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Experimental Physiology 91.1 pp 103-109
DOI: 10.1113/expphysiol.2005.032052
© The Physiological Society 2006
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Effects of rhythmic muscle compression on cardiovascular responses and muscle oxygenation at rest and during dynamic exercise

Takeshi Nishiyasu1, Tsuyoshi Maekawa2, Ryoko Sone3, Nobusuke Tan3 and Narihiko Kondo4

1 Laboratory of Exercise Physiology, Institute of Health and Sport Sciences, University of Tsukuba 1-1-1, Tennodai, Tsukuba City, 305-8574, Japan 2 School of Medicine3 Faculty of Education, Yamaguchi University, Japan 4 Faculty of Developmental Sciences, Kobe University, Japan


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
We examined the way in which the duration of rhythmic muscle compressions affects cardiovascular responses and muscle oxygenation at rest and during dynamic exercise. We measured the mean arterial pressure (MAP), heart rate (HR) and oxygenation of the vastus lateralis muscle (by near-infrared spectroscopy) in eight healthy male subjects at rest and during supine bicycle exercise (50 and 100 W at 60 r.p.m.) while applying pulsed muscle compressions at 1000 ms intervals. Compression pressure and durations were 150 mmHg and 300, 600, 900 and 1000 ms (1000 ms being static continuous compression), respectively. During exercise, the pulsed leg compression was synchronized to each thigh extensor muscle contraction. The observed changes in muscle oxygenation were dependent on compression duration (increased at 300 ms, no change at 600 ms and decreased at 900 or 1000 ms) and were different from those seen at rest (increases at < 1000 ms and decrease at 1000 ms). This suggests that the effects of external pulsed muscle compression may have a duration threshold below which muscle pumping counteracts the obstruction to flow caused by the compression, and that the threshold is set at a shorter compression duration during exercise than at rest. Although HR and MAP did not change during pulsed compression at rest, during exercise they both increased progressively as compression duration increased. Thus, while exercising, the increased MAP and HR seen during the compression could be due to the combination and interaction of mechanical effects and the muscle mechanoreflex and/or metaboreflex.

(Received 29 August 2005; accepted after revision 5 October 2005; first published online 6 October 2005)
Corresponding author T. Nishiyasu: Laboratory of Exercise Physiology, Institute of Health and Sport Sciences, University of Tsukuba 1-1-1, Tennodai, Tsukuba City, 305-8574, Japan. Email: nisiyasu{at}taiiku.tsukuba.ac.jp


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
During rhythmic exercise, heart rate (HR), mean arterial pressure (MAP) and blood flow in the active muscles increase in proportion to graded increases in workload (Pluto et al. 1988; Rowell et al. 1996), as does the intramuscular pressure within the active muscles (Sejersted & Hargens, 1995; Ballard et al. 1998). In addition, the intramuscular veins and arteries are mechanically compressed by the muscle contractions, which probably impedes blood flow during the contraction phase; certainly blood flow is diminished during isometric muscle contraction at above 20% maximum voluntary contraction (Barcroft & Millen, 1939). Nonetheless, because the resistance vessels within active muscles are dilated by various local mechanisms, vascular conductance during the exercise actually increases more than 10-fold compared to conductance at rest (Rowell, 1993; Laughlin et al. 1996; Delp & Laughlin, 1998). This means that, although blood flow is impeded by mechanical compression during each muscle contraction, the total blood flow in the active muscles during usual rhythmic exercise is markedly increased thanks to the abrupt increases in blood flow during the relaxation phase (Rowell, 1993; Laughlin et al. 1996).

