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Role of speed vs. grade in relation to muscle pumpfunction at locomotion onset DON D. SHERIFF AND AMY L. HAKEMANDepartment of Exercise Science, University of Iowa, Iowa City, Iowa 52242 Received 20 July 2000; accepted in final form 1 March 2001 Sheriff, Don D., and Amy L. Hakeman. Role of speed
transduction of vasodilator chemicals (4, 16). The rel- vs. grade in relation to muscle pump function at locomotion ative contribution of each of these two mechanisms is onset. J Appl Physiol 91: 269–276, 2001.—We sought to unclear. On the basis of the known delay in the onset of clarify the roles of contraction frequency (speed) and contrac- arteriolar vasodilation in response to electrically in- tion force (grade) in the rise in muscle blood flow at the onset duced twitch contractions in anesthetized animals (6, of locomotion. Shoemaker et al. (Can J Physiol Pharmacol 76: 12), Sheriff and co-workers (18) reasoned that the on- 418–427, 1998) explored this relationship in human hand- set of locomotion might provide a short window of grip exercise and found that the time course of the rise inmuscle vascular conductance was similar when a light opportunity before vasodilation occurs in which to eval- weight was lifted in a fast cadence and a heavy weight was uate the isolated influence of the muscle pump on lifted in a slow cadence (total work constant). This indicates muscle blood flow. This possibility is supported by the that muscle pumping (contraction frequency) was of limited observation that the isolated muscle pump can elicit importance in governing the time course. Rather, vasodilator immediate increases in muscle blood flow in a setting substances released in proportion to the total work per- where vasodilation alone would be ineffective in rais- formed appeared to determine the pattern and extent of the ing flow (19). On the basis of the biphasic pattern of rise in conductance. We hypothesized that conductance rise in muscle vascular conductance at the onset of would rise faster during locomotion at a high speed (fre- mild treadmill locomotion in dogs with autonomic quency) and low grade (force) than at a low speed and high blockade, Sheriff and co-workers (18) attributed the grade, despite similar total increases in conductance, owing immediate rise in calculated vascular conductance in to more effective muscle pumping at faster contraction rates.
response to mild exercise to the action of the muscle Seven male rats performed nine 1-min bouts of treadmill pump. A second, delayed rise in conductance was at- locomotion across a combination of three speeds (5, 10, and20 m/min) and three grades (Ϫ10, 0, and ϩ15°) in random tributed to the action of vasodilator substances, lead- order. Locomotion at 10 m/min and 0° grade and 20 m/min ing to an increase in vessel diameter. Consistent with and Ϫ10° grade led to an equal rise in terminal aortic vas- this idea, they observed in a limited number of animals cular conductance. However, the equal rise was achieved that a doubling of treadmill speed led to an approxi- more quickly at the higher running speed, suggestive of more mate doubling of the rise in vascular conductance effective muscle pumping. Across the nine combinations of achieved in the first 2–3 s of locomotion. That is, a exercise, speed began to exert a statistically significant in- doubling of contraction frequency appeared to lead to a fluence on conductance by the 3rd s of locomotion. Grade did proportional increase in the effectiveness of muscle not begin to exert an influence until the 12th s of locomotion pumping. In response to moderate exercise, conduc- (similar to the delays reported for arteriolar dilation to mus- tance rose smoothly (monotonically) to steady-state cle contraction). Additional experiments in dogs provided values, suggesting that vasodilation is initiated after a similar results. Thus the muscle pump appears to initiate the far shorter delay when work rate is increased above a increase in blood flow in proportion to contraction frequency mild intensity (no window of opportunity for evaluat- dog; rat; nitric oxide; muscle blood flow; iliac artery; terminal Recently, Shoemaker et al. (21) explored the rela- aorta; arterial pressure; vasodilation; vascular conductance tionship between muscle pumping and vasodilation atthe onset of handgrip exercise performed by humansubjects. In separate trials, these investigators had THE ONSET OF LOCOMOTION and most forms of dynamic subjects lift and lower a light weight in a fast cadence exercise are accompanied by a rapid increase in the and a heavy weight in a slow cadence, such that the blood flow to the muscles engaged in producing move- total work performed was equal in the two conditions.
