| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 School of Sport and Exercise Science, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
(Received 23 September 2004;
accepted after revision 26 January 2005; first published online 11 February 2005)
Corresponding author M. P. D. Bell: School of Sport and Exercise Science, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. Email: mpb106{at}bham.ac.uk
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The contribution of a mechanically mediated afferent reflex is more difficult to assess in human exercise as central command will always accompany voluntary muscular contraction and so may obscure the influence of concurrent mechanoreceptor activation. This may explain the difficulties encountered in identifying the role of the muscle mechanoreflex on cardiovascular control in man. Observations that electrically evoked exercise, which removes central command, can elicit similar cardiovascular responses to those produced voluntarily (albeit with a one-beat delay in the case of the increase in heart rate (HR) at exercise onset) (Iwamoto et al. 1987; Bull et al. 1989) suggest that other mechanisms can ‘deputise’ for central command under these conditions. The immediacy of the HR rise during evoked exercise suggests mechanoreflex involvement, and a vagal mediation of this response is becoming increasingly clear (Hollander & Bouman, 1975; Maciel et al. 1987; Al Ani et al. 1997; Gladwell & Coote, 2002). This reflex vagal withdrawal has also been demonstrated in resting subjects using sustained passive stretch of the muscle (Murata & Matsukawa, 2001; Gladwell & Coote, 2002). Although afferent activity has been noted in response to both stretch and compression of animal skeletal muscle (Kniffki et al. 1978; Kaufman et al. 1983), external compression of human skeletal muscle has been found to be a relatively ineffective stimulus for HR change (McClain et al. 1994; Williamson et al. 1994; Carrington et al. 2003). Nevertheless, external compression of muscle has consistently been shown to elicit a rise in blood pressure in both animals (Osterziel et al. 1984; Stebbins et al. 1988) and man (McClain et al. 1994; Williamson et al. 1994).
During exercise, both mechanosensitive and metabosensitive pathways may be simultaneously activated, and so the interaction of these two inputs during exercise becomes important. Blood pressure and muscle sympathetic nerve activity (MSNA) response to a standard external muscular compression stimulus or voluntary contraction are augmented during conditions that would be expected to enhance metaboreceptor activity (McClain et al. 1994; Williamson et al. 1994; Herr et al. 1999), suggesting an interaction between mechanoreception and metaboreception. However, these studies have not attempted to examine carefully this interaction nor could they quantify the dependence of the mechanoreflex response on the concurrent level of muscle metaboreflex stimulation or in the case of Herr et al. (1999) exclude a role for central command.
Therefore, in this study we sought to perform a systematic investigation of the influence of the level of muscle metaboreflex stimulation on the cardiovascular response observed during a standard external mechanical stimulus. By performing various intensities of ischaemic isometric exercise we sought to adjust the degree of muscle metaboreflex activation and to then impose a standard external compression during PECO. We hypothesised that one of three responses to the combination of metabolic and mechanical stimuli were possible. (1) A constant compression-induced cardiovascular response during PECO, independent of preceding exercise intensity, indicating no metabolic sensitivity of the response to standardised compression. (2) An increase in the cardiovascular response to standardised compression, dependent upon the preceding exercise, suggesting metabolite sensitisation of the mechanoreceptive pathway. (3) An attenuating response to mechanical compression as exercise intensity increased, indicating that metabolic and mechanically activated (polymodal) afferents compete for a common pathway.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Prior to experimental measurements, subjects were habituated with all apparatus and protocols. They then returned on a further eight occasions to perform a series of trials assigned in a randomised order. Each of these trials involved a period of isometric calf exercise at a predetermined level of maximal voluntary contraction (MVC). The MVC of each subject was determined prior to each trial using a purpose-designed dynamometer as previously described by Bull et al. (1989). Subjects were instrumented and seated in the apparatus with the thigh of their dominant leg horizontal and their lower leg secured at an angle of 85 deg to the foot. The upward force generated by plantar flexion of the foot was then transduced and displayed on a chart recorder, and sampled by an analog to digital converter (1401 plus, Cambridge Electronic Design, Cambridge, UK) and personal computer. Subjects' MVCs were assessed as the best of at least three efforts (required to be within ± 5% of one another) with a 1-min rest between efforts.