Rhythmic muscle compression can affect cardiovascular responses in several ways. As mentioned above, natural compression during muscle contraction decreases blood flow in the active muscle. However, rhythmic muscle compression can increase blood flow via the so-called muscle pump function (Stegall, 1966; Folkow et al. 1979). How the duration of the each compression affects muscle blood flow and muscle metabolism remains unknown, however. Systemic arterial blood pressure can also be affected by the duration of each muscle compression; prolonged hindrance to blood flow during more prolonged muscle contractions can lead to increases in systemic vascular resistance and, in turn, increases in systemic arterial blood pressure. Moreover, the reduction in muscle blood flow caused by prolonged mechanical compressions can change the metabolic state of the active muscle, leading to activation of the muscle metaboreflex, a neural cardiovascular reflex that originates from active muscles (Alam & Smirk, 1937; Rowell & O'Leary, 1990; O'Leary & Sheriff, 1995; Nishiyasu et al. 1998, 2000), while the muscle deformation itself can lead to activation of the muscle mechanoreflex, a second neural cardiovascular reflex originating in active muscles (McCloskey et al. 1972; Mitchell & Schmidt, 1983; Osterziel et al. 1984; Stebbins et al. 1988; Williamson et al. 1994b). Although it has been postulated that during periods of rhythmic muscle compression, increasing the duration of each compression can increase both mechanical and neural cardiovascular reflex effects, it is not known how the duration of compression affects muscle metabolism and systemic cardiovascular responses.

The aim of the present study was to test the hypothesis that rhythmic mechanical compression of leg muscles would itself induce cardiovascular responses during dynamic leg exercise in humans. In particular, we focused on the relationship between the duration of the imposed compression pulse and the bodily response to the exercise (i.e. changes in metabolic state and cardiovascular parameters).


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
We studied eight male healthy volunteers whose mean age, height and body weight were 23 ± 2 years, 170 ± 2 cm and 62 ± 2 kg, respectively. None of the subjects was receiving medication, and none smoked. The study was approved by the Human Subjects Committee at Yamaguchi University and conformed to the Declaration of Helsinki, and each subject gave informed written consent.

After entering the test room, in which the ambient temperature was kept at 27 ± 0.5°C, the subject lay down in a supine position. Each subject wore a thigh cuff (19 cm wide) fitted to each leg. While the subject rested for at least 30 min, the electrodes used to measure HR (ECG lead II) and record electromyograms (EMGs), a blood pressure cuff and near infrared spectroscopy (NIRS) probes were applied.

Figure 1 shows the experimental set-up used for the exercise session. At rest and during dynamic exercise (50 and 100 W; 60 r.p.m.) pulsed compressions (150 mmHg; 60 compressions min–1) were applied to the legs. The duration of the compression pulse was 300, 600, 900 or 1000 ms (the last being effectively static continuous compression) both at rest and during dynamic exercise. The exercise protocols were repeated with and without (control) pulse compression with an interval of at least 20 min in between.



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  		Figure 1.  Schematic illustration of the experimental set-up
The subjects performed cycle ergometry with pulsed compression of the legs (application of each leg compression was synchronized to the thigh extensor muscle contraction in the same leg).

 
During the protocols, MAP, HR and oxygenation index from NIRS (Jobsis, 1977) were measured continuously; gas parameters were measured only during exercise. Before the start of the two exercise protocols, the correct placement of the photoelectric sensors (Fig. 1) was determined with the aid of the EMG signal and cuff pressure, so that the onset of the increase in cuff pressure was synchronized with the start of each extensor muscle contraction in the same leg. Photo-reflectors were fixed to the side of each pedal, and the subjects were asked to keep their body position constant during the experiment. During the exercise protocols, the operation of the electric valves controlling cuff pressure was initiated by a signal from the photoelectric sensor. During the pulsed-compression exercise protocol, exercise was performed for 4 min without leg compression, and then pulsed leg compressions (150 mmHg) of increasing duration (300, 600, 900 or 1000 ms) were applied at 1000 ms intervals over a period of 2 min, while the exercise continued; in practice, during the 1000 ms condition, we stopped applying the pressure within 1 min or less because of the difficulty of pedalling. Finally, the exercise was continued for two more minutes without leg compression. MAP, HR and gas parameters (oxygen uptake, {eph_198_mu1}, and minute ventilation rate, {eph_198_mu2}) were measured continuously throughout the protocol. During the control exercise protocol, the exercise was conducted for the same period without pulsed compression.