ment. The rise in blood flow is largely attributable to a They found that the time course of the rise in vascular rise in the calculated vascular conductance across mus- conductance was similar between the two conditions, cle, which in turn is attributable to the muscle pump indicating that muscle pumping was of limited impor- (10, 15, 18, 23) and inhibition of arteriolar smoothmuscle after the production, release, diffusion, and The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby Address for reprint requests and other correspondence: D. D.
marked ‘‘advertisement’’ in accordance with 18 U.S.C. Section 1734 Sheriff, 518 Field House, UI Exercise Science, Iowa City, IA 52242.
8750-7587/01 $5.00 Copyright 2001 the American Physiological Society tance in governing the time course of the rise in con- serted centrally into the vessel under isoflurane anesthesia ductance. Rather, vasodilator substances released in for measurement of systemic arterial pressure. Although this proportion to the total work performed appeared to be procedure likely reduced the blood flow to the distal tissues, the dominant mechanism responsible for the pattern even for the brief duration of low-intensity exercise employed and extent of the increase in muscle vascular conduc- in the present study, it is unlikely that the pattern (timecourse) of blood flow response measured at the level of the terminal aorta would be substantially altered by this proce- In the present study, we sought to pursue the follow- dure. The catheter was tunneled to an exit site on the back.
ing two goals. First, we sought to clarify the relative The animal was allowed to recover for Ն3 h or overnight.
role of speed (contraction frequency) vs. grade (contrac- Data collection. The animal was lightly anesthetized (1% tion force) in governing the rise in muscle blood flow at isoflurane), the catheter was connected to a pressure trans- the onset of locomotion. The rationale was that differ- ducer (model P10EZ, Ohmeda, Madison, WI), and the flow ences in contraction frequency would lead primarily to transducer was connected to a flowmeter (model T106, Tran- changes in the effectiveness of the muscle pump (at sonic). The animal was then placed in the treadmill and, after least in the first few seconds of locomotion), whereas regaining full consciousness, was allowed Ն30 min to re- differences in contraction force would lead primarily to cover. The pressure transducer was connected to a signalconditioner (model 6600, Gould Instrument Systems, Valley changes in arteriolar diameter [perhaps only after View, OH). Signals were displayed on a chart recorder (model some delay (25)]. On the basis of these premises, alter- MT95K2, Astro-Med, West Warwick, RI), digitized at 1 kHz, ations in speed and grade should provide insight into and written to a fixed disk of a microcomputer with the use of the relative roles of the muscle pump vs. vasodilation commercially available software (PONEMAH Physiology in raising muscle blood flow at locomotion onset. Be- Platform, P3, Gould Instrument Systems).
cause the blood flow-raising action of the muscle pump Experimental protocols. The animals performed nine 1-min is proposed to be most effective during locomotory bouts of treadmill exercise across a combination of three exercise (10), we deemed that it would be useful to speeds (5, 10, and 20 m/min) and three grades (Ϫ10, 0, and apply the approach employed by Shoemaker et al. (21) ϩ15°) in random order. For the high grade, two rats ran at in their handgrip study to locomotory exercise. We ϩ10° and five rats ran at ϩ15°; the group mean data arereported as ϩ15° for convenience. The stride frequency for hypothesized that conductance would rise faster dur- rats at these three speeds is ϳ1, 2, and 3 strides/s (3). The ing locomotion at a high speed and low grade than at a animals were allowed to recover for Ն3 min between bouts.
low speed and high grade, despite similar total in- Data analysis. Terminal aortic vascular conductance was creases in conductance, owing to more effective muscle calculated as terminal aortic flow divided by arterial pres- pumping at faster contraction rates associated with sure. Arterial pressure, terminal aortic flow, and terminal higher treadmill speeds. Second, because nitric oxide aortic vascular conductance were each averaged over 1-s (NO) synthase (NOS) inhibition has recently been re- periods beginning 10 s before the onset of locomotion until ported to slow the vasodilation in response to locomo- tion (17), we inhibited NOS in an effort to extend theshort window of opportunity for evaluating muscle pump function at the onset of locomotion at moderate Six mongrel dogs (18–24 kg body wt) of either gender were intensities of locomotion. Experiments were carried selected for their willingness to run on a motor-driven tread- out in chronically prepared, conscious rats and dogs.
mill (model J6, Proform). The dogs were familiarized withtreadmill running in a series of training sessions before the following aseptic surgical procedures were performed.
Surgical preparation. Dogs were anesthetized with thio- All procedures met National Institutes of Health guide- pental, intubated, ventilated, and maintained with halo- lines and were reviewed and approved by the InstitutionalAnimal Care and Use Committee of the University of Iowa.
thane. Ultrasonic transit-time blood flow transducers (Tran-sonic) and vascular occluder cuffs were placed bilaterally on the iliac arteries through a midline abdominal incision. Inone dog, these devices were implanted on the terminal aorta, Seven male Sprague-Dawley rats (250–300 g) were se- and the measured values of blood flow in this dog were on lected for their willingness to run on a motor-driven tread- average three times greater than in the other dogs. Blood mill (model 1010 Modular Treadmill, Columbus Instruments, flows measured in this dog were divided by a factor of 3 before Columbus, OH). The rats were familiarized with treadmill they were averaged with the results from the remaining running before the following aseptic surgical procedures animals. A catheter was inserted into the aorta for measure- ment of systemic arterial pressure and in a femoral artery Surgical preparation. Rats were anesthetized with isoflu- and vein for measurement of hindlimb perfusion pressure rane. An ultrasonic transit-time blood flow transducer (model and infusion of drugs, respectively. All leads were tunneled to 1.5RB, Transonic, Ithaca, NY) was implanted in each animal exit sites on the back. Skin patches delivering a total of 75 on the terminal aorta through a midline abdominal incision.
␮g/h of fentanyl were placed on the dogs for 72 h after The probe cable was tunneled to an exit site on the back. The surgery to control postoperative pain, and the dogs were animal was given nalbuphine hydrochloride (1 mg/kg sc) for given cephalexin (500 mg po twice a day) continually after control of postoperative pain. The animal was allowed to surgery throughout the time that data were collected.
recover until an acceptable blood flow signal was acquired Data collection. Catheters were connected to pressure (usually 2–3 days). On the day before or on the morning of a transducers (model P10EZ, Ohmeda) and flow transducers day when an experiment was to be carried out, a femoral were connected to flowmeters (model T106, Transonic). Sig- artery was ligated, and a PE-10 catheter was directly in- nals were displayed on a pen recorder and digitized at 250 Hz. Average values of each signal were written to a fixed diskof a microcomputer twice per second.
Experimental protocols. The animals performed treadmill exercise at three intensities (3.2 km/h and 0% grade, 6.4km/h and 0% grade, and 6.4 km/h and 10% grade) for 3 minin no regular order. The animals were allowed to recover for Ն3 min before exercise was repeated at a different exerciseintensity. The animals were then given intravenous hexame-thonium (10 mg/kg), atropine (0.1 mg/kg), and captopril (1mg/kg) to block autonomic function and the renin-angioten-sin system, respectively (17, 20). The efficacy of these drugswas inferred from the exaggerated fall in arterial pressurethat accompanied locomotion after autonomic blockade. Thethree bouts of exercise were then repeated. Some animals ranfor only 1 min at some workloads, owing to reduced exercisecapacity after autonomic blockade. Animals were then givennitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv) to inhibitNO production, and exercise was repeated as describedabove. The efficacy of NOS inhibition was inferred from therise in arterial pressure elicited by this drug. On a separateday, animals performed locomotion as described above withand without L-NAME alone. Drugs were acquired from SigmaChemical (St. Louis, MO).