Each trial comprised a 2.5-min period of rest, followed either by a 1.5-min period of rest (control) or by voluntary exercise at one of the following exercise intensities: 20, 30, 40, 50, 60, 70 or 80% of subjects' predetermined MVC. Immediately prior to the commencement of exercise, a thigh cuff (Hokansen CC22) was inflated to supra-systolic pressure (200 mmHg, Hokansen E20 Rapid Cuff Inflator supplied by AG101 Cuff Inflator Air Source), and this cuff remained inflated throughout the exercise period and for a further 3 min post exercise. After the first minute of PECO, a second cuff (Hokansen CC22) situated around the calf, was rapidly inflated to 300 mmHg, and this calf compression was maintained for 1 min. On deflation of the calf cuff, and with the thigh cuff inflation maintained, subjects rested for further 1-min period prior to thigh cuff deflation. The subjects then remained seated for a 2-min recovery period.
Blood pressure was continuously monitored on a beat-to-beat basis throughout the protocol, using a 2300 Finapres (Ohmeda) placed around the middle finger of the left hand, which was supported at heart level by means of an adjustable stand. ECG was monitored using a three-lead ECG (Cardiorater CR7, Cardiac Records). The signal was amplified and sampled (1000 Hz) by an analog to digital converter and analysed on a personal computer using Spike 2 data analysis software (Cambridge Electronic Design).
Statistics
Data for blood pressure changes during protocol are presented as group mean 15-s ensemble average changes from rest (S.D.), unless otherwise stated. The terms PRE-COMP, COMP and POST-COMP refer to the group mean values relative to rest for the 1-min periods preceding compression, during compression and following compression, respectively. Statistical analysis was achieved by repeated measures analysis of variance (ANOVA) of rest, end exercise, PRE-COMP, COMP and POST-COMP blood pressure changes relative to rest (Table 1, Figs 2 and 3) and linear regression of group mean post-exercise blood pressure values with the compression-induced blood pressure increases (Fig. 4). Orthogonal polynomial comparisons of the ANOVA data from Fig. 2 were examined to determine the significance and contribution of any quadratic and/or linear trends. Planned contrasts of the compression-induced blood pressure changes were performed to determine whether each value was significantly different from the preceding value (Fig. 3). The criterion for statistical significance was P < 0.05.
|
|
|
|
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
All subjects were able to perform the control trial and 90 s of sustained isometric exercise at intensities from 20 to 70%. At 80% MVC subjects were unable to sustain a constant force for the whole exercise period, with force declining rapidly after the first 20–30 s of the contraction. In those who completed the 70 and 80% MVC trials the force levels at exercise onset obviously differed but due to the rapid fatigue of the muscle at 80% MVC the force–time integral over the duration of exercise was found to be not significantly greater than that at 70% MVC. Three subjects were unable to complete the 80% MVC trial and withdrew from the study, without having completed all of their randomised trials. This therefore resulted in only eight of the subjects completing all eight trials. However all 11 subjects completed trials from 30 to 70% MVC.
Blood pressure
Figure 1 shows the mean changes in mean arterial pressure (MAP) during the course of the protocol during the 50% trial (this is representative of the directional changes observed during all trials though obviously the magnitude of the changes differed between conditions). During the rest period MAP averaged 92 (6) mmHg, and did not differ significantly between trials. Upon exercise MAP increased progressively throughout the exercise period and the end-exercise values were significantly (P < 0.01) dependent upon the intensity of exercise performed, with the exception of the 80% MVC trial which was not significantly different from the 70% MVC trial (Table 1). Subsequently, during the 1 min PRE-COMP period, MAP recovered to a level that was still significantly higher than during rest. The magnitude of the increase from rest was significantly associated with the preceding exercise intensity (P < 0.01), for PRE-COMP, COMP and POST-COMP. However, there was no difference between the responses following 70 and 80% MVC in the eight subjects who performed all trials (Table 1). In this group of subjects, COMP elicited a significant increase in MAP in all trials compared with both the PRE-COMP and POST-COMP MAP levels (P < 0.01 in both cases). The magnitude of this effect was dependent on the preceding exercise intensity performed (P < 0.05). However, there was no significant difference in the magnitude of response between 70 and 80% MVC trials, or between 0, 20 and 30% MVC trials. Upon cessation of compression (POST-COMP), MAP fell back towards PRE-COMP values but in all cases MAP remained slightly, though significantly (P < 0.01), above PRE-COMP levels (Table 1). On removal of the circulatory occlusion, blood pressure rapidly returned to resting levels following all exercise trials.
|
When the MAP increase due to compression was examined in relation to the change in baseline MAP during the combined PECO period (the post exercise ‘background’ level), a clear linear relationship was found between baseline MAP change and compression-induced MAP increase (Fig. 4). It is also clear that there was very little difference between the MAP increases caused during PECO following the 30 and 40% MVC trials; accordingly, the COMP-induced MAP change is also very similar.
Heart rate
At rest, the average HR was 64 (10.5) beats min–1. This did not differ between trials. During exercise, HR increased from resting values progressively during the 1.5-min isometric contraction at all exercise intensities, but was unchanged during the control trial. At exercise cessation, HR returned to resting levels within 30 s. HR was significantly higher during the first 30 s of PRE than in the rest of PECO in each trial, as it did not fall instantaneously following exercise cessation (see Fig. 1). However, there is no statistically significant variation in HR between the subsequent 30 s averages during PECO (encompassing PRE-COMP, COMP and POST-COMP). Overall taken as 1-min averages, HR during these three periods (PRE-COMP, COMP and POST-COMP) did not differ significantly. Furthermore, these 1-min average values during PECO were not different to those obtained during the rest period.
In the 11 subjects who completed trials at 30 to 70% MVC, the results obtained were similar in direction and magnitude to those presented for end exercise in Table 1 for the eight subjects who completed trials at 0 to 80% MVC.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
External compression of muscle is an established tool for evoking increases in intramuscular pressure (Matsen et al. 1976; Reneman et al. 1980), and would therefore be assumed to evoke responses from pressure-sensitive afferents (Paintal, 1960; Kniffki et al. 1978). The most novel finding of this study is that the effect of compression on MAP is dependent on the preceding exercise intensity (Fig. 3).
Other studies have observed augmented MSNA responses to external compression (McClain et al. 1994; Fu et al. 1998). Such modulation of sympathetic outflow could conceivably account for the blood pressure changes reported in the present study.