Measurements

Throughout this study, systemic arterial blood pressure (systolic blood pressure, SAP, and diastolic blood pressure, DAP) was measured using a finger pressure monitor (Finapress, Ohmeda, Englewood, CO, USA), and MAP was calculated according to the formula: MAP = DAP + (SAP – DAP)/3. HR and MAP were averaged at 1 min intervals throughout the study. During exercise, {eph_198_mu3} and {eph_198_mu4} were measured using a gas analysing system (Minato RM300I, Tokyo, Japan) with a mass spectrometer (Arco system, Chiba, Japan). A portable computer-controlled spectrometer (Niro-300, Hamamatsu Photonics Ltd, Hamamatsu, Japan) was used to measure NIRS signals. The Niro-300 uses specially resolved spectroscopy (SRS) to provide not only the usual measurements of changes in haemoglobin concentration, but also an absolute signal for the tissue oxygenation index (TOI), which is related to the averaged regional haemoglobin saturation (Kirkpatrick et al. 1996; Owen-Reece et al. 1999). The SRS technique incorporates several detectors housed within a single probe placed over an area of 8 x 8 mm and situated 4–5 cm from the light source optical fibre. A combination of these multidistance measurements of optical attenuation with the usual multiwavelength spectroscopy data enables calculation of the relative concentrations of deoxyhaemoglobin and oxyhaemoglobin in the illuminated tissue; thus, TOI is regarded as an index of the mean tissue haemoglobin saturation (Owen-Reece et al. 1999). In practice, TOI showed a high correlation with O2 saturation values obtained from the blood gas analyser in measurements made on phantoms containing intralipid and blood (Suzuki et al. 1999). The ends of the optical fibres were fixed to the skin on the vastus lateralis muscle at a mean interfibre distance of 5 cm.

Statistics

A two-way analysis of variance for repeated measurements was used for comparison of data. Post hoc determination of the significance of differences between means was carried out using a protected least significant difference test. All values are presented as means ± S.E.M., and the null hypothesis was rejected at P < 0.05.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
At rest, TOI increased during pulsed compressions of < 1000 ms, but declined at 1000 ms (static continuous compression; Fig. 2). HR and MAP did not change during pulsed compression at rest.



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  		Figure 2.  Tissue oxygenation index (TOI) obtained during rhythmic external compression on the thigh muscles
*P < 0.05 versus the initial resting value.

 
During both 50 and 100 W control exercise protocols, TOI declined within 1 min after the onset of exercise and remained at the new level throughout the exercise period (Fig. 3). TOI was lower during 100 W exercise than during 50 W exercise. During 100 W exercise with pulsed compressions of 300 ms, TOI increased to levels greater than were seen during control exercise, whereas TOI was unchanged from control values with compressions of 600 ms. By contrast, TOI markedly declined during both 50 and 100 W exercise with pulsed compressions of 900 or 1000 ms. After release of the pressure, TOI returned to the control level seen before application of the pressure.



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  		Figure 3.  TOI at rest and during exercise (50 and 100 W) obtained during the control and pulsed-pressure protocols
*P < 0.05 versus the control exercise protocol.

 
HR, MAP, {eph_198_mu5} and {eph_198_mu6} all increased within 1 min after the onset of the control exercise protocol and remained at the new level throughout the exercise period (Figs 4 and 5). During exercise with pulsed leg compressions, however, MAP increased progressively as the duration of the compressions increased (50 W; > 300 ms), while HR increased at compression durations > 300 ms. The levels of both HR and MAP were greater during 100 than 50 W exercise (Fig. 4). {eph_198_mu7} increased slightly with compressions of 1000 ms during 100 W exercise and after release of the compression during both 50 and 100 W exercise protocols. {eph_198_mu8} increased with pulsed compression of 900 or 1000 ms in the 50 and 100 W exercise protocols.



