Tens

Effect of Burst-Mode TranscutaneousElectrical Nerve Stimulation onPeripheral Vascular Resistance

Background and Purpose. Based on changes in skin temperature alone, someauthors have proposed that postganglionic sympathetic vasoconstrictor fiberscan be stimulated transcutaneously. Our goal was to determine the effects oflow-frequency (2 bursts per second), burst-mode transcutaneous electricalnerve stimulation (TENS) on calf vascular resistance, a more direct marker ofsympathetic vasoconstrictor outflow than skin temperature, in subjects with noknown pathology. Subjects. Fourteen women and 6 men (mean age531 years,SD513, range51858) participated in this study. Methods. Calf blood flow,arterial pressure, and skin temperature were measured while TENS wasapplied over the common peroneal and tibial nerves. Results. Blood flowimmediately following stimulation was not affected by TENS applied justunder or just above the threshold for muscle contraction. Transcutaneouselectrical nerve stimulation applied at 25% above the motor threshold causeda transient increase in calf blood flow. Regardless of stimulation intensity,TENS had no effect on arterial pressure; therefore, calf vascular resistancedecreased only during the trial that was 25% above the motor threshold.Regardless of stimulation intensity, TENS failed to alter dorsal or plantar skintemperature. Discussion and Conclusion. These results demonstrate that theeffects of TENS on circulation depend on stimulation intensity. When theintensity was sufficient to cause a moderate muscle contraction, a transient,local increase in blood flow occurred. Cooling of the dorsal and plantar skinoccurred in both the stimulated and control legs, most likely because skintemperature acclimatized to ambient room temperature, rather than becauseof any effect of TENS on circulation. The data, therefore, call into questionthe idea that postganglionic sympathetic efferent fibers are stimulated whenTENS is applied at clinically relevant intensities to people without symptomsof cardiovascular or neuromuscular pathology. [Sherry JE, Oehrlein KM,Hegge KS, Morgan BJ. Effect of burst-mode transcutaneous electrical nervestimulation on peripheral vascular resistance. Phys Ther. 2001;81:11831191.]

Key Words: Electrical stimulation, Physical therapy, Regional blood flow, Sympathetic nervous system,

Vascular resistance.

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Julie E Sherry

Kristin M Oehrlein

Kristin S Hegge

Barbara J Morgan

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Transcutaneous electrical nerve stimulation(TENS) is typically used for alteration of painperception.1,2 Several investigators,38 however,have reported that TENS can affect the periph-

eral vascular system. Wong and Jette5 reported that 3forms of TENS applied at the motor threshold that resultin muscle contractions (high frequency585 pulses persecond [pps], low frequency52 pps, and burst mode52bursts per second [bps]) decreased blood flow in sub-jects with no known pathology. In contrast, Kaada6reported that low-frequency (25 pps) and burst-mode(2 bps) TENS, applied over peripheral nerves withintensities high enough to produce visible muscle con-tractions, increased blood flow in patients with diabeticpolyneuropathy and Raynaud phenomenon. Based onchanges in skin temperature alone, the investigators inboth studies hypothesized that TENS alters vasoconstric-tor activity in sympathetic nerves. These investigators,however, did not directly measure sympathetic activity orcalculate vascular resistance. More recent studies7,8 havedemonstrated that TENS increases both skin tempera-ture and skin blood flow in subjects with no knownpathology and in patients with chronic leg ulcers. Unfor-tunately, these authors did not report whether thestimulation elicited a muscle contraction; therefore, thepotential mechanism underlying their results is difficultto ascertain.

The question of whether sympathetic nerve fibers inperipheral nerves can be stimulated transcutaneouslywas addressed in a recent study9 in which continuous-mode, high-frequency TENS (110 pps) was applied overthe peripheral nerves of subjects with no known pathol-ogy at levels just above and just below the motor thresh-

old. Indergand and Morgan9 demonstrated that TENS,applied in this manner, does not alter skin leg bloodflow or vascular resistance in the leg, or skin tempera-ture, suggesting that sympathetic vasoconstrictor fibersare not activated during transcutaneous stimulation. Itis possible, however, that the mode of TENS used(ie, continuous-mode, high-frequency stimulation at110 pps) failed to cause vasoconstriction because of thenonphysiologic pattern of stimulation. Naturally occur-ring sympathetic action potentials occur in bursts ratherthan in continuous trains.10 Studies using direct nervestimulation in experimental animals have demonstratedthat vascular smooth muscle is more responsive to irreg-ular bursts of stimulation ranging from 2 to 5 bps than tocontinuous stimulation with the same average stimula-tion frequency.11,12