The afferent origin of this reflex is unclear. If the effect of compression was mediated by ‘pure’ mechanoreceptors, sensitive only to mechanical stress, then a constant compression stimulus would be expected to elicit a constant response (our hypothesis 1, see Introduction). However, as the MAP response instead varies depending on the blood pressure level onto which the compression is superimposed (Fig. 4), it appears that there is some influence of the mechanical reflex by local muscular metabolic conditions (our hypotheses 2 and 3, see Introduction). Adreani & Kaufman (1998) investigated the discharge properties of group III and IV afferents during dynamic exercise and found them to be augmented during occlusion, suggesting that retention of exercise-induced metabolite accumulation can enhance the response of these afferents. Kaufman et al. (1983), measuring afferent impulses in cats, found that during static muscular contraction, approximately half of group III afferent exhibited a ‘secondary’ response; after their initial response, their firing rate increased again with a latency suggesting the involvement of increasing metabolic levels. These studies indicate the presence of a metaboreflex–mechanoreflex interaction. The precise nature of this interaction is as yet unclear. However, in light of our earlier hypotheses, the sensitisation effect of the metaboreceptor activation shows no signs of saturation within the range of exercise intensities we studied, and we must therefore conclude that the activation of the afferent population does not reach saturation (hypothesis 3), as would evince a distinct polymodal afferent population. However, we are careful not to negate this possibility, as we found that the force–time integrals between 70 and 80% MVC were no different, and consequently the post-exercise blood pressure was no different, therefore this protocol is limited in the metaboreceptor activation it can induce. Perhaps in future studies a greater post-exercise blood pressure rise can be evoked and a saturation effect will be seen. Based on the available data we must conclude that a sensitisation of the mechanoreflex response to external compression has occurred (hypothesis 2). Compression-induced MAP changes at 0, 20, 30 and 40% MVC are small and do not significantly differ from one another. From these results therefore it would appear that a minimum metabolic accumulation is necessary to provoke this response, and that, in this human calf muscle model, 30–40% MVC isometric contractions are sufficient to induce this requisite accumulation. Figures 3 and 4 indicate that above this level the response to compression increases linearly with exercise intensity or blood pressure increase induced by this exercise. Williamson et al. (1994) used external compression of the lower leg of up to 90 mmHg, and observed compression-induced MAP responses; these responses were, however, abolished when occlusion was removed. The aforementioned study of McClain et al. (1994) found that no compression-induced MSNA response was observed at rest. Mense & Stahnke (1983) noted this interaction in cats, observing the responses of afferents that during ischaemic work were augmented by accumulation of some unspecified substance sufficiently as to allow a previously ineffective mechanical stimulus to become potent. Overall this evidence and our present findings that responses to compression are not manifest in the absence of metaboreceptor stimulus suggest that the observed effects of compression are not mediated exclusively by mechanoreceptors. Putative factors in this response include bradykinin (Mense & Meyer, 1988) and arachidonic acid (Rotto et al. 1990), which have thus far been shown to exhibit these sensitisation properties when exogenously administered. However, the identity of this substance has yet to be conclusively ascertained in vivo.
The present findings suggest that the compression-induced MAP effect does not attenuate over the period of time involved in this study (there was no significant difference between the four 15-s average MAP values during the 1 min of compression), and that the afferent response does not adapt as long as the metabolic and mechanical stimuli remain intact. This is contrary to the reported effects of another form of mechanoreceptor stimulus, that of passive muscular stretch. Stretch has repeatedly been reported to evoke a vagally induced HR increase at the onset of exercise (Stebbins et al. 1988; Al Ani et al. 1997; Gladwell & Coote, 2002), a response which attenuates over time. This suggests that these modes of mechanical stimulation evoke distinct and separate afferent populations. Indeed recent observations from our laboratory show that responses to stretch during PECO are independent of preceding exercise intensity (Fisher et al. 2004).
Another pertinent point of this study is that this compression-induced blood pressure increase was unaccompanied by bradycardia, as would be expected from an unmodified baroreflex. McWilliam & Yang (1991) showed that baroreflex-induced R–R interval prolongation in response to a standard baroreflex stimulus could be attenuated by peroneal stimulation of group III and IV afferents. They concluded that vagal baroreflex sensitivity was reduced by activation of group III and IV afferents. Previous work from this laboratory has also shown a decrease in baroreflex sensitivity during external compression (Carrington et al. 2003). Other work suggests a resetting of the baroreflex stimulus response to a higher blood pressure ‘set point’ (Potts & Mitchell, 1998). Either of these outcomes could clarify our observations that the HR during COMP remains unaltered despite a progressively augmented MAP response. Unfortunately the duration of the PECO phases in the present experiments made it impossible to perform sequence analysis to ascertain baroreflex sensitivity.
Although this protocol employs a relatively high compression stimulus, it must be noted that subjects did not report that they perceived it as painful. Neither did the compression elicit any change in HR, as might be expected from nociceptor stimulation. Indeed the metabolic and mechanical stimuli which we applied in this study can occur in human muscle under normal working conditions and therefore can be regarded as falling within the normal ergoreceptive range. Matsen et al. (1976), and Sadamoto et al. (1983) have shown that degree of external compression has a linear relationship with the resultant intramuscular pressure, and that most (> 90%) of the pressure applied is transmitted to the muscle. We would therefore expect the intramuscular pressure during the compression stage of this study to approach 300 mmHg. Accordingly, several studies have demonstrated that intramuscular pressure values measured during voluntary exercise can approach and even exceed this magnitude (Sadamoto et al. 1983; Sejersted et al. 1984; Aratow et al. 1993; Ballard et al. 1998). Sadamoto et al. (1983) extrapolated their results from plantar flexion of the foot at levels up to 80% of MVC to estimate intramuscular pressure in the soleus and gastrocnemius of 271 mmHg. Even this may be less than the true value during high intensity muscle contractions as it has been observed that linear extrapolation of submaximal intramuscular pressure values may underestimate the value at MVC (Sejersted et al. 1984). Additionally, Barcroft & Millen (1939) demonstrated that circulation to the human calf muscles was occluded at only 20% MVC. Therefore we can conclude that the ischaemic, high intramuscular pressure conditions of our PECO phase with external compression are commonly replicated during voluntary exercise and are therefore of physiological relevance.
In conclusion, the novel finding of the present study is that a standardised stimulus, external muscle compression, is capable of eliciting a pressor response, the magnitude of which depends upon the prevailing level of muscle metaboreflex stimulation. Other studies have shown that external compression of human muscle is capable of eliciting a cardiovascular response (McClain et al. 1994; Williamson et al. 1994) and that the blood pressure changes appear to vary with both the muscle mass compressed (Williamson et al. 1994) and the degree of external compression of the muscle (Stebbins et al. 1988). Dependence of the response to compression upon intramuscular metabolic conditions may now also be considered a factor in this increasingly complex story. We suggest that this metaboreflex-dependent response cannot be served by a distinct, solely mechanosensitive afferent population but instead must reflect the involvement of muscle afferents receptive to a combination of mechanical and metabolic stimuli.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Alam M & Smirk FH (1937). Observations in man upon a blood pressure raising reflex arising from the voluntary muscles. J Physiol 89, 372–383.
Al Ani M, Robins K, al Khalidi AH, Vaile J, Townend J & Coote JH (1997). Isometric contraction of arm flexor muscles as a method of evaluating cardiac vagal tone in man. Clin Sci 92, 175–180.[Medline]
Aratow
M, Ballard
RE, Crenshaw
AG, Styf
J, Watenpaugh
DE, Kahan
NJ
&
Hargens
AR (1993). Intramuscular pressure and electromyography as indexes of force during isokinetic exercise. J Appl Physiol
74, 2634–2640.
Ballard
RE, Watenpaugh
DE, Breit
GA, Murthy
G, Holley
DC
&
Hargens
AR (1998). Leg intramuscular pressures during locomotion in humans. J Appl Physiol
84, 1976–1981.
Barcroft H & Millen JLE (1939). The blood flow through muscle during sustained contraction. J Physiol 97, 17–31.
Bull
RK, Davies
CTM, Lind
AR
&
White
MJ (1989). The human pressor response during and following voluntary and evoked isometric contraction with occluded local blood supply. J Physiol
411, 63–70.
Carrington
CA, Ubolsakka
C
&
White
MJ (2003). Interaction between muscle metaboreflex and mechanoreflex modulation of arterial baroreflex sensitivity in exercise. J Appl Physiol
95, 43–48.