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  		Figure 4.  Heart (HR) and mean arterial pressure (MAP) at rest and during exercise (50 and 100 W) obtained during the control and pulsed-pressure protocols
*P < 0.05 versus the control exercise protocol.

 


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  		Figure 5.  Minute oxygen consumption {eph_198_mu14} and minute ventilation {eph_198_mu15} at rest and during exercise (50 and 100 W) obtained during the control and pulsed-pressure protocols
*P < 0.05 versus the control exercise protocol.

 

   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Rest session

At rest, pulsed compressions elicited increases in TOI when their duration was < 1000 ms. Because we used 150 mmHg as the external compression pressure and the MAP at rest was under 80 mmHg, blood flow to the lower legs was occluded during each compression. As a consequence, when the compression duration was 900 ms, blood flowed to the lower legs for only 100 ms of the 1000 ms compression cycle. Because it is highly unlikely that metabolic activity declined during pulsed compression at rest, the observed increase in oxygenation of the resting muscles almost certainly reflects increased blood flow (Nishiyasu et al. 1999). At rest, the metabolic rate in muscles is very low. That the obstruction caused by external compressions of < 1000 ms within a 1000 ms cycle did not significantly affect oxygen delivery to the muscles suggests that the muscle pumping effect induced by the compressions counteracted the obstruction. An additional potent explanation (besides a muscle pumping effect) is that compression may cause distortion of the vascular endothelium which could trigger the release of vasodilator substances such as nitric oxide (Tschakovsky & Sheriff, 2004). At rest, therefore, the effects of external pulsed compression of the lower legs may have a duration threshold (900–1000 ms within a 1000 ms cycle) below which muscle pumping and/or other mechanisms counteract the obstruction to flow caused the external compression.

Exercise sessions

When the compression duration was 300 or 600 ms during exercise, TOI did not change or was increased (at 300 ms). The MAP was under 110 mmHg, so that during compressions the blood flow to the lower legs would have been occluded, as at rest. Given that the length of the muscle contraction phase during 75 W bicycle exercise is reportedly < 350 ms (Nishiyasu et al. 2001), during 50 and 100 W bicycle exercise in the present study, 300 ms external compressions probably would not exert an obstruction-induced effect and could even increase the muscle pumping effect. With compression periods of 600 ms during exercise, the effects of increased muscle pumping may counteract those of the increased obstruction resulting from the more prolonged compressions.

During exercise protocols with compression periods of 300 or 600 ms, {eph_198_mu9} and {eph_198_mu10} were not different from control values, indicating that there were no metabolic changes within the muscles. By contrast, with compressions of 900 or 1000 ms during exercise, TOI markedly declined, reflecting the reduced blood flow in the lower legs. This suggests that the aforementioned duration threshold is shorter during exercise (600–900 ms) than at rest (900–1000 ms), most likely because of the increased oxygen demand within active muscles.

That TOI did not change or even increased during exercise with compression periods of 300–600 ms suggests that pulsed compressions of this duration do not lead to changes in the metabolic state in the muscle or to activation of the muscle metaboreflex; the increases in MAP and HR seen in this situation must have been due to other mechanisms. Because the intramuscular pressure in active muscles increases in proportion to the workload (Sjogaard et al. 1986; Sejersted & Hargens, 1995; Ballard et al. 1998), a graded increase in intramuscular pressure during graded dynamic exercise would be expected to contribute to a graded reflex increase in MAP. In practice, during dynamic exercise, intramuscular pressure varies rhythmically in the active muscles, increasing only during the contraction phase. In that regard, using the decerebrate unanaesthetized cat made to walk on a treadmill, Pickar et al. (1994) found that group III afferents with endings in the triceps surae muscles discharged in synchrony with the contraction phase of the step cycle. In addition, Victor et al. (1989) showed that in anaesthetized cats muscle mechanoreceptors with group III afferents contribute to the reflex stimulation of renal sympathetic outflow evoked by muscle contractions, and Adreani et al. (1997) showed that in the unanaesthetized decerebrate cat mild dynamic exercise alone is sufficient to activate the group III and IV muscle afferents that probably evoke reflex effects on systemic arterial pressure. Thus, the increase in MAP and HR seen during dynamic exercise with pulsed compression could be mediated by group III and IV muscle afferents activated by the external compression. Interestingly, McClain et al. (1994) showed in humans that, although external forearm compression (> 110 mmHg) at rest did not affect sympathetic activity, it augmented muscle sympathetic activity when applied during an isometric handgrip contraction. They suggested that the mechanoreceptor reflex response is augmented by muscle compression during exercise, probably due to sensitization of group III and IV afferents. Other recent studies also support the notion of metabolite-mediated sensitization of the mechanoreceptive pathways (Adreani & Kaufman, 1998; Fisher & White, 2004; Bell & White, 2005). In the present study, although application of pulsed compression at rest did not evoke a blood pressure response, pulsed compression during dynamic exercise did. Thus, the enhanced blood pressure response elicited by applying pulsed compressions with durations of 300 or 600 ms during exercise might reflect an interaction between the mechanoreflex and other factors related to exercise.

Both MAP and HR were markedly increased during pulsed leg compressions with durations of 900 or 1000 ms. That there was a concomitant decline in TOI indicates that by decreasing vascular conductance pulsed compressions reduced blood flow in the active muscles, which would in turn produce an increase in systemic blood pressure with no change in cardiac output (not measured). The decrease in blood flow in the active muscles also would change the metabolic state to a more glycolytic one, in which case the muscle metaboreflex could be activated. It was previously reported that partial occlusion of the lower legs by application of lower body positive pressure during dynamic leg exercise can elicit a pressure-dependent pressor response with enhanced ventilation (Eiken & Bjurstedt, 1987; Rowell et al. 1991; Sundberg & Kaijser, 1992; Williamson et al. 1994a; Nishiyasu et al. 2000). The increase in {eph_198_mu11} seen with pulsed compressions of 900 and 1000 ms in the present study is consistent with those findings. In addition, as the duration of the compression pulse was increased, the period of deformation of the muscles also increased, suggesting that stimulation of the muscle mechanoreflex was also increased. Thus, the marked increase in MAP and HR seen with pulsed compressions of 900 and 1000 ms could be due to the interaction of mechanical effects with the muscle metaboreflex and mechanoreflex.

Limitations

We used 150 mmHg for the external compression at rest and during exercise. During bicycle exercise at < 100 W, the intramuscular pressure during contractions is much lower than 150 mmHg (Sejersted & Hargens, 1995; Ballard et al. 1998), which means that blood flow to the lower legs was occluded during the compression periods. However, the MAP increased during pulsed leg compressions of >900 ms and eventually exceeded 150 mmHg, in which case blood flow would not have been completely occluded.

The fact that {eph_198_mu12} was not different during exercise with pulsed compressions of < 1000 ms from that during control exercise suggests that the external compressions synchronized to the thigh extensor muscle contractions did not change the mechanical workload during exercise, and subjects did not find the compressions uncomfortable as long as the duration was < 1000 ms. However, subjects could not sustain the workload when the external compression was 1000 ms (i.e. static continuous compression), and {eph_198_mu13} was slightly increased in that case. Thus, the increase in MAP and HR seen with 1000 ms compressions during exercise may be due in part to the increased mechanical workload caused by the static continuous compression itself and in part to increased central command.


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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
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   Acknowledgements
 
We should like to sincerely thank the volunteer subjects. We also greatly appreciate the help of Dr William Goldman (English editing and critical comments). This study was supported by grants from COE projects and the Ministry of Education, Science and Culture of Japan.




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