Data analysis. Iliac vascular conductance was calculated as iliac blood flow divided by arterial pressure. We evaluatedthe effect of L-NAME treatment on the time course of the risein iliac vascular conductance graphically on the basis ofcalculations of iliac vascular conductance for each exercise Fig. 1. Hemodynamic responses from 1 rat to 9 bouts of treadmill bout averaged over 1-s periods from 10 s before until the end locomotion graded across 3 speeds and 3 grades. Terminal aortic flow of the first 60 s of exercise. Values are means Ϯ SE.
and vascular conductance rose in response to locomotion, whereasfemoral arterial pressure tended to fall slightly. There was consid-erable overlap in the steady-state values of flow and conductance Tests for statistical significance were done by paired t-tests, except as follows. For each 1-s time period of the data 0.150 Ϯ 0.022 and 0.162 Ϯ 0.023 ml ⅐ minϪ1 ⅐ mmHgϪ1 presented in Figs. 3 and 5, treatment effects were tested for 10 m/min and 0° grade and 20 m/min and Ϫ10° statistically by multiple linear regression (22) with a com- grade, respectively (P ϭ 0.19). Exercise vascular con- puter spreadsheet program (Microsoft Excel 97, Redmond,WA). Dummy variables were used as independent variables ductance (averaged over the final 10 s of locomotion) to account for interindividual variability among animals (22).
was 0.271 Ϯ 0.034 and 0.277 Ϯ 0.038 ml ⅐ minϪ1 ⅐ For Fig. 3, treadmill speed (5, 10, or 20 m/min), grade (Ϫ10, mmHgϪ1 for 10 m/min and 0° grade and 20 m/min and 0, or ϩ10°), and sequence order (1–9) were used to encode Ϫ10° grade, respectively (P ϭ 0.60). The increase in treatment effects. For Fig. 5, treadmill speed (3.2 or 6.4 hindlimb conductance from rest to exercise was km/h) and treadmill grade (0 or 10%) were used to encode 0.121 Ϯ 0.016 and 0.115 Ϯ 0.021 ml ⅐ minϪ1 ⅐ mmHgϪ1 treatment effects. Values are means Ϯ SE.
for 10 m/min and 0° grade and 20 m/min and Ϫ10°grade, respectively (P ϭ 0.53). Femoral arterial pres- sure was similar during the two bouts. Figure 2 depicts the time course of the rise in hindlimb conductance aspercent increase, and it can be seen that the similar Figure 1 depicts arterial pressure, hindlimb blood increases in conductance followed different time flow, and hindlimb vascular conductance in a rat per- courses. That is, conductance at the slower speed and forming treadmill exercise graded across nine combi- higher grade was significantly less (P Ͻ 0.05) than nations stemming from three speeds (5, 10, and 20 conductance at the faster speed and lesser grade early m/min) and three grades (Ϫ10, 0, and ϩ15°). All speeds and grades led to immediate increases in blood flow Figure 3 depicts group mean data showing the and calculated vascular conductance. The steady-state changes in hindlimb blood flow, femoral arterial pres- values of these variables reveal considerable overlap sure, and hindlimb vascular conductance from seven among the different combinations of speed and grade.
rats. Figure 3, left, shows the isolated influence of Data collected in response to locomotion at 10 m/min speed on the rise in blood flow and conductance; i.e., and 0° grade and 20 m/min and Ϫ10° grade were each trace represents the response to the three indi- selected to illustrate how different combinations of vidual bouts at the three different grades, averaged speed and grade can lead to a similar rise in vascular together. The statistical analysis (which included the conductance with a variable pattern of response. Rest- data from the intermediate speed) indicates that speed ing vascular conductance (averaged over the 10 s im- began to exert a significant influence (P Ͻ 0.05) on mediately preceding the onset of locomotion) was conductance as soon as the 3rd s of locomotion, and this together. The statistical analysis (which included thedata from the intermediate grade) indicates that gradedid not begin to exert a significant effect (P Ͻ 0.05) onthe rise in conductance until the 12th s of locomotion.
Figure 4 depicts the time course of the rise in hind- limb vascular conductance averaged from five dogsperforming treadmill exercise at 6.4 km/h and 10%grade before and after inhibition of NOS (autonomicfunction intact). When NOS function was intact, con-ductance rose progressively over the first 10 s of loco-motion with an apparent overshoot. After inhibition ofNOS, the time course of the rise in conductance exhib-ited a biphasic pattern. Conductance initially (1–3 s) Fig. 2. Time course of rise in hindlimb vascular conductance as rose to a steady level that persisted for ϳ5 s, after percent increase in response to locomotion at 10 m/min and 0° grade which conductance began a second rise to a steady- and 20 m/min and Ϫ10° grade in rats. Resting vascular conductance, state value with no apparent overshoot.
exercise vascular conductance, and change in vascular conductance Figure 5 depicts the rise in conductance across the from rest to exercise were not significantly different between the 2conditions. Rise in vascular conductance follows a slower time course three workloads after inhibition of NOS and autonomic during locomotion at 10 m/min and 0° grade than during locomotion blockade. The immediate rise in conductance in the first few seconds of locomotion at 6.4 km/h was approx-imately twice as great as the rise that accompanied influence persisted throughout the remainder of exer- locomotion at 3.2 km/h. Furthermore, the immediate cise. Figure 3, right, depicts the isolated influence of rise in conductance was identical for locomotion at 6.4 grade on the rise in blood flow and conductance; i.e., km/h and 0% grade and for locomotion at 6.4 km/h and each trace represents the response to the three indi- 10% grade. Thereafter, under all three conditions, con- vidual bouts at the three different speeds, averaged ductance underwent further increases.
Fig. 3. Isolated influence of speed andgrade on the hemodynamic response tolocomotion in rats. Left: each trace rep-resents responses to individual bouts atthe 3 different grades, averaged to-gether. Right: each trace represents re-sponses to individual bouts at the 3 dif-ferent speeds at a single grade, averagedtogether. Error bars for intermediatespeed and grade have been deleted toimprove clarity.
characteristics, which are relatively slow (half-relax-ation times of 5–40 s) (11). Therefore, we reasoned thata fixed rise in vascular conductance should follow asimilar time course, regardless of the specific mechan-ics of locomotion if vasodilation were the sole or over-whelming cause of the rise in conductance. In supportof this rationale is the observation that vasodilatoryresponses induced by four different chemical sub-stances follow a relatively similar time course (25).
Also, even though a change in arteriolar diameter canbe detected immediately after an electrically induced1-s tetanic contraction of surrounding skeletal musclefibers, the vasodilation that is expressed lasts for ϳ50s (6). These observations imply that the microvascula-ture possesses relatively sluggish response character- Fig. 4. Influence of nitric oxide synthase (NOS) inhibition on the istics and thus functions as a low-pass filter.
time course of the rise in hindlimb vascular conductance in response The muscle pump exerts important influences on the to locomotion of moderate intensity in dogs. NOS inhibition elimi- pressure-volume (capacitive) (20) and the pressure- nated the rise in conductance normally seen at 3–7 s but did not flow characteristics (18, 19) of the peripheral circula- affect the overall rise in conductance. Nitro-L-arginine methyl ester(L-NAME) exerted a statistically significant effect (P tion. A number of investigators employing a broad s. Resting conductance was 2.60 Ϯ 0.19 and 1.23 Ϯ 1.23 mixture of different exercise conditions have concluded ml ⅐ minϪ1 ⅐ mmHgϪ1 in control and after L-NAME, respectively.
that the muscle pump can augment blood flow acrossmuscle (5, 15, 18, 19, 23). Laughlin (10) postulated that DISCUSSION
the blood flow-raising function of the muscle pump ismost effective during locomotory-type exercise. A com- The major new findings of our study are twofold.