Burst-mode TENS stimulates peripheral nerve fibersusing relatively high carrier frequencies (80100 pps),modulated burst frequencies (25 bps), and intensitiesabove or below the motor threshold.13 This pattern ofexternal stimulation more closely mimics physiologicsympathetic nerve activity than continuous-mode high-or low-frequency stimulation does. The purpose of ourstudy, therefore, was to investigate the effects of burst-mode TENS on calf blood flow, arterial pressure, andskin temperature in subjects with no known pathology.

Methods

SubjectsTwenty adults, 6 men and 14 women (mean age531years, SD513, range51858 years), served as subjects.All subjects said that they were nonsmokers, were not

JE Sherry, PT, MS, is a faculty associate, Physical Therapy Program, Department of Surgery, University of Wisconsin-Madison. She is also a staffphysical therapist at the UW-Research Park Spine Physical Therapy Clinic, University of Wisconsin Hospitals and Clinics. Address allcorrespondence to Ms Sherry at 4176 Medical Sciences Center, 1300 University Ave, Madison, WI 53706-1532 (USA) ([email protected]).

BJ Morgan, PT, PhD, is Associate Professor, Physical Therapy Program, Department of Surgery, University of Wisconsin-Madison.

KM Oehrlein and KS Hegge were physical therapist students at the University of Wisconsin-Madison at the time this research was conducted.

This work was performed in partial fulfillment of the degree requirements for Ms Sherrys Master of Science degree in kinesiology at the Universityof Wisconsin-Madison.

All authors provided writing and data collection. Ms Sherry and Dr Morgan provided research design. Ms Sherry, Ms Oehrlein, and Ms Heggeprovided data analysis. Ms Sherry provided project management, and Dr Morgan provided facilities/equipment and consultation. Patricia Mecumprovided secretarial assistance, and Nick Puleo provided technical assistance in the laboratory.

The study was approved by the Human Subjects Committees of the Center for Health Sciences, University of Wisconsin-Madison, and theMiddleton Memorial Veterans Administration Hospital.

Oral presentation of this research was made at the Combined Sections Meeting of the American Physical Therapy Association; February 5, 2000;New Orleans, La.

This article was submitted June 8, 2000, and was accepted November 22, 2000.

1184 . Sherry et al Physical Therapy . Volume 81 . Number 6 . June 2001

currently using prescription medications, and did nothave a pathology such as neuromuscular or cardiovascu-lar disease. All subjects provided informed consent priorto participation.

General ProceduresSubjects were studied in a supine position, at least 2hours after a meal, in a temperature-controlled labora-tory (2461C). This was done in an effort to minimizethe potential effects of digestion or thermoregulatoryactivity and to create a stable hemodynamic state. Allvariables were measured continuously throughout alltrials. Blood pressure was measured at 1-minute intervalsusing an automated sphygmomanometer (Dinamapmodel 1846 SX/P*).

In order to detect transient blood pressure changes thatcould influence blood flow, beat-by-beat arterial pressurewas also measured by photoelectric plethysmography(Finapres model 2300). Calf blood flow was measuredby venous occlusion plethysmography (model 271 ple-thysmograph) every 15 seconds during baseline andrecovery periods. We were unable to record blood flowmeasurements during the stimulation period becausethe electrically stimulated muscle contractions affectedthe stability of the strain gaugederived plethysmo-graphic tracing. Other details concerning the methods,rationale, and assumptions for venous occlusion ple-thysmography have been published previously.14,15

Skin temperature was measured every minute with atemperature monitor and 5-mm-diameter thermistorprobes placed 2.54 cm (1 in) proximal to the firstmetatarsal head on both the dorsal and plantar aspectsof both feet. These areas of skin are innervated by theperoneal and tibial nerves, respectively.16 Skin tempera-ture and calf blood flow were measured from both legssimultaneously; therefore, the unstimulated right legserved as a concurrent control during the TENS appli-cations. Because respiratory factors such as hypoventila-tion, hyperventilation, and the Valsalva maneuver areknown to alter sympathetic outflow, vascular resistance,and arterial pressure,17,18 the subjects were instructed tomaintain a stable breathing pattern throughout the datacollection period. In this study, a stable breathing patternwas defined as the absence of sustained changes in rateor depth of breathing as well as constant end-tidal CO2levels. To ensure adherence to this instruction, respira-tion was monitored throughout all trials using a bellowspneumograph\ wrapped around the abdomen at the

level of the diaphragm. In addition, breath-by-breathend-tidal CO2 was monitored by a nasal cannula andcapnometer (model 8800#).

