Effects of ultrasound and trolamine salicylate phonophoresis on delayed-onset muscle soreness.

Phonophoresis consists of using ultrasound to drive a drug through the skin and into underlying tissues. [1,2] In theory, ultrasound can enhance the transdermal delivery of certain pharmacologic agents to skeletal muscle tissue, bursae, tendons, and so on.

Thus, phonophoresis offers the potential advantage of delivering a pharmacologic agent in a relatively safe, painless, and easy manner to structures that lie somewhat deep within the body.

Several forms of drugs have been administered with phonophoresis. [2,3] Studies using animal models have suggested that ultrasound may enhance the percutaneous absorption of local anesthetics and anti-inflammatory steroids. Novak [4] documented the ability of ultrasound to increase the amount of lidocaine that was transmitted through the skin and into the quadriceps femoris muscles of rabbits. Ultrasound was able to drive topically administered cortisol to depths of 5 to 6 cm in porcine tissues. [5] Studies using human subjects have attempted to document the clinical effectiveness of phonophoresis in treating certain conditions. Griffin et al [6] found that ultrasonically driven hydrocortisone was superior to ultrasound alone in alleviating pain and inflammation in patients with arthirtic disorders. Kleinkort and Wood [1] found that hydrocortisone phonophoresis was effective in treating patients with various inflammatory conditions. In a case report, Wing [7] described using hydrocortisone phonophoresis to treat a patient who had temporomandibular joint pain.

Some preliminary evidence, therefore, exists that phonophoresis may improve percutaneous delivery and enhance the effects of local anesthetics and anti-inflammatory steroids. There is, however, a relative paucity of well-controlled studies that have evaluated the effectiveness of phonophoresis with other agents. There are essentially no reports of whether ultrasound phonophoresis enhances the analgesic and anti-inflammatory effects of the group of drugs known as salicylates.

Salicylates are a family of compounds that includes aspirin (acetylsalicylic acid) and drugs with effects similar to those of aspirin. In general, the salicylates evoke a number of pharmacologic effects, including analgesia and decreased inflammation. [8,9] These effects are believed to be due to the blockage of the production of prostaglandins. [10,11] Prostaglandins, which are normally produced locally at the site of injury and infection, play a principal role in mediating the inflammatory response. [12,13] Aspirin and similar drugs are potent inhibitors of the enzyme that synthesizes prostaglandins. Salicylates are therefore believed to attenuate pain and inflammation through their inhibitory effect on prostaglandin biosynthesis.

One type of aspirinlike drug, trolamine salicylate, has been manufactured as a topical cream under a variety of trade names. These preparations typically contain 10% trolamine salicylate and are available without a prescription.

Trolamine salicylate creams are applied to the skin's surface so that the drug is absorbed through the skin and into underlying tissues. The principal desired effect of topically applied salicylates is to decrease pain and inflammation in muscles and other subcutaneous tissues. [14,15] Investigations in animal models have indicated that a topical application of 10% trolamine salicylate has the ability to penetrate through skin and into muscle tissues even in the absence of ultrasound. [14,16] If utrasound can enhance the percutaneous absorption of this drug, phonophoresis may increase its analgesic and anti-inflammatory effects.

The clinical efficacy of any therapeutic intervention such as salicylate phonophoresis must be determined in some form of sample population. In this study, we elected to use a model of experimentally induced delayed-onset muscle soreness (DOMS). This model has been used previously by investigators [15,17] to assess various treatment regimens, including the effectiveness of topically applied salicylates. Delayed-onset muscle soreness is described as a sensation of pain and stiffness in skeletal muscle following a session of rigorous or unaccustomed exercise. [15,18] The term "delayed onset" refers to the fact that peak levels of soreness typically occur around 24 to 72 hours following the exercise session. Delayed-onset muscle soreness does appear, however, to be a transient disorder, and there are no apparent permanent effects of this condition. [18,19]

The exact factors responsible for DOMS are not fully understood. [18,20] Although earlier theories suggested that this phenomenon is caused by the accumulation of metabolites such as lactic acid, it is now believed that DOMS occurs following the generation of high levels of tension by muscles. [18,21,22] Large increases in tension, such as those occurring during eccentric contractions, are believed to alter the structure and transport characteristics of the sarcolemma. [18] Alterations in sarcolemmal structure and function may lead to disruption and leakage of the muscle cell membrane as well as activation of proteolytic enzymes that facilitate further intracellular damage and disarray of myofibrillar structure. [18,20,23] This damage to the muscle cell also appears to invoke an inflammatory response, as evidenced by the infiltration of monocytes, subsequent conversion of monocytes to macrophages, and activation of mast cells and histocytes in and around the muscle cell. [24,25]. This inflammatory response promotes swelling in the interstitium and leads to the production of nociceptive substances such as kinins, histamine, and prostaglandins. [18] The initial damage caused by mechanical factors such as eccentric contractions appears to initiate a series of cellular responses that in turn contribute to the painful symptoms associated with DOMS.

The fact that DOMS is associated with symptoms suc as pain as well as cellular changes consistent with an inflammatory response makes this phenomenon an acceptable model for studying the effect of nonsteroidal anti-inflammatory--analgesic preparations such as trolamine salicylate. [15] We must emphasize that DOMS was induced in our study as an experimental clinical model to test the effectiveness of a specific intervention: salicylate phonophoresis. Our selection of salicylate phonophoresis does not mean that this intervention is necessarily advocated for use in this specific problem (ie, patients exhibiting DOMS), but merely that this model may be helpful in documenting the efficacy of salicylate phonophoresis in a clinical model of musculoskeletal pain and stiffness.

The primary purpose of this study was to determine the effect of salicylate phonophoresis as compared with ultrasound used alone on DOMS. We attempted to determine whether phonophoresis increases the effectiveness of trolamine salicylate cream in attentuating the muscle soreness that typically occurs 1 to 2 days after some forms of exercise. The effect of salicylate phonophoresis was compared with the effect of ultrasound used alone to help determine any possible effect of ultrasound on DOMS. This comparison was done so that any ultrasound effects could be distinguished from the pharmacologic effects of trolamine salicylate when both are used together in the form of salicylate phonophoresis.

Method

Subjects

The subjects in this study were 40 college-aged women. Only female subjects were selected in order to eliminate any potential gender-related differences in perception of muscle soreness. The subjects were not engaged in any tema sports or in a formal weight-training program. All subjects had normal upper-extremity function bilaterally and had not sustained any recent injury to either upper extremity. Each subject provided informed consent in accordance with institutional policy.

Overview of Experimental

Design

Subjects participated in this study on 4 consecutive days. The procedures used on each day are outlined in Figure 1. Muscle soreness was initiated on day 1 after baseline measurements for muscle soreness and active elbow range of motion (ROM) were recorded. Measurements of muscle soreness and ROM were taken each succeeding day prior to any other procedure or treatment. Subjects received three consecutive treatments beginning on day 1, with approximately 24 hours separating each treatment. The type of treatment depended on the assigned group for each subject. The last set of measurements taken on day 4 was not followed by a treatment. Specific aspects of the experimental design and procedures are described as follows.

Treatment Groups

Subjects were assigned randomly to one of four treatment groups. Each group corresponded to one of the possible combinations of the two principal factors in this study: ultrasound (either sham or real) and treatment cream (either placebo or trolamine salicylate). Subjects in group 1 (n=10) received sham ultrasound with placebo cream. Group 2 (n=10) received sham ultrasound with 10% trolamine salicylate cream. Group 3 (n=10) received ultrasound with placebo cream as the coupling medium. Group 4 (n=10) received salicylate phonophoresis using ultrasound with 10% trolamine salicylate cream as the coupling medium.

Treatment Creams

The trolamine salicylate cream (Aspercreme *) used in this study contains 10% trolamine salicylate in a base consisting primarily of water and lanolin. The placebo cream we used is a commercially available ultrasound coupling medium (Rich-Mar Lotion (+) that is similar in composition and appearance to the trolamine salicylate preparation. Transmission of ultrasound through the placebo cream and the trolamine salicylate cream was measured using an ultrasound power meter (Model UPM-30 (++)). Transmission characteristics of the placebo and salicylate creams are presented in Table 1.

Treatment Procedures

One arm of each subject was selected randomly for treatment. The contralateral arm served as a comparison (control) within each subject. The designated treatment (according to the subject's assigned group) was applied to the anterior surface of the distal half of the arm and proximal one fourth of the forearm (ie, the distal portion of the muscle belly and the distal attachment of the elbow flexors). This area was typically reported after muscle soreness was initiated on day 1 as the location of greatest soreness in all subjects. Subjects were seated during each treatment with the treated arm supported on an adjacent table.

All treatments were given for 5 minutes. A Rich-Mar Model No. IV ultrasound machine (+) with a fixed frequency of 1 MHz and a [10-cm.sup.2] sound head was used to administer the treatments. Treatment procedures commenced with the therapist aplying a fixed amount (10-12 mL) of either placebo or salicylate cream to the skin and then applying the ultrasound head over the cream using small, continuous, circular movements. For groups receiving ultrasound, treatment was initiated at 1.5 [W/cm.sup.2] of continuous-wave ultrasound, and the intensity was decreased if the subject experienced anything other than a sensation of mild warmth. The duration and intensity of ultrasound

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treatment were selected based on suggested clinical treatment characteristics, [2,226] and the range of intensities used in this study was equivalent to that of intensities used in previous clinical studies using phonophoresis techniques. [1,6,7] Sham ultrasound consisted of performing the ultrasound treatment without the machine being turned on. Treatments were given by two therapists (BGL and JJC) using a standardized set of procedures, with the same therapist performing all the treatments on any given subject.

Subjects were not informed of the group to which they were assigned and were therefore blinded to both the ultrasound and salicylate treatments. Subjects were unaware of whether ultrasound was applied, because the ultrasound machine was shielded from their view. The salicylate and placebo creams were applied via coded bottles that were indentical in appearance. Salicylate treatment was applied in a double-blind fashion, because the therapist applying the treatment was also unaware of the contents of the applicator bottles.

Inducement of Delayed-Onset

Muscle Soreness

Repeated eccentric contractions were used to induce DOMS bilaterally in the elbow flexors. The elbow flexors were isolated using a preacher curl bench. This device enabled the subject to sit with her arms resting on a padded board and positioned in front of the body at a 45-degree angle downward from the axilla. Resistance was applied bilaterally to the elbow flexors by having the subject grasp a barbell and alternately flex and extend both elbows throughout a full ROM.

With the subject positioned on the preacher curl device, a one-repetition maximum (1-RM) of the elbow flexors was determined. The 1-RM represented the amount of weight the subject could lift concentrically one time before the elbow flexors became fatigued. Using a weight equivalent to the 1-RM, the subject performed repeated eccentric contractions of the elbow flexors. Each subject performed only eccentric contractions by slowly lowering the barbell from a fully flexed to a fully extended elbow position. After each eccentric contraction, the weight was returned to a starting position of full elbow flexion by one of the investigators. Each subject performed three sets of 10 repetitions of the exercise, with a 2-minute rest between each set.

Subject's Rating

of Muscle Soreness

A visual analogue scale (VAS) was used to assess muscle soreness in each subject on each day of the study. The validity and reliability of this tool in measuring experimentally induced pain have been established elsewhere. [27] A recent investigation [28] also used a VAS to measure exercise-induced muscle soreness, thus documenting the application of this tool in measuring DOMS. The VAS used in our study consisted of a continuous horizontal line 150 mm in length, with anchor points of "no soreness" and "worst possible soreness" at the left and right ends of the line, respectively. An identical set of instructions was read to each subject prior to completing each VAS, and subjects indicated the amount of soreness by placing a slash somewhere along the VAS. Relative soreness was then calculated by measuring the distance of the slash from the left end of the VAS. Subjects completed a separate VAS for each upper extremity, and they were not allowed to compare one VAS result with another.

Measurement of

Elbow Range of Motion

The effect of DOMS on active elbow ROM was determined using a universal goniometer. The goniometer axis was placed over the lateral epicondyle of the humerus, with the stationary and movable arms aligned along the lateral midline of the humerus and the radius, respectively. Active ROM was measured as the total excursion from full elbow flexion to full elbow extension. A standardized testing procedure was established to ensure proper identification of bony landmarks and goniometer alignment. Subjects were given identical instructions prior to each measurement, and a single measurement of total joint excursion was recorded at each session. All ROM measurements were recorded by two therapists (BGL and JJC), with the same therapist performing each measurement on any given subject. The reliability of goniometer measurement of active elbow ROM using this standardized procedure has been established by several investigators. [29-31]

Statistical Analysis

The VAS values recorded from the treated and control (contralateral) arms of the subjects within each group on each day of the study were compared using a Student's paired t test. This statistcal analysts was used to allow a comparison of soreness between each subject's arms without attempting to compare one subject with another or values recorded from one day to another. Differences between the VAS values for the two arms were considered significant at the .05 level of probability. Goniometric measurements of elbow ROM were analyzed for each arm within each group using a two-way analysis of variance (ANOVA). This type of ANOVA was selected to allow comparison of baseline values of elbow ROM recorded on day 1 for each arm and group to be compared with subsequent values on days 2, 3 and 4. The days of the study were regarded as treatment effects, and subjects were considered as block effects to account for intersubject variability. Post hoc analysis consisted of Duncan's Multiple-Range Test. Differences were considered significant at the .05 level of probability.

Results

Changes in muscle soreness, as indicated by the VAS values obtained for the control and treated arms of the subjects in each group on each day of the study, are illustrated in Figure 2. Soreness increased from negligible levels on day 1 to appreciable levels in both arms in all groups by day 2. Most groups reported peak levels of soreness on day 3, reaching levels that ranged between 29% and 45% of the maximum possible rating (150 mm). Soreness began to decline toward baseline values by day 4 of the study.

The VAS ratingf of elbow flexor soreness for the control and treated arms on day 2 through day 4 are presented for each group in Table 2. Baseline soreness levels recorded on day 1 are not shown in the table, because these values were essentially zero for all arms and groups. In group 1, no consistent or significant differences were found between the subjects' treated and control arms throughout the study. In group 2, soreness was essentially the same between the treated and control arms on day 2, but soreness in the treated arm was reported to be 11% less on day 3 and 21% less on day 4 relative to the control arm. These differences, however, were not statistically significant. In group 3, soreness in the treated arm was 15%, 25%, and 6% greater in the treated arm versus the control arm on days 2, 3, and 4, respectively. The increased soreness in the treated arm of the group 3 subjects on day 3 was significant (P<.05). The subjects in group 4 did not display any consistent or significant differences in soreness between the treated and control arms throughout the study.

Results of the goniometric measurement of elbow ROM are shown in Table 3. Elbow ROM in the control arm was significantly reduced relative to day 1 baseline values in most groups following indicement of DOMS. In three of the four groups (groups 1, 3, and 4), ROM in the control arm was significantly reduced on days 2 and 3, with two groups (groups 1 and 3) continuing to display a significant decrease on day 4. Elbow ROM values for the control arm in group 2 were not significantly different from one another throughout the 4 days of the study. In the

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treated arm, elbow ROM was significantly less on day 2 and day 3 relative to day 1 baseline values in groups 1, 2, and 3. Elbow ROM remained significantly less on day 4 in group 3. The ROM values for the treated arms of the subjects in group 4, however, did not decrease significantly until day 3, and elblow ROM had returned to levels that were not significantly different from baseline values by day 4.

Discussion

The primary purpose of this study was to determine the effectiveness of trolamine salicylate photophoresis in decreasing pain and stiffness associated with DOMS. Delayed-onset muscle soreness was used in this study as an experimental model that could be induced in a relatively easy and predictable fashion in a group of nondisabled volunteers. The execricse protocol used in this study was successful in creating appreciable levels of soreness bilaterally in the subjects' elbow flexors (Fig. 2). The time course of DOMS seen in this study was consistent with that reported by other investigators using similar exercise protocols. [15,17] Thus, the model of DOMS used in our study offered an opportunity to assess the effectiveness of a particular therapeutic intervention: salicylate phonophoresis.

As indicated in Figure 2, some variability existed in the soreness perceived in each group. Subjects in group 1 reprted values that ranged between 22% and 43% lower than similar values reported by the other three groups. It is not clear why subjects in group 1 typically indicated lower values for soreness on each day of the study. These values, however, did follow the same relative trend as that seen in the other groups. For example, VAS values for the subjects in group 1 indicated that soreness was apparent by day 2, peaked by day 3, and began to subside by day 4. The trend of lower VAS values also was consistent in both arms of the subjects in group 1, thus allowing a comparison between the control and treated arms within this group. It appears, therefore, that the average perception of soreness was simply lower in these subjects than in the other subjects, although the reasons for this distinction are unknown.

The ability of trolamine salicylate to reduce DOMS in the absence of ultrasound should be examined before considering the effects of trolamine salicylate phonophoresis. In this study,

[TABULAR DATA OMITTED]

the group that received trolamine salicylate without ultrasound (group 2) did not display any significant differences in muscle soreness between the control and treated arms. Closer inspection, however, reveals that the degree of soreness was progressively reduced in the treated arm versus the control arm on each successive day of the study. In group 2, soreness was reduced 1%, 11%, and 21% in the treated arms on days 2, 3, and 4, respectively (Tab. 2). Although this trend was not statistically significant, a previous investigation of the effectiveness of trolamine salicylate on DOMS indicated that topical application of this drug 4 times per day can decrease the severity and duration of muscle soreness. [15] In our study, trolamine salicylate was applied only once each day. Consequently, trolamine salicylate does appear to have pharmacologic properties thqat attenuate the effects of DOMS, but these effects may not have been obvious in group 2, given the application schedule used in this study. The principal focus of this study, however, was to examine the effects of administering trolamine salicylate with ultrasound, and the results from the subjects receiving salicylate phonophoresis must now be considered.

The basic hypothesis being tested in this study was that, if trolamine salicylate phonophoresis were effective, DOMS would be diminished in the arms of subjects receiving this treatment (ie, group 4). The VAS findings indicated that DOMS was not reduced in group 4. The results from this group must be considered, however, in relation to the findings from the group that received ultrasound applied through a standard coupling medium (ie, group 3). It was found that soreness was increased in the arms of subjects in group 3. Presented here are a possible explanation for the increased soreness in subjects receiving ultrasound and a discussion of how this finding may relate to the results obtained for subjects receiving trolamine salicylate phonophoresis.

Although it is not clear exactly how ultrasound facilitated an increase in DOMS in this study, ultrasound's ability to increase tissue heating may have contributed to the factors producing DOMS. It has been shown that elevated local and systemic temperatures attributable to extreme muscular exertion can directly damage skeletal muscle structure and elicit cellular changes that are similar to those seen in DOMS. [18,32] Increased temperatures could also contribute to the pain associated with DOMS by enhancing the inflammatory response and by increasing the stimulation of pain-transmitting neurons (ie, types C and A delta). 18,33] Nonthermal effects of ultrasound, such as acoustic streaming and caitation, have been suggested as being able to influence cellular membrane transport and may be deleterious if the membrane structure has been previously compromised. [34] It appears that one or more of the characteristics associated with ultrasound may have accelerated the mechanisms underlying DOMS in some way, thus accounting for the increased soreness observed in this study.

Although soreness was increased in the arms of subjects receiving ultrasound applied through a standard coupling medium, soreness was not increased in subjects receiving ultrasound applied through trolamine salicylate cream (ie, salicylate phonophoresis). This finding suggests that the ability of ultrasound to augment DOMS was offset by the pharmacologic action of trolamine salicylate. Because trolamine salicylate appears to exert its beneficial effects by inhibiting prostaglandin biosynthesis, the role of prostaglandins must be considered in light of these findings. Postaglandins are a group of pharmacologically active compounds that are routinely found at sites of inflammation and tissue injury. [12,13,35] The exact role of prostaglandins in mediating inflammation is not known, but these compounds are generally believed to accelerate the pain and swelling associated with an inflammatory response. [12,36,37] As discussed earlier, cellular changes consistent with an inflammatory response have been noted in DOMS, and this response may involve the production of substances such as prostaglandins. In our study, ultrasound appeared to augment some of the factors involved in DOMS. The ability of ultrasound to augment DOMS may be due, at least in part, to the increased production of pro-inflammatory substances such as prostaglandins. Because trolamine salicylate decreases the formation of prostaglandins, an increase in soreness was prevented and trolamine salicylate were applied simultaneously.

Thus, trolamine salicylate phonophoresis did not attenuate soreness, but it appeared to blunt any increase in soreness that would have occurred if salicylate had not been used concurrently with the ultrasound. Clinical implications of this finding are discussed later.

An alternative explanation for the findings of this study is based on the different ultrasound transmission characteristics of the placebo and trolamine salicylate preparations. Various pharmaceutical products exhibit a wide range of abilities to transmit ultrasound, with some preparation transmiting little or no ultrasound and other preparations transmitting ultrasound to a moderate degree. [38] Over the range of ultrasound intensities used in this study, transmission of ultrasound through the trolamine salicylate cream was typically 25% to 37% less than transmission through the standard coupling agent used as a placebo cream. Hence, the increased soreness seen in the subjectsw receiving standard ultrasound may not have occurred when ultrasound was applied through the trolamine salicylate cream simply because one found to one third less ultrasound was reaching the affected tissues. Consequently, it is not known whether soreness would have ill been attenuated in group 4 if transmission of ultrasound through the trolamine salicylate cream was equal to transmission of ultrasound through the placebo cream.

Delayed-onset muscle soreness is typically associated with pain and stiffness that leads to a transient decrease in joint ROM in affected areas. [17,39] In this study, untreated (control) arms of the subjects in three of the four groups (ie, groups 1, 3, and 4) experienced a significant decrease in active elbow ROM that in most cases persisted through day 4. Why the control arms of the subjects in group 2 did not exhibit any appreciable decrement in ROM throughout this study is not apparent.