Coote
JH, Hilton
SM
&
Perez-Gonzalez
JF (1971). The reflex nature of the pressor response to muscular exercise. J Physiol
215, 789–804.
Coote
JH
&
Perez-Gonzalez
JF (1970). The response of some sympathetic neurones to volleys in various afferent nerves. J Physiol
208, 261–278.
Fisher JP, Bell MPD & White MJ (2004). The cardiovascular response to human calf muscle stretch is independent of the level of concurrent muscle metaboreflex stimulation. J Physiol 560P, C14.
Fu
Q, Sugiyama
Y, Kamiya
A, Shamsuzzaman
AS
&
Mano
T (1998). Responses of muscle sympathetic nerve activity to lower body positive pressure. Am J Physiol
275, H1254–H1259.
Gladwell
VF
&
Coote
JH (2002). Heart rate at the onset of muscle contraction and during passive muscle stretch in humans: a role for mechanoreceptors. J Physiol
540, 1095–1102.
Goodwin
GM, McCloskey
DI
&
Mitchell
JH (1972). Cardiovascular and respiratory responses to changes in central command during isometric exercise at constant muscle tension. J Physiol
226, 173–190.
Herr
MD, Imadojemu
V, Kunselman
AR
&
Sinoway
LI (1999). Characteristics of the muscle mechanoreflex during quadriceps contractions in humans. J Appl Physiol
86, 767–772.
Hollander
AP
&
Bouman
LN (1975). Cardiac acceleration in man elicited by a muscle-heart reflex. J Appl Physiol
38, 272–278.
Iwamoto
GA, Mitchell
JH, Mizuno
M
&
Secher
NH (1987). Cardiovascular responses at the onset of exercise with partial neuromuscular blockade in cat and man. J Physiol
384, 39–47.
Kaufman
MP, Longhurst
JC, Rybicki
KJ, Wallach
JH
&
Mitchell
JH (1983). Effects of static muscular contraction on impulse activity of groups III and IV afferents in cats. J Appl Physiol
55, 105–112.
Kaufman
MP, Rybicki
KJ, Waldrop
TG
&
Ordway
GA (1984). Effect of ischemia on responses of group III and IV afferents to contraction. J Appl Physiol
57, 644–650.
Kniffki KD, Mense S & Schmidt RF (1978). Responses of group IV afferent units from skeletal muscle to stretch, contraction and chemical stimulation. Exp Brain Res 31, 511–522.[Medline]
Krogh A & Lindhard JA (1917). Comparison between voluntary and electrically evoked muscular work in man. J Physiol 51, 182–201.
Maciel BC, Gallo JL, Marin Neto JA & Martins LE (1987). Autonomic nervous control of the heart rate during isometric exercise in normal man. Pflugers Arch 408, 173–177. 10.1007/BF00581348[CrossRef][Medline]
McClain
J, Hardy
C
&
Sinoway
L (1994). Forearm compression during exercise increases sympathetic nerve traffic. J Appl Physiol
77, 2612–2617.
McCloskey
DI
&
Mitchell
JH (1972). Reflex cardiovascular and respiratory responses originating in exercising muscle. J Physiol
224, 173–186.
McWilliam
PN
&
Yang
T (1991). Inhibition of cardiac vagal component of baroreflex by group III and IV afferents. Am J Physiol
260, H730–H734.
Matsen FA III, Mayo KA, Sheridan GW & Krugmire RB Jr (1976). Monitoring of intramuscular pressure. Surgery 79, 702–709.[Medline]
Mense
S
&
Meyer
TE (1988). Bradykinin-induced modulation of the response behaviour of different types of feline group III and IV muscle receptors. J Physiol
398, 49–63.
Mense
S
&
Stahnke
M (1983). Responses in muscle afferent fibres of slow conduction velocity to contractions and ischaemia in the cat. J Physiol
342, 383–397.
Murata J & Matsukawa K (2001). Cardiac vagal and sympathetic efferent discharges are differentially modified by stretch of skeletal muscle. Am J Physiol 280, H237–H245.
Osterziel KJ, Julius S & Brant DO (1984). Blood pressure elevation during hindquarter compression in dogs is neurogenic. J Hypertens 2, 411–417.[Medline]
Paintal AS (1960). Functional analysis of group III afferent fibres of mammalian muscles. J Physiol 152, 250–270.
Potts
JT
&
Mitchell
JH (1998). Rapid resetting of carotid baroreceptor reflex by afferent input from skeletal muscle receptors. Am J Physiol
275, H2000–H2008.
Reneman RS, Slaaf DW, Lindbom L, Tangelder GJ & Arfors KE (1980). Muscle blood flow disturbances produced by simultaneously elevated venous and total muscle tissue pressure. Microvasc Res 20, 307–318. 10.1016/0026-2862(80)90031-X[CrossRef][Medline]
Rotto
DM, Schultz
HD, Longhurst
JC
&
Kaufman
MP (1990). Sensitization of group III muscle afferents to static contraction by arachidonic acid. J Appl Physiol
68, 861–867.
Rowell
LB, Hermansen
L
&
Blackmon
JR (1976). Human cardiovascular and respiratory responses to graded muscle ischemia. J Appl Physiol
41, 693–701.
Rowell
LB
&
O'Leary
DS (1990). Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes. J Appl Physiol
69, 407–418.
Sadamoto T, Bonde-Petersen F & Suzuki Y (1983). Skeletal muscle tension, flow, pressure, and EMG during sustained isometric contractions in humans. Eur J Appl Physiol Occup Physiol 51, 395–408.[CrossRef][Medline]
Sejersted
OM, Hargens
AR, Kardel
KR, Blom
P, Jensen
O
&
Hermansen
L (1984). Intramuscular fluid pressure during isometric contraction of human skeletal muscle. J Appl Physiol
56, 287–295.
Stebbins
CL, Brown
B, Levin
D
&
Longhurst
JC (1988). Reflex effect of skeletal muscle mechanoreceptor stimulation on the cardiovascular system. J Appl Physiol
65, 1539–1547.
Williamson
JW, Mitchell
JH, Olesen
HL, Raven
PB
&
Secher
NH (1994). Reflex increase in blood pressure induced by leg compression in man. J Physiol
475, 351–357.
This article has been cited by other articles:
|
|
 |
|
  J. Cui, R. Moradkhan, V. Mascarenhas, A. Momen, and L. I. Sinoway Cyclooxygenase inhibition attenuates sympathetic responses to muscle stretch in humans Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2693 - H2700. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. C. Drew, M. P. D. Bell, and M. J. White Modulation of spontaneous baroreflex control of heart rate and indexes of vagal tone by passive calf muscle stretch during graded metaboreflex activation in humans J Appl Physiol, March 1, 2008; 104(3): 716 - 723. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Cui, V. Mascarenhas, R. Moradkhan, C. Blaha, and L. I. Sinoway Effects of muscle metabolites on responses of muscle sympathetic nerve activity to mechanoreceptor(s) stimulation in healthy humans Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2008; 294(2): R458 - R466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Nishiyasu, T. Maekawa, R. Sone, N. Tan, and N. Kondo Effects of rhythmic muscle compression on cardiovascular responses and muscle oxygenation at rest and during dynamic exercise Exp Physiol, January 1, 2006; 91(1): 103 - 109. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P Fisher, M. P. D Bell, and M. J White Cardiovascular responses to human calf muscle stretch during varying levels of muscle metaboreflex activation Exp Physiol, September 1, 2005; 90(5): 773 - 781. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
MAP (S.E.M) during compression (mmHg) = 0.33 x MAP change from baseline during PECO (mmHg) – 1.45 mmHg. n= 11; R2= 0.93; P < 0.01.