The physiologic variability of blood flow, blood pressure,and end-tidal CO2 measurements was assessed by calcu-lating the coefficients of variation ([standard deviation/mean] 3 100) for repeated measurements made underbaseline conditions. This provided us with an estimate ofbaseline physiologic variability against which we couldcompare the effects of TENS. The mean values for thecoefficient of variation were 14.9% for leg blood flow,2.6% for blood pressure, and 5.1% for end-tidal CO2measurements. Reliability was not determined usingstandard statistical methods.

Transcutaneous Electrical Nerve StimulationPrior to electrode placement, the skin was cleansed withalcohol, and the course of the tibial and peroneal nerveswas mapped out with a 2-channel portable electricalstimulator (Eclipse model 7723**) equipped with ahandheld probe. During the nerve mapping, the stimu-lation intensity was turned up until a muscle contractionwas visible. Optimal electrode placement was confirmedby determining the location of the most vigorous con-traction. Then, 2 self-adhesive gel electrodes (ComfortEase 5- 3 6.4-cm disposable, pin-connector, polymer-gelelectrodes) were placed over the tibial and peronealnerves. A shared dispersive electrode (10- 3 5-cmcarbon-rubber electrode) was placed on the posteriorcalf, approximately 9 cm above the calcaneus. Thus, onechannel was used to stimulate the tibial nerve and theother channel to stimulate the peroneal nerve. Constantcurrent output with a balanced, biphasic asymmetricalwaveform was used. Prior to this study, this waveform wasverified by an oscilloscope in our laboratory by the leadauthor. A burst frequency of 2 bps, a carrier frequency of85 pps, and a phase duration of 250 microseconds wereused. All measurements, except those made with theautomated blood pressure cuff, were continuouslyrecorded on a chart recorder (model TA4000) with apaper speed of 2.5 mm/s. In addition, analog signalswere digitized (model 3000A PCM recording adap-tor) at a rate of 128 Hz with 12-bit resolution andsaved on magnetic tape (model HR-D860U videocas-sette recorder\\).

TENS ProtocolsWhile resting in a supine position with the hips andknees flexed to approximately 70 degrees, each subject

* Critikon Inc, PO Box 318000, Tampa, FL 33631. Finapres, Ohmeda Dr, Madison, WI 53707. Parks Medical Electronics Inc, PO Box 5669, Aloha, OR 97006. YSI Inc, 1725 Brannum Ln, Yellow Springs, OH 45387.\ Lafayette Instrument Co Inc, 3700 Sagamore Pkwy N, PO Box 5729, Lafayette,IN 47903.

# Sims BCI Inc, N7 W22025 Johnson St, Waukesha, WI 53186.** Medtronic Inc, 710 Medtronic Pkwy NE, Minneapolis, MN 55432. Empi Inc, 599 Cardigan Rd, St Paul, MN 55126. Gould Inc, 3631 Perkins Ave, Cleveland, OH 44114. AR Vetter Co, Box 143, Redersburg, PA 16872.\\ JVC Company of America, 41 Slater Dr, Elmwood Park, NJ 07407.

Physical Therapy . Volume 81 . Number 6 . June 2001 Sherry et al . 1185

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underwent 3 separate trials of 5 minutes of burst-modeTENS. During one trial TENS was just below the motorthreshold (ST), in another trial TENS was just above themotor threshold (MT), and in another trial TENS was25% above the motor threshold (125% MT). The motorthreshold for each nerve was defined as the analogreading on the electrical stimulator at the lowest inten-sity that elicited a visible muscle contraction. For the STtrial, the intensity was first increased to the motorthreshold, then decreased until the muscle contractiondisappeared. For the 125% MT trial, the TENS analogoutput necessary for motor threshold stimulation wasmultiplied by 1.25. We believe this method provided uswith a way to easily reproduce the relative intensity ofstimulation provided from subject to subject. Wedeemed this method to be appropriate because theTENS unit analog intensity scale and current outputwere found to be linearly related across all stimulationintensities. Order of the trials was randomized by abalanced Latin square design.19 Each 15-minute TENSprotocol included 5 minutes of baseline data collection,5 minutes of electrical stimulation, and 5 minutes ofrecovery data collection. A 10-minute rest period wasgiven between each trial to ensure adequate return tosteady state.

Static Handgrip ProtocolIn order to verify that the right and left legs wouldrespond to a known vasoconstrictor stimulus, each sub-ject performed 2 minutes of static handgrip exercises at30% of his or her predetermined maximal voluntarycontraction. The trial consisted of a 2-minute baselineperiod, a 2-minute handgrip period, and a 2-minuterecovery period. We believe that this trial also verifiedthat our instruments were sensitive enough to recordsubtle changes in leg blood flow.

Data Analysis

TENS trials. Minute values of arterial pressure obtainedby the automated sphygmomanometer were convertedto mean arterial pressure (MAP) by the followingformula20:

MAP 5 diastolic BP 1 @~systolic BP

2 diastolic BP)/3]

MAP values taken simultaneously with blood flow mea-surements were used in all calf vascular resistance calcu-lations. Calf vascular resistance was calculated by thefollowing formula20:

Calf vascular resistance 5 MAP/calf blood flow

Because we were unable to take calf blood flow measure-ments during the electrically induced muscle contrac-

tions, we compared blood flow measurements immedi-ately before and immediately after stimulation. For eachleg, the change in calf blood flow immediately after 5minutes of stimulation was computed by subtracting thefinal 30 seconds of baseline measurement from the first30-second interval of recovery. In addition, in order todetermine how long this change persisted, the change incalf blood flow was computed by subtracting the mea-surement of blood flow during the final 30 seconds ofbaseline from the measurement taken during the second30 seconds of recovery. Once the overall change wasdetermined, a paired t test was used to compare the left(stimulated) and right (unstimulated, control) legs.19This procedure was repeated for calf vascular resistance(Tab. 1).

The change in MAP was calculated by subtracting thepressure measurement obtained during the final minuteof the baseline period from both the pressure measure-ment obtained during the final minute of stimulationand the pressure measurement obtained during the firstminute of recovery. Then, a paired t test19 was used tocompare the difference between these 2 time periods(Tab. 2).

Skin temperature measurements were recorded fromeach of the 4 sites every minute. For each leg, the changein dorsal and plantar skin temperature from the finalminute of the baseline period to the final minute ofstimulation was computed. Paired t tests were used tocompare the left (stimulated) and right (control) legsfor dorsal and plantar regions.19 To ensure that therewas not a delayed effect, this process was repeated tocompare the change in skin temperature from the finalminute of the baseline period to the first minute of therecovery period.

Static handgrip trial. For each leg, changes in arterialpressure, calf blood flow, and calf vascular resistanceover time were calculated by subtracting the measure-ment obtained during the final 30 seconds of thehandgrip trial and the final 30 seconds of the recoveryperiod from those obtained during the baseline period.These values were then compared by a paired t test.19 Inall text and figures, data are presented as means 6standard deviation. Probability values of less than .05were considered statistically significant.

Results

TENS ApplicationsBurst-mode TENS applied at an intensity 25% above themotor threshold caused a transient increase in calf bloodflow and a decrease in vascular resistance in the stimu-lated leg, but not in the unstimulated control leg. Thesechanges returned to baseline within 1 minute after the


cessation of stimulation (Tab. 1, Figs. 1 and 2). Incontrast, TENS applied at intensities equal to, or justbelow, the motor threshold did not affect calf blood flowor vascular resistance (Tab. 1, Figs. 1 and 2). Meanarterial pressure was unaltered by TENS at any intensitylevel (Tab. 2). Likewise, dorsal and plantar foot temper-ature was unaltered by TENS at any intensity level(Tab. 2).

Static Handgrip ExerciseAs expected, 2 minutes of static handgrip exerciseproduced an increase in arterial pressure and vascularresistance in both legs from the baseline period to thefinal 30 seconds of the handgrip exercise (Tab. 3).Although vascular resistance in both legs increased 70%during the handgrip exercise, there was no concomitantchange in dorsal or plantar skin temperature.

DiscussionSeveral investigators38 have hypothesized that transcu-taneous stimulation of peripheral nerves, at variousintensities and frequencies, can either increase ordecrease activity in postganglionic vasoconstrictor neu-rons. However, the ability of transcutaneous stimulationto activate sympathetic vasoconstrictor fibers has not

been demonstrated. For this reason, we investigated theeffects of 3 different intensity levels of burst-mode TENSon calf blood flow, vascular resistance, and skin temper-ature. We chose burst-mode stimulation in order tomimic the naturally occurring, burst-like pattern ofaction potentials in sympathetic nerves.10 We reasonedthat vasoconstriction would be more likely to occur withburst-mode than with constant-frequency TENS becausearterial smooth muscle is more responsive to irregular,low-frequency bursts of stimulation.11,12 Our major find-ing is that burst-mode TENS produced vasodilation inthe leg; however, this effect depended on stimulationintensity. When TENS was applied at or below the motorthreshold, circulation was not affected. In contrast, whenTENS was applied at an intensity 25% above the motorthreshold, there was a transient vasodilation that lastedless than 1 minute. Regardless of stimulation intensity,TENS had no effect on skin temperature.

A frequently recommended electrode placement for theclinical use of TENS is directly over the peripheral nervethat serves the painful area.13 Investigators who observeddecreases in skin temperature during motor thresholdTENS have raised the concern that TENS may decreaseblood flow to a painful extremity by direct stimulation of

Table 1.Hemodynamic Responses to Submotor Threshold (ST), Motor Threshold (MT), and 25% Above Motor Threshold (125% MT) TranscutaneousElectrical Nerve Stimulation (TENS) in the Left (Stimulated) and Right (Control) Legs of Subjects Without Known Cardiovascular or NeuromuscularPathologya

Baselineb Recovery 1c Recovery 2d

ST (n520)

Calf blood flow (mL/100 mL/min)Left leg 2.460.9 2.360.9 2.260.9Right leg 2.260.9 2.261.3 2.060.9

Calf vascular resistance (mm Hg/mL/100 mL/min)Left leg 37.7614.7 38.7617.4 39.2613.8Right leg 44.9621.4 42.5619.2 47.6621.4

MT (n520)



125% MT (n520)



a Values shown are mean6SD.b Last 30 seconds of baseline period.c First 30 seconds of recovery period.d Second 30 seconds of recovery period.


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sympathetic vasoconstrictor fibers.5 Our results suggestotherwise. Although we did not measure sympatheticoutflow, we calculated vascular resistance, a variable thatprovides a more direct estimate of sympathetically medi-ated vasoconstriction than does skin temperature. Calfvascular resistance was not altered by burst-mode TENSapplied at or slightly below motor threshold. Applicationof TENS at 25% above the motor threshold causedvasodilation, not vasoconstriction.

Hemodynamic Responses to Burst-Mode TENSOur findings of vasodilation in response to electricalstimulation that was 25% above motor threshold areconsistent with previous reports that TENS increaseslocal blood flow when the stimulation intensity is wellabove the motor threshold.21,22 Because we did notobserve systemic cardiovascular responses to any of the 3stimulation intensity levels, we assume that the reduc-tions in vascular resistance produced in the TENS trialthat was 25% above motor threshold were caused mainlyby local mechanisms. The muscle pump,23,24 accumu-lation of local metabolic vasodilator substances,25,26 and

flow-induced vasodilation produced by local release ofrelaxing factors derived from the endothelium arepotential mechanisms for the observed vasodilation.27,28

Skin Temperature Responses to Burst-Mode TENSEven though we provided at least 1 hour for acclimati-zation to the laboratory (2461C) prior to data collec-tion, we observed no effects of burst-mode TENS on skintemperature. Our findings differ from those of otherinvestigators who reported decreases5 or increases6 inskin temperature after low-frequency TENS. Following30 to 45 minutes of TENS applied at intensities highenough to elicit visible muscle contractions in patientswith diabetic polyneuropathy or Raynaud phenomenon,Kaada6 reported a rise in skin temperature of 7 to 10C.One of the authors proposed explanations for theobserved increase in skin temperature was a neurohu-moral mechanism, because the post-stimulation temper-ature rise persisted for periods of 4 to 8 hours.6 We thinkthat this prolonged time course is incompatible with apure neural event.

Table 2.Mean Arterial Pressure (MAP) and Thermal Responses to Submotor Threshold (ST), Motor Threshold (MT), and 25% Above Motor Threshold(125% MT) Transcutaneous Electrical Nerve Stimulation (TENS) in the Left (Stimulated) and Right (Control) Legs of Subjects Without KnownCardiovascular or Neuromuscular Pathologya

Baselineb Stimulationc Recoveryd

ST (n520)

Dorsal foot temperature (C)Left leg 29.462.2 29.662.2 29.562.2Right leg 29.562.2 29.462.2 29.462.2

Plantar foot temperature (C)Left leg 28.762.2 28.662.2 28.662.2Right leg 28.962.6 28.961.7 28.962.6

MAP (mm Hg) 7969 7969 8069

MT (n520)



MAP (mm Hg) 7969 7864 7969

125% MT (n520)



MAP (mm Hg) 8064 7969 7969

a Values shown are mean6SD.b Final minute of baseline period.c Final minute of stimulation.d First minute of recovery period.


We designed our study to assess the feasibility of trans-cutaneous stimulation of sympathetic fibers; therefore,stimulation was applied for only 5 minutes. Our resultsdid not demonstrate any immediate hemodynamic effectfrom application of burst-mode TENS at or below themotor threshold. Our findings are inconsistent withthose of Wong and Jette,5 who reported that 25 minutesof motor threshold stimulation at high, low, and burstfrequencies all caused a decrease in skin temperature of2 to 3C in humans who were healthy. These authors5proposed that the observed decrease in skin tempera-ture was due to direct activation of vasoconstrictornerves in the stimulated arm. However, the time con-stant for activation of sympathetic fibers18,29,30 and forvasoconstriction following direct stimulation of sympa-thetic nerves is known to be less than 10 seconds.31 Skintemperature was not continually monitored in the exper-iments of Wong and Jette5; therefore, the authors wereunable to report on the time course for the effect on skintemperature.

Similar to Indergand and Morgan,9 we also observed asmall, progressive decrease in skin temperature over the2- to 3-hour data collection period. There are 2 reasons

why it is unlikely that this change was caused by electricalstimulation of sympathetic vasoconstrictor fibers. First,we did not notice any short-lived increases or decreasesin temperature that coincided with the onset or cessa-tion of the stimulation. Any measurable decrease in skintemperature was not apparent until after the commence-ment of the second trial, at least 25 minutes after thestart of data collection. This decrease persisted through-out all subsequent trials. Second, and more importantly,comparable decreases were observed in the stimulatedleg and the contralateral, unstimulated, leg. If we weredirectly stimulating sympathetic vasoconstrictor nerves,we would expect to see an effect only in the stimulatedleg.

Although we chose to use clinically relevant stimulationparameters that we believe would mimic the naturallyoccurring burst-like pattern of sympathetic nerves, theintensity may not have been sufficient to elicit actionpotentials in sympathetic nerve fibers. Our failure toobserve vasoconstrictive effects of TENS may beexplained by the strength-duration curve for peripheralnerve fibers.13,30 Postganglionic sympathetic fibers,

Figure 1.Bar graphs depicting the group mean values for the change in leg bloodflow (upper panel) and vascular resistance (lower panel) from baselineto immediately after stimulation between the stimulated leg (open bars)and control leg (closed bars). All 3 stimulation intensities of transcuta-neous electrical nerve stimulation (TENS) are depicted. ST5submotorthreshold, MT5motor threshold, and 125% MT525% above motorthreshold. Values shown are mean 6 standard deviation. *Paired t test,df519, P,.05, stimulated leg versus control leg.

Figure 2.Bar graph depicting the group mean values for the change in leg bloodflow (upper panel) and vascular resistance (lower panel) from baselineto 30 seconds after stimulation between the stimulated leg (open bars)and control leg (closed bars). All 3 stimulation intensities of transcuta-neous electrical nerve stimulation (TENS) are depicted. ST5submotorthreshold, MT5motor threshold, and 125% MT525% above motorthreshold. Values shown are mean6standard deviation. Paired t test,df519, P..05, stimulated versus control leg.


