Alleviating Muscle Soreness
Cause and Cure
By Shirley Vanderbilt
Originally published in Massage Bodywork magazine, October/November 2003.
Copyright 2003. Associated Bodywork and Massage Professionals. All rights reserved.
One of the most frequent and recurring injuries brought on by exercise is delayed onset muscle soreness (DOMS). Elite athletes and weekend warriors alike can be affected by this type of muscle strain, which is commonly associated with a return to training or the implementation of a new form of exercise activity. Although symptoms can vary in intensity, the general presentation includes stiffness, aching and tenderness, especially with movement and palpation, peaking at about 24-48 hours post-exercise and then gradually dissipating over the next few days. At times, discomfort can be severe enough to restrict normal movement but rarely requires medical care.1,2
For the average exercise novice or enthusiast, DOMS may only be an uncomfortable or inconvenient case of overindulging in an activity and underestimating its effects. The amateur athlete can rest a few days and with lesson learned, use better judgement when reinstituting their activity program. But for the professional with a rigorous training schedule, the situation is far more serious. DOMS has the potential to affect performance and injury risk through several factors: Perceived functional impairment; reduction in joint range of motion (ROM); reduction of strength and power; and compensatory changes in muscle recruitment with the strain of unfamiliar stress to other muscles.3
Most researchers agree on a multi-factor hypothesis (as yet unproven) for DOMS, beginning with the concept of initial muscle and connective tissue damage caused by eccentric exercise. Karoline Cheung et al. note, "Eccentric activity is characterized by an elongation of the muscle during simultaneous contraction. Thus if the external load exceeds the muscle's ability to actively resist the load, the muscle is forced to lengthen and active tension is generated."4 Several biochemical disruptions within the body's system are attributed to muscle injury, including ion imbalance, which activates an enzyme that can further degrade muscle protein, and an elevation in circulating neutrophils (white blood cells) leading to inflammation.5
According to J.E. Hilbert et al., "Within 8 hours of the initial injury, chemoattractants released by the damaged muscle tissue attract neutrophils which adhere to the endothelium of nearby blood vessels in a process called adhesion or margination." In this process, the neutrophils infiltrate the muscle tissue to eliminate damaged cells, but if the neutrophil action gets out of hand, healthy tissue can also be destroyed causing further muscle damage.6 It is theorized the combination of these and other mechanical disruptions along with edema and increased temperature in the area activates pain receptors in the muscle fiber and tendon junctions, resulting in the DOMS sensation.7
The lactic acid theory as a cause for DOMS has been put to rest. Lactic acid levels return to normal within an hour after exercise -- with or without massage -- and show no relationship to soreness up to 72 hours later.8 Although this myth has continued to make the rounds in massage circles, researchers do not currently factor it in to their multi-model hypothesis on DOMS.
Trial and Error
While a variety of treatments for DOMS have been studied, their proven success in relieving symptoms has been minimal. Research on the standard R.I.C.E. approach (rest, ice, compression and elevation) has shown no attenuation of symptoms other than a temporary analgesic effect. Stretching, widely recommended as a preventative, can actually induce muscle soreness. Other approaches with mixed or negative results include ultrasound, electric current techniques, homeopathy and hyperbaric oxygen therapy. Light exercise appears to provide temporary relief of pain, although findings in this area also vary from study to study.9
Massage, as a treatment for DOMS, has also had its ups and downs in clinical trials. In a systematic review published in 1998, Edzard Ernst examined the findings of seven previously published reports deemed to be valid, though flawed, controlled studies in this area. A major problem, as so often found with massage research, is small sample size. Nevertheless, Ernst notes the conceivable positive impact of massage on the hypothesized biochemical process of DOMS.10
Among the studies included in the Ernst review was a report by L.L. Smith et al. indicating that massage, administered two hours after injury, "decreased muscle soreness and increased the circulating neutrophil count, which suggests the treatment reduced neutrophil margination."11 In the final count, Ernst dismisses these results primarily because of the small sample of only 19 subjects. But despite its size limitation, this study served as a springboard for another recent (albeit equally small) project that we will examine here.
Massage and DOMS
Neutrophil margination is one of several markers of DOMS tracked by researchers Hilbert et al. in a paper published in 2003. The researchers were specifically interested in the effect of massage on neutrophil levels, muscle soreness, ROM and peak torque during the experience of DOMS. Noting a relationship between muscle damage, inflammation and muscle function, the study team proposed that theoretically, "If massage is rendered during the early stages of inflammation, the mechanical pressure applied with the massage might decrease neutrophil margination, thereby reducing inflammation and DOMS."12
Citing variations in previous studies regarding treatment length, application time and technique, the Hilbert team chose to use Swedish massage techniques already proven to be effective in reducing muscle soreness. In an attempt to improve on the Smith study, they also elected to forego a simple scale measurement of soreness in favor of the Differential Descriptor Scale (DDS) which takes into account both sensory and emotional aspects of pain. As their goal included assessment of not only physiological but also psychological effects of massage, they added the Profile of Mood States (POMS) to round out the psychological measurement.13
A group of 18 young adult subjects (male and female) were recruited for randomized assignment to either a massage or control group. Prior to initiation of the experimental treatment, all subjects were administered the DDS and POMS for evaluation of mood and muscle soreness and also assessed to determine baseline values for hamstring ROM and peak torque measurements. ROM was determined through the use of a standard uni-level inclinometer while performing a straight leg raise, for an average of three trials.14
For ROM baselines, subjects were instructed in the use of an isokinetic device designed to measure ROM and induce muscle soreness. After an initial warmup of eight submaximal and two maximal eccentric contractions with the right hamstrings, followed by a rest, subjects completed five maximal contractions, with the highest value obtained serving as their peak torque. Neutrophil count was documented for each subject by means of a 5 ml. blood sample, as examined by a trained laboratory technician.15
Following establishment of baseline values, subjects were instructed to begin the project with isokinetic warmup protocols using the same mechanism as for the baseline assessment of peak torque. To induce muscle damage, they continued with six sets of 10 maximal eccentric contractions, with one minute of rest between sets. This was followed by a five additional maximal eccentric contractions to establish peak torque at zero hours post-exercise. After a two-hour break, peak torque was again measured in the same manner as described.16
Subjects were then administered massage or a control treatment, according to their assignment. Massage techniques consisted of five minutes of effleurage and one minute of tapotement followed by 12 minutes of petrissage and an additional two minutes of effleurage. Treatment was administered by a senior physical therapy student with timing of strokes standardized to an audiotape. For the control group, the therapist applied lotion to the subjects' legs, then instructed them to rest while listening to the same audiotape used in the massage sessions. Both groups were advised the treatment might reduce inflammation from DOMS.17
Immediately after treatment, the POMS was again administered. Measurements were then taken at six and 24 hours post-exercise to document neutrophil count, peak torque, soreness, ROM and mood state. A final assessment of all measurements, excluding neutrophil count, was made at 48 hours post-exercise.18
Hilbert's team found no change in neutrophil count, although this had been a positive finding in the Smith trial. However, the present study involved a greater quantity of injured muscle mass. Researchers suggest this could account for the discrepancy, as there would be a greater inflammatory response in the larger muscle mass, possibly "making it more difficult to discern a treatment effect on neutrophil margination." Additionally, there was no discerned effect on peak torque or ROM. "Based on the current theory for DOMS," the team says, "the inability of massage to alter circulating neutrophil levels suggests that muscle damage induced by inflammation would not be attenuated," as was the case here.19
Researchers did find a decrease in perceived muscle soreness at 48 hours post-exercise, adding to what the team calls a growing body of evidence for this effect and lending to the premise that "the effects of massage may indeed be more psychological than physiological."20 This finding, suggests the team, could be due to improved sleep patterns, increased endorphin and serotonin levels, and decreased stress hormone levels. "Additionally, massage may activate pressure instead of pain receptors, thereby lowering soreness intensity."21
The Final Score
The whole point of research is to start with what we know and hopefully move to a new level, adding to the base from which we began. It appears there is still much to learn about DOMS. Researchers believe that by pinpointing the cause, we will be closer to identifying an effective treatment.
In their review of DOMS treatment strategies, Cheung et al. pose a number of interesting questions yet to be answered: Is the combination of models a valid explanation for the mechanism of DOMS? (A clarification of the specific timing of biochemical and mechanical events, from injury to full-blown symptoms, is essential to treatment.) Is DOMS preventable and what prophylactic strategies should we be using? And if we assume "that DOMS induces temporary alterations in joint kinematics and muscle activation patterns," what are the implications for a return to exercise activity?22
Once again we hark to the old refrain, "More research needed." As flawed and small as these studies are, they provide the building blocks for larger, more solid attempts to establish what is and what isn't valid in the field of massage therapy and bodywork.
Shirley Vanderbilt is a staff writer for Massage Bodywork magazine.
References
1 Cheung, Karoline et al. Delayed onset muscle soreness: Treatment strategies and performance factors. Sports Medicine 2003;33(2):146-7.
2 Hilbert, J.E. et al. The effects of massage on delayed onset muscle soreness. British Journal of Sports Medicine 2003 Feb;37(1):72.
3 Cheung, 150-3.
4 Ibid., 147, 149.
5 Hilbert, 72.
6 Ibid.
7 Cheung, 149-50.
8 Ibid., 147-8.
9 Ibid., 153-60.
10 Ernst, E. Does post-exercise massage treatment reduce delayed onset muscle soreness? A systematic review. British Journal of Sports Medicine 1998 Sep;32(3):212-4
11 Hilbert, 72.
12 Ibid.
13 Ibid.
14 Ibid., 72-73.
15 Ibid., 73.
16 Ibid.
17 Ibid.
18 Ibid.
19 Ibid., 74.
20 Ibid.
21 Ibid., 75.
22 Cheung, 160-1.
Copyright 2003. Associated Bodywork and Massage Professionals. All rights reserved.
One of the most frequent and recurring injuries brought on by exercise is delayed onset muscle soreness (DOMS). Elite athletes and weekend warriors alike can be affected by this type of muscle strain, which is commonly associated with a return to training or the implementation of a new form of exercise activity. Although symptoms can vary in intensity, the general presentation includes stiffness, aching and tenderness, especially with movement and palpation, peaking at about 24-48 hours post-exercise and then gradually dissipating over the next few days. At times, discomfort can be severe enough to restrict normal movement but rarely requires medical care.1,2
For the average exercise novice or enthusiast, DOMS may only be an uncomfortable or inconvenient case of overindulging in an activity and underestimating its effects. The amateur athlete can rest a few days and with lesson learned, use better judgement when reinstituting their activity program. But for the professional with a rigorous training schedule, the situation is far more serious. DOMS has the potential to affect performance and injury risk through several factors: Perceived functional impairment; reduction in joint range of motion (ROM); reduction of strength and power; and compensatory changes in muscle recruitment with the strain of unfamiliar stress to other muscles.3
Most researchers agree on a multi-factor hypothesis (as yet unproven) for DOMS, beginning with the concept of initial muscle and connective tissue damage caused by eccentric exercise. Karoline Cheung et al. note, "Eccentric activity is characterized by an elongation of the muscle during simultaneous contraction. Thus if the external load exceeds the muscle's ability to actively resist the load, the muscle is forced to lengthen and active tension is generated."4 Several biochemical disruptions within the body's system are attributed to muscle injury, including ion imbalance, which activates an enzyme that can further degrade muscle protein, and an elevation in circulating neutrophils (white blood cells) leading to inflammation.5
According to J.E. Hilbert et al., "Within 8 hours of the initial injury, chemoattractants released by the damaged muscle tissue attract neutrophils which adhere to the endothelium of nearby blood vessels in a process called adhesion or margination." In this process, the neutrophils infiltrate the muscle tissue to eliminate damaged cells, but if the neutrophil action gets out of hand, healthy tissue can also be destroyed causing further muscle damage.6 It is theorized the combination of these and other mechanical disruptions along with edema and increased temperature in the area activates pain receptors in the muscle fiber and tendon junctions, resulting in the DOMS sensation.7
The lactic acid theory as a cause for DOMS has been put to rest. Lactic acid levels return to normal within an hour after exercise -- with or without massage -- and show no relationship to soreness up to 72 hours later.8 Although this myth has continued to make the rounds in massage circles, researchers do not currently factor it in to their multi-model hypothesis on DOMS.
Trial and Error
While a variety of treatments for DOMS have been studied, their proven success in relieving symptoms has been minimal. Research on the standard R.I.C.E. approach (rest, ice, compression and elevation) has shown no attenuation of symptoms other than a temporary analgesic effect. Stretching, widely recommended as a preventative, can actually induce muscle soreness. Other approaches with mixed or negative results include ultrasound, electric current techniques, homeopathy and hyperbaric oxygen therapy. Light exercise appears to provide temporary relief of pain, although findings in this area also vary from study to study.9
Massage, as a treatment for DOMS, has also had its ups and downs in clinical trials. In a systematic review published in 1998, Edzard Ernst examined the findings of seven previously published reports deemed to be valid, though flawed, controlled studies in this area. A major problem, as so often found with massage research, is small sample size. Nevertheless, Ernst notes the conceivable positive impact of massage on the hypothesized biochemical process of DOMS.10
Among the studies included in the Ernst review was a report by L.L. Smith et al. indicating that massage, administered two hours after injury, "decreased muscle soreness and increased the circulating neutrophil count, which suggests the treatment reduced neutrophil margination."11 In the final count, Ernst dismisses these results primarily because of the small sample of only 19 subjects. But despite its size limitation, this study served as a springboard for another recent (albeit equally small) project that we will examine here.
Massage and DOMS
Neutrophil margination is one of several markers of DOMS tracked by researchers Hilbert et al. in a paper published in 2003. The researchers were specifically interested in the effect of massage on neutrophil levels, muscle soreness, ROM and peak torque during the experience of DOMS. Noting a relationship between muscle damage, inflammation and muscle function, the study team proposed that theoretically, "If massage is rendered during the early stages of inflammation, the mechanical pressure applied with the massage might decrease neutrophil margination, thereby reducing inflammation and DOMS."12
Citing variations in previous studies regarding treatment length, application time and technique, the Hilbert team chose to use Swedish massage techniques already proven to be effective in reducing muscle soreness. In an attempt to improve on the Smith study, they also elected to forego a simple scale measurement of soreness in favor of the Differential Descriptor Scale (DDS) which takes into account both sensory and emotional aspects of pain. As their goal included assessment of not only physiological but also psychological effects of massage, they added the Profile of Mood States (POMS) to round out the psychological measurement.13
A group of 18 young adult subjects (male and female) were recruited for randomized assignment to either a massage or control group. Prior to initiation of the experimental treatment, all subjects were administered the DDS and POMS for evaluation of mood and muscle soreness and also assessed to determine baseline values for hamstring ROM and peak torque measurements. ROM was determined through the use of a standard uni-level inclinometer while performing a straight leg raise, for an average of three trials.14
For ROM baselines, subjects were instructed in the use of an isokinetic device designed to measure ROM and induce muscle soreness. After an initial warmup of eight submaximal and two maximal eccentric contractions with the right hamstrings, followed by a rest, subjects completed five maximal contractions, with the highest value obtained serving as their peak torque. Neutrophil count was documented for each subject by means of a 5 ml. blood sample, as examined by a trained laboratory technician.15
Following establishment of baseline values, subjects were instructed to begin the project with isokinetic warmup protocols using the same mechanism as for the baseline assessment of peak torque. To induce muscle damage, they continued with six sets of 10 maximal eccentric contractions, with one minute of rest between sets. This was followed by a five additional maximal eccentric contractions to establish peak torque at zero hours post-exercise. After a two-hour break, peak torque was again measured in the same manner as described.16
Subjects were then administered massage or a control treatment, according to their assignment. Massage techniques consisted of five minutes of effleurage and one minute of tapotement followed by 12 minutes of petrissage and an additional two minutes of effleurage. Treatment was administered by a senior physical therapy student with timing of strokes standardized to an audiotape. For the control group, the therapist applied lotion to the subjects' legs, then instructed them to rest while listening to the same audiotape used in the massage sessions. Both groups were advised the treatment might reduce inflammation from DOMS.17
Immediately after treatment, the POMS was again administered. Measurements were then taken at six and 24 hours post-exercise to document neutrophil count, peak torque, soreness, ROM and mood state. A final assessment of all measurements, excluding neutrophil count, was made at 48 hours post-exercise.18
Hilbert's team found no change in neutrophil count, although this had been a positive finding in the Smith trial. However, the present study involved a greater quantity of injured muscle mass. Researchers suggest this could account for the discrepancy, as there would be a greater inflammatory response in the larger muscle mass, possibly "making it more difficult to discern a treatment effect on neutrophil margination." Additionally, there was no discerned effect on peak torque or ROM. "Based on the current theory for DOMS," the team says, "the inability of massage to alter circulating neutrophil levels suggests that muscle damage induced by inflammation would not be attenuated," as was the case here.19
Researchers did find a decrease in perceived muscle soreness at 48 hours post-exercise, adding to what the team calls a growing body of evidence for this effect and lending to the premise that "the effects of massage may indeed be more psychological than physiological."20 This finding, suggests the team, could be due to improved sleep patterns, increased endorphin and serotonin levels, and decreased stress hormone levels. "Additionally, massage may activate pