of isometric calf plantar flexor exercise subjects were told to stop contracting their calf muscles. The thigh cuff then remained inflated for a further 3.5 min. After 90 s of this postexercise circulatory occlusion (PECO) phase the foot was passively dorsiflexed to the predetermined angle by the isokinetic dynamometer at a velocity of 30 deg s–1. This position was maintained for 60 s, following which a further 60 s of PECO was conducted. The thigh cuff was then released and a 2 min recovery period was performed. Each subject performed two trials at exercise intensities of 30, 50 and 70% MVC. Two rest trials were also conducted where no exercise was performed (0% MVC). No more than two trials were performed on any day and these were separated by at least 20 min, and re-establishment of resting baseline was ensured before commencing the subsequent trial. The order of all trials was counterbalanced according to a Latin square design.
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Heart rate (HR) was measured using a three-lead ECG (Cardiorater CR7, Cardiac Records Ltd, London, UK) in lead II position. Blood pressure was non-invasively monitored from the middle finger of the right hand supported at the height of the heart, using a Finapres system (Ohmeda 2300, Louisville, CO, USA). The phase of the respiratory cycle was measured using a band placed around the chest and attached to a strain gauge. Ankle plantar flexor torque, angle and speed of rotation were monitored using a Biodex System 3 Pro, isokinetic dynamometer (Biodex Medical Systems, Shirley, NY, USA). All outputs underwent analog-to-digital conversion using a 1401plus (Cambridge Electronic Design 1401plus, CED, Cambridge, UK). HR was sampled at 1000 Hz, whilst all other signals were sampled at 100 Hz. Data was recorded using Spike 2 software (CED) and analysed using custom-written script files and Microsoft Excel macros. HR variability was calculated over pertinent time points during the protocol using the square root of the mean of the sum of successive differences (RMSSD). This estimate of short-term high-frequency variations in HR is an index of vagal tone (Task Force of European Society of Cardiology, 1996). HR variability analysis was recorded using Nevrokard® HRV software (version 6.4.0, Medistar, Slovenia).
Electromyogram (EMG) was recorded from the gastrocnemius and soleus muscles of the right leg during the 0% trial. EMG was detected using custom-built bipolar, silver surface electrodes (10 mm diameter, 17 mm centre to centre) containing a skin-mounted preamplifier (x1000) encapsulated in epoxy resin (Johnson et al. 1977). Prior to application of the surface electrodes, the site was prepared by removal of dead skin by gentle abrasion and cleaning with alcohol. Conducting gel was applied to the electrodes before they were placed on the central portion of each muscle belly in a direction parallel to muscle fibre orientation. Movement artefacts were minimized by taping the electrodes and wires to the skin. Analog EMG signals were amplified and converted to digital, at a sampling frequency of 1700 Hz, then recorded using Spike 2 software.
Statistical analysis
Using a custom-written Spike 2 file, raw data files were analysed to produce beat-to-beat values for HR, systolic blood pressure (SBP), mean arterial pressure (MAP) and diastolic blood pressure (DBP). Ensemble averages were calculated over 15 s epochs for each subject and then averaged to produce a group mean ± S.E.M. Time series analysis for the effect of time and condition during each experimental phase was performed using repeated measures ANOVA with Greenhouse–Geisser correction (Ludbrook, 1994). Post hoc analysis was performed using Student's paired t tests with a Bonferroni correction. Differences in the group minute averages taken before, during and after Stretch were analysed using MANOVA. Statistical significance was taken as P < 0.05.
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Results |
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The MVC recorded prior to commencing the experimental protocol was not significantly different between conditions (142.3 ± 11.5, 137.9 ± 12.1 and 134.9 ± 10.9 N m for 30, 50 and 70% MVC, respectively). These values are similar to those reported previously for the ankle plantar flexors (Sale et al. 1982; Harridge & White, 1993). The MVCs yielded target forces of 42.7 ± 3.4, 68.9 ± 6.1 and 94.4 ± 7.6 N m for the 30, 50 and 70% conditions, respectively. The foot position during calf muscle Stretch was not significantly different between conditions. During Stretch the subjects did not report any sensations of pain and no increase in EMG was detected in the rest (0%) condition.
No significant difference was found in the torque produced during Stretch in the 70, 50 and 30% trials, which reached 31.5 ± 0.02, 36.1 ± 1.1 and 30.3 ± 0.8 N m, respectively. This equated to 22, 26 and 22% of the MVC produced prior to the 70, 50 and 30% trials, respectively. However, there was a significant effect of time on torque over the Stretch period when it was expressed as 15 s averages. In all conditions, the torque elicited by Stretch fell from initial levels, but was maintained at 89 ± 1.1% of this value by the end of the Stretch period.
Cardiovascular measurements
There were no significant differences between resting values for MAP, DBP and HR prior to the 0, 30, 50 and 70% MVC trials (Table 1). The group mean resting SBP was significantly higher in the 70% trial in comparison with the 0% trial.
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Discussion |
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The simplest explanation of our findings is that stretch stimulates a mechanically sensitive afferent population of nerves whose response is unaffected, i.e. not sensitized, by the metabolic conditions within the muscle. Gladwell & Coote (2002) and Gladwell et al. (2005) showed that passive calf muscle stretch causes a vagally mediated HR increase in humans. Our data show that this HR rise was maintained when muscle metaboreflex activation was elevated to different levels. Kaufman & Rybicki (1987) demonstrated that whilst ischaemia increased the responses of 47% of the group IV afferents recorded during evoked exercise, the activity of only 13% of group III afferents was increased. Those group III afferents that were not sensitized by ischaemia were particularly responsive to tendon stretch. Additionally, Leshnower et al. (2001) were unable to demonstrate that the metabolic sensitization of mechanically sensitive muscle afferents translated into a greater cardiovascular response. When muscle stretch was combined with evoked muscle contractions in anaesthetized cats, the cardiovascular responses to this combined mechanical stimulus were no greater than those produced by constant passive stretch at a matched tension. Furthermore, in man, both Williamson et al. (1994) and Gallagher et al. (2001) demonstrated that the application of lower body positive pressure, thought to activate muscle mechanoreceptors and some muscle metaboreceptors (unavoidably, because of venous outflow restriction), produced similar increases in blood pressure at rest and during dynamic exercise of increasing intensity. These findings seemingly support a view that mechanical stimulation, i.e. passive stretch, might have a consistent effect irrespective of the metabolic background.
Contrary to this view, many previous studies in animals have demonstrated that the responses of mechanically sensitive group III muscle afferents to muscle contraction are potentiated by muscle ischaemia and intra-arterial injection of arachidonic acid or bradykinin (Mense & Stahnke, 1983; Kaufman & Rybicki, 1987; Rotto et al. 1990; Adreani & Kaufman, 1998). In addition, Herr et al. (1999) argued that in human subjects the muscle mechanoreflex could be sensitized by the metabolites produced during exercise. This belief was based upon their observations that muscle sympathetic nerve activity (MSNA) increased during repeated isometric quadriceps contractions at 25% MVC, where metabolic stimulation would be expected to increase from trial to trial though mechanical stimulation would be constant. However, a limitation of this study was that central command was present during exercise and this too would be expected to increase progressively throughout the trials, eventually reaching a level that could influence MSNA (Victor et al. 1995; Gandevia, 2001; Adam & De Luca, 2003). An important advantage of the present study is that central command was excluded during PECO and Stretch; therefore our observations must be accounted for purely by muscle afferent activation.
There was a trend for the Stretch-induced HR increase to be smaller in the 70% condition (Fig. 5), which may suggest the inhibitory involvement of the baroreflex. During isolated muscle metaboreflex activation (PECO), the sympathetically mediated blood pressure elevation would increase baroreceptor activation (Mark et al. 1985), causing a reflex increase in vagal tone (Nishiyatsu et al. 1994; Fig. 6). Indeed, Gladwell et al. (2005) showed that when transmural pressure at the carotid sinus was increased using neck suction, thus increasing baroreflex activation and the level of vagal tone, the tachycardic response to passive muscle stretch was attenuated. However, in the present study RMSSD was not significantly different between conditions during the whole PECO1 phase, suggesting that the progressive elevations in blood pressure we achieved following exercise of increasing intensity and the increased baroreflex stimulation this must have caused were not sufficient to alter significantly this index of vagal tone prior to Stretch.
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The present findings could be seen to be in conflict with a recent report from our own laboratory in which we showed that the blood pressure responses to external calf muscle compression were augmented when muscle metaboreflex activation was progressively increased (Bell & White, 2005). A possible explanation for this may be that the muscle afferent populations activated by external compression at 300 mmHg and passive stretch are different. From the recent work by Gladwell et al. (2005) and Hayes et al. (2005) it seems that muscle stretch stimulates a unique population of the faster conducting group III mechanosensitive afferents which Gladwell et al. (2005) would wish to term tentonoreceptors. It is possible that those afferents which are activated by compression are more of the polymodal variety (Fig. 6) and perhaps, therefore, can be sensitized by metabolic conditions in the muscle; those activated by stretch may be thought of as ‘purer’ mechanoreceptors and so perhaps cannot be sensitized.
Limitations
A potential limitation of the present study is that we were unable to make measurements of intramuscular metabolites. However, human studies have demonstrated that isometric exercise of a similar intensity and duration clearly elicits increases in adenosine (Costa et al. 2001) and potassium (Fallentin et al. 1992) and a decrease in pH (Victor et al. 1989). Furthermore, since the classic studies of Alam & Smirk (1937) it has been established that the elevation in BP during PECO can only be explained by increased metabolic concentration, since central command and muscle mechanoreflex are inactive at this time (Alam & Smirk, 1937; Rowell et al. 1976, 1981). It follows that a graded blood pressure augmentation during PECO, reported in the present study, must be the result of an increasing metabolite accumulation.
We were unable to make MSNA measurements, though we have reported DBP as a proxy. DBP is commonly regarded as a more accurate reflection of the change in total peripheral resistance than systolic BP (Lind 1983; Carrington et al. 2001), and vascular resistance has been positively correlated with MSNA (Seals, 1989). We have previously recorded MSNA activity during 30% MVC isometric calf exercise and subsequent PECO, finding an increase of 
40% in total activity during PECO (Fisher, 2004), and we would expect much higher levels than this in the 50 and 70% trials.
Finally, EMG was not measured from the hamstrings during Stretch. This was because a cuff was inflated around the thigh at this time. However, it is unlikely that the cardiovascular responses during Stretch were due to small inadvertent hamstring contraction, since Fallentin et al. (1985) demonstrated that low-level contraction (7% MVC) produced no effect on MAP or HR over the first 5 min of contraction in human subjects.
Conclusion
The novel results of the present study show that the HR and blood pressure responses to calf muscle stretch are independent of the level of concurrent metaboreflex activation.
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, 0%; 
, 30%; 
, 50%; and •, 70% MVC. The light and dark shaded areas indicate the postexercise occlusion phases (PECO1 and PECO2) and PECO plus stretch phase (Stretch), respectively. *Significant effect of time; 
significant effect of condition (P < 0.05).
, 70% MVC. * Significant effect of time; 