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because of their fiber diameter and conduction velocity,are C fibers.29,30 In order to overcome the high externalresistance of these thin fibers, stimulation intensitiesmight have to be higher than those we used. Thesehigher intensities probably would have elicited painfulsensations; none of our subjects, however, told us thatthe stimulation was painful. Our findings do not supportthe possibility raised by other investigators5 that transcu-taneous electrical stimulation over peripheral nervesmight have a vasoconstrictive effect. Our findings, as wellas previous work from our laboratory,9 both of which arebased on more direct markers of sympathetic activitythan skin temperature, lead us to question whether thisis possible. Our data indicate that burst-mode electricalstimulation applied transcutaneously over peripheralnerves at clinically relevant pulse durations and frequen-cies does not cause vasoconstriction or cooling of theskin. In contrast, when the intensity of burst-mode TENSis increased to a level well above motor threshold, thereis a transient vasodilatory effect, without any accompa-nying change in skin temperature.

LimitationsThe strain gauges used to register limb circumferenceduring venous occlusion plethysmography are very sen-sitive to movement artifact; therefore, this techniquecannot be used to measure blood flow during musclecontraction.14,15 We took measurements immediatelyfollowing the cessation of stimulation (within 1 second).We contend that these blood flow measurements closelyapproximate the undisturbed flow rate immediatelyprior to venous occlusion (ie, during musclecontraction).14,15

Venous occlusion plethysmography measures blood flowin the entire limb15; therefore, separate measurementsof blood flow to muscle and skin cannot be obtainedwith this technique. We cannot determine, based on ourdata, whether the exercise-induced increases in bloodflow occurred primarily in muscle, skin, or both vascularbeds. We consider it unlikely, however, that changes inskin blood flow contributed to the observed changes inblood flow to a meaningful extent. The room tempera-ture was maintained at a comfortable 24C, and distrac-tions inherent in the laboratory were kept to a mini-mum. Therefore, fluctuations in skin blood flow causedby thermoregulatory and arousal responses wereminimized.18

In our experiments, there was intersubject variation inthe level of force produced by the muscle contractionsduring the stimulation trial set at 25% above motorthreshold. We do not believe that this failure to controlthe absolute level of force production diminishes theimportance of our findings. Our intent was not to strictlycontrol for motor output between subjects, but toapproximate the intensity of muscle contractions thatmight be observed in clinical practice as well as providea measurable means for reproduction of ourexperiment.

We considered the possibility that an inability to respondto vasoconstrictor stimuli was responsible for the nega-tive findings in our subjects. Therefore, we assessed theirresponsiveness to 2 minutes of static handgrip exercise,an intervention that is known to cause time-dependent,sympathetically mediated vasoconstriction in the calf.9,10

Table 3.Hemodynamic and Thermal Responses to Static Handgrip Exercise (n520) in the Left (Stimulated) and Right (Control) Legs of Subjects WithoutKnown Cardiovascular or Neuromuscular Pathologya

Baselineb Handgripc Recoveryd


Mean arterial pressure (mm Hg) 85613 117622 101622




a Values shown are mean6SD.b Final 30 seconds of baseline period.c Final 30 seconds of handgrip exercise.d Final 30 seconds of recovery period.


In all subjects, we observed an increase in vascularresistance throughout the second minute of isometricexercise in both legs. Therefore, we believe it is unlikelythat our negative findings can be attributed to a nonspe-cific failure of vasoconstrictor mechanisms.

ConclusionOur data are consistent with evidence obtained throughdirect stimulation of peripheral nerves: namely, that theactivation threshold for sensory and motor fibers isbelow that of nociceptive C fibers.30 We demonstratedthat burst-mode TENS, applied at 3 different intensitylevels that our subjects did not perceive as painful, doesnot cause vasoconstriction or cooling of the skin. There-fore, our data indicate that the belief that postganglionicsympathetic nerves can be stimulated transcutaneouslyin subjects with no known health problems using clini-cally relevant stimulation parameters is incorrect. Wecannot exclude the possibility that, if TENS were ofsufficient stimulation intensity to cause a painfulresponse, it could stimulate sympathetic vasoconstrictorfibers. Future studies should investigate the immediateand long-term effects of burst-mode TENS on skintemperature, limb blood flow, and vascular resistance insubjects with known pathology.

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