mon assumption is that contraction frequency consti- First, the time course of the rise in muscle vascular tutes a major determinant of muscle pump efficacy (5, conductance is significantly altered by the mechanical 8, 18, 21) just as cardiac frequency can constitute a factors (speed and grade) by which a given rate of work major determinant of cardiac pump efficacy, and sev- is achieved during locomotion in rats. Second, aug- eral studies have provided evidence in support of this mented NO formation exerts a significant effect on the idea (5, 8, 18). For example, Gotschall and co-workers rise in conductance during the initial stages (3–10 s) in (8) examined the importance of cycling cadence at a response to a moderate intensity of treadmill locomo- fixed workload and found that higher cadences were tion and appears to account for all the dilation that associated with a higher total vascular conductance, normally occurs over this period in dogs. Moreover, the which they attributed to more effective muscle pump- absence of the normal influence of NO reveals that themuscle pump likely accounts for all the rise in bloodflow in the first 8 s of locomotion in these conditions.
The increases in muscle blood flow and muscle vas- cular conductance achieved during dynamic exerciseare tightly coupled to the amount of work performed bymuscle, and metabolic vasodilation is an importantregulatory mechanism by which muscle blood flow iscoupled to local energy demands. The common view isthat vasodilator substances within active muscle accu-mulate in a manner governed by the balance betweenthe energy expended by the muscle and the blood flowthrough the muscle and that metabolic vasodilationconstitutes the primary determinant of the vascularconductance achieved during locomotion. Because ar-terial pressure changes far less than does muscle bloodflow in the transition from rest to locomotion (20% vs.
Fig. 5. Rise in hindlimb vascular conductance in response to loco- 200%), the blood flow achieved is also tightly coupled motion graded across 2 speeds and 2 grades after inhibition of NOS to the rise in vascular conductance. For these reasons, and autonomic blockade. Doubling of treadmill speed from 3.2 to 6.4 we chose muscle vascular conductance as an index of km/h led to an approximate doubling of the rise in conductance the work rate imposed by the various combinations of achieved in the first 5 s of locomotion. Increasing treadmill grade speed and grade employed in our study. Also, the time from 0 to 10% at a fixed treadmill speed did not affect the rise invascular conductance over this time period. Speed began exerting a course of the relaxation of vascular smooth muscle significant effect (P Ͻ 0.05) on conductance at 4 s, whereas grade did appears to be constrained by relatively fixed dynamic not begin to exert an effect until 18 s.
ing. The importance of contraction force on the bloodflow-raising function of the muscle pump is unclear,although this variable is known to be relatively unim-portant in determining the efficacy of the muscle pumpin altering the pressure-volume characteristics of thecirculation [i.e., mild contractions are as effective asforceful contractions in emptying muscle veins (2)].
We found that contraction frequency exerts an influ- ence on muscle vascular conductance as soon as the 3rds of locomotion. In contrast, the influence of musclecontraction frequency on arteriolar dilation per se isindistinct. For example, the changes in arteriolar di-ameter in response to contractions at 2 and 4/s (similarto the contraction frequencies of the rats in the presentstudy) are identical for the first 40 s, whereas the risein diameter is more extensive over this period during Fig. 6. Influence of speed and grade on the rise in hindlimb vascular contractions at 8/s (6). On the basis of this finding, the conductance in response to locomotion in rats. Results are averaged observation that conductance is different across vari- together over time periods when a factor (speed or grade) does notexert a statistically significant influence, and the results are split ous treadmill speeds relatively early during locomotion over time periods when a factor does exert a significant influence.
argues that this difference stems from the influence ofcontraction frequency on the effectiveness of musclepumping, and not on arteriolar vasodilation.
gether into a single trace. At the point in time when We found that treadmill grade (contraction force) did speed begins to exert a significant influence (3rd s), the not begin to exert a significant effect on conductance single trace splits into three traces, one new trace for until 13 s after the onset of locomotion. If contraction each of the three speeds. Finally, at the point in time force constituted an important determinant of the effi- when grade begins to exert a significant influence (12th cacy of muscle pumping, we would expect this variable s), the traces representing locomotion at the low and to exert an effect on conductance with little or no time high speeds are each split into three, one new trace for delay. The delayed nature of the influence of contrac- each of the three grades. The responses from the three tion force on conductance is consistent with the idea grades at the intermediate speed remain averaged that this factor exerts its influence by modulating the together to improve clarity. As can be seen, a similar release of vasodilator substances. The fact that the rise in conductance can be achieved via many paths, delay we report here is similar to the delays reported for arterioles to begin dilating in response to twitch The qualitatively different results from the study by contractions at similar frequencies strengthens this Shoemaker et al. (21) and the present study likely stem from the different modes of exercise employed in the Recently, Shoemaker et al. (21) found that contrac- two studies. In the study by Shoemaker et al., the tion frequency did not affect the pattern or extent of subjects raised and then lowered a weight over a 1-s the rise in muscle blood flow during forearm exercise period and then relaxed the muscle for 1 s before performed by human subjects. Rather, the rise in mus- another duty cycle was begun. Thus for each duty cycle, cle blood flow during work at a fixed rate followed the the muscle was continuously activated for 1 s, during same time course, regardless of whether the work was which it performed a concentric contraction followed by performed with a light weight at a fast cadence or with an eccentric contraction, after which it relaxed at fixed a heavy weight at a slow cadence. This led these inves- length. In contrast, the pattern of activation and the tigators to conclude that vasodilator responses are im- mode of shortening and lengthening are substantially portant early during dynamic exercise, and this influ- different during locomotion. Generally, muscles en- ence likely obscures any muscle pump effect that is gaged in producing locomotion tend to perform brief dependent on contraction frequency. In contrast, we concentric contractions, relax, and then undergo forced found that the time course of the rise in vascular reextension by antagonistic muscles while they are conductance varied significantly with changes in con- relaxed (or are relaxing). For example, during locomo- traction rate and grade, even when the eventual rise in tion at 8.5 km/h (2.2 strides/s) in dogs, the gluteus vascular conductance, and thus presumably the total medius muscle (a hip extensor) expresses electromyo- work rate, was the same (Fig. 2). Furthermore, the genic activity for 27% (120 ms) of the stride period and faster rise in conductance at the faster treadmill speed the muscle shortens while it is active (7). The muscle is is consistent with the idea that the muscle pump is then quiescent for Ͼ150 ms before it begins to re- more effective at higher contraction rates. To illustrate lengthen as the leg is pulled forward by the hip flexors.
these points graphically, Fig. 6 replots the vascular For this muscle to accumulate 1 s of electromyographic conductance data from the nine bouts of exercise as activity (as presumably occurs in the 1st duty cycle in follows. Over the period of time when neither speed nor the study of Shoemaker et al.), it would take over eight grade exerted a significant influence (from the begin- strides and thus would not occur until the 4th s of ning until the 3rd s), all the runs were averaged to- exercise. The forceful reextension of muscle may be a critical factor in promoting effective muscle pumping in time, an observation that underscores the view that during locomotion (10). Histological evaluation of the redundant control mechanisms are involved in the influence of changes in muscle length on lymphatic regulation of muscle blood flow (9).