Results from the goniometric testing of the treated arms lend additional support to the idea that trolamine salicylate counteracted some of the effects of ultrasound on DOMS. Subjects who received ultrasound through a standard coupling medium (ie, group 3) were found to have a significant reduction in elbow ROM in the treated arm by day 2 of this study, and this decrase in elbow ROM persisted through day 3 and day 4. In contrast, subjects who received trolamine salicylate phonophoresis (ie, group 4) did not exhibit a significant reduction in elbow ROM until day 3, and their elbow ROM returned to levels that were not significantly different from baseline values by day 4. The observed decrease in elbow ROM occurred later and waxs resolved more rapidly in subjects receiving salicylate phonophoresis than in subjects treated only with ultrasound. This finding suggests that salicylate phonophoresis was able to blunt some of the effects of ultrasound on DOMS at least in the early and later stages of this phenomenon. The inability of salicylate phonophoresis to prevent a decrease in elbow ROM on day 3 may be related to the fact that the cellular changes underlying DOMS typically reach peak levels about 48 hours after the initial exercise session. [18] These levels correspond to the measurements taken on day 3 of this study, and the pharmacologic effects of trolamine salicylate may have been unable to offset the deleterious effects of ultrasound during peak levels of cellular activity in DOMS.

Clinical Implications

Ultrasound used alone appeared to actually augment the development of DOMS when this treatment was given immediately after the exercise session and again at 24 hours and 48 hours following exercise. Clinicians therefore may choose to avoid applying ultrasound through a standard coupling medium to muscle groups that are in the process of developing DOMS. Application of ultrasound through trolamine salicylate cream during the time that DOMS was developing appeared to blunt the increased soreness that occurred when ultrasound was used alone. Salicylate phonophoresis however, does not appear to be an effective method of preventing the development of DOMS, because soreness was not diminished in the arms of subjects receiving daily treatments of ultrasound applied through salicylate cream. Thus, this treatment regimen probably will not lessen the severity of muscle soreness that develops following a specific exercise session.

The results of this study may have additional clinical implications when DOMS is considered as an experimental model of musculoskeletal pain and stiffness. Delayed-onset muscle soreness appears to have certain attributes that mimic other inflammatory conditions. Therefore, it is interesting to speculate whether the opposing effects of trolamine salicylate and ultrasound could be useful when applied simultaneously in a clinical setting. Presumably, the ultrasound would still be able to exert some beneficial effects (eg, increased tissue heating, increased blood flow), whereas any acceleration of the inflammatory response would be counteracted by the trolamine salicylate

For example, conditions such as rheumatoid arthritis, bursitis, and tenosynovitis might benefit from the increased heating and blood flow produced by the ultrasound, whereas the trolamine salicylate might negate any tendency for the ultrasound to also increase the inflammatory response underlying these conditions. This implication is speculative, and subsequent studies involving salicylate phonophoresis may help shed additional light on the effectiveness of this technique in resolving clinical disorders for which a reduction in pain and inflammation is desirable.

Conclusion

This study found that ultrasound used alone increased the symptoms associated with DOMS. These increases were not observed when ultrasound was administered through a topically applied anti-inflammatory-analgesic agent (ie, trolamine salicylate). These results suggest that the ability of ultrasound to enhance the mechanisms underlying DOMS may be offset by the pharmacologic activity of trolamine salicylate. Clinical implications of these findings are that the technique of salicylate phonophoresis may be indicated when it is desirable to administer ultrasound without promoting cellular changes that mimic an inflammatory response. Future studies should further investigate the use of this therapeutic intervention on other musculoskeletal conditions that exhibit an inflammatory response as an underlying mechanisms.

(*) Thompson Medical Co, PO Box 5264, New York, NY 10150.

(+) Rich-Mar Corp, PO Box 879, Inola, OK 74036.

(++) Ohmic Instruments Co, St Michaels, MD 21663.

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CD Ciccone, PhD, PT, is Associate Professor, Department of Physical Therapy, School of Health Sciences and Human Performance, Ithaca College, Ithaca, NY 14580 (USA). Address all correspondence to Dr Ciccone.

BG Leggin and JJ Callamaro were physical therapy students, Program in Physical Therapy, Ithaca College, when this study was conducted.

The results of this study were presented in a platform presentation at the Annual Conference of the American Physical Therapy Association, Anaheim, California, June 24-28, 1990.

This study was approved by the Human Subjects Research Committee of Ithaca College.

This article was submitted December 27, 1990, and was accepted May 6, 1991.