volume (13) and microscopy evaluation of the influence In the present study, we confirm and extend the of changes in muscle length on the geometry of mi- previous findings of Sheriff et al. (18). Figure 5 shows, crovessels (14) lend credence to the suggestion that on the basis of the measurement of iliac artery blood skeletal muscle and its vasculature function as a “bel- flow and without the competing influence of the auto- nomic nervous system and the early contribution ofNO, that an approximate doubling of stride frequency (treadmill speed) leads to an approximate doubling ofthe initial (2- to 3-s) rise in conductance. Importantly, In a previous study using a limited number of ani- when the influence of NO is lacking, increasing tread- mals, Sheriff et al. (18) found that doubling treadmill mill grade at a fixed speed does not alter the initial (1- speed from a low to a moderate level led to a doubling to 10-s) rise in conductance. Thus all the other numer- of the immediate rise in hindlimb conductance in dogs ous potential vasodilator substances (16) fail to elicit walking on the flat. These investigators attributed this any measurable change in conductance until ϳ8 s into initial (2- to 3-s) rise in blood flow and calculated the exercise bout. Beyond 8 s, these other dilators conductance to more effective muscle pumping at the eventually exert a profound effect, eliciting a second higher contraction frequency. After a delay of ϳ10 s, rise in conductance that is approximately twice as during which time conductance was relatively un- large for work at 10% grade as on the flat. In our changed, they observed that conductance underwent a opinion, it is unlikely that vasodilation causes (or even second rise that they attributed to the action of vaso- contributes to) the initial (1- to 2-s) rise in conductance dilator substances. They also found that vascular con- under these conditions, and it is even more unlikely ductance rose more smoothly to its steady-state level in that vasodilation ceases for 5 s and then begins dogs walking uphill at a moderate speed, suggesting again. For example, recent elegant studies by Welsh that vasodilation might begin much sooner at this and Segal (24) provide compelling evidence that workload (thereby encroaching on the short window of there is a 2- to 3-s delay attributable to electrome- opportunity for gauging the effectiveness of the muscle chanical coupling within vascular smooth muscle pump). Importantly, recent evidence indicates thatNOS inhibition slows the rate of vasodilation during cells in response to vasodilator substances. Also, locomotion (17). It is believed that the muscle pump Wunsch et al. (25) recently demonstrated a delay of elicits an immediate increase in blood flow and, as a ϳ4 s before the onset of dilation of isolated arterioles consequence, there is a rise in shear stress on endo- after direct application of chemical vasodilator sub- thelial cells, which augments the release of NO. In stances. On the basis of these arguments, our results this way, NO acts as an amplifier that reinforces the support the proposal of Sheriff et al. that the muscle influence of the muscle pump on blood flow. In the pump elicits all the initial (1- to 3-s) increase in present study, we sought to shut off this amplifier by calculated conductance (blood flow) during mild in- inhibiting NOS as a means of possibly extending the tensities of locomotion and extends this to moderate window of opportunity for evaluating muscle pump intensities of locomotion when NO function is inhib- effectiveness at the onset of locomotion at this higher ited. The discrepancy between the delayed vasodila- tory responses resulting from direct application of We found that NO exerts an important influence vasodilator substances to isolated arterioles (25) and early during the transition from quiet standing to the more immediate vasodilation observed in arte- locomotion as reported previously (17). The focus of our rioles after 1-s electrically evoked contractions of previous study was on evaluating the contribution of surrounding skeletal muscle (6) remains to be ex- NO to the rise in vascular conductance that accompa- nies locomotion; the focus here is on evaluating what Finally, our results may help explain why the search the absence of NO reveals about muscle pump function.
for the chemical substances that account for active As seen in Fig. 4, NOS inhibition does not alter the hyperemia has proven so elusive (9). Our results initial (1- to 2-s) rise in conductance. However, NOS strongly suggest that the muscle pump can initiate a inhibition appears to eliminate the entire rise in con- significant (2-fold) increase in blood flow, which in turn ductance normally seen in seconds 3–7 at this intensity stimulates augmented NO release and a further rise in of locomotion. These results are consistent with the blood flow. If feedforward control such as this matches idea that the muscle pump initiates an immediate the rise in blood flow to the rise in oxygen demand in a increase in blood flow (virtual conductance) that is close temporal relationship, a chemical error signal subsequently reinforced by augmented NO formation may not arise over a wide range of intensities of loco- induced by an increase in endothelial wall shear stress motion. Indeed, the tendency for vascular conductance that arises as a consequence of the increase in blood to exhibit an overshoot early during mild locomotion flow. Beyond 7 s, conductance begins a second rise when sympathetic function is intact (18) indicates that during NOS inhibition that is similar in rate and muscle may be relatively overperfused early during extent to the rise seen in control conditions but delayed We thank Tony Smith for expert technical assistance.
14. Nakao M and Segal SS. Muscle length alters geometry of
This work was supported by National Heart, Lung, and Blood arterioles and venules in hamster retractor. Am J Physiol Heart Circ Physiol 268: H336–H344, 1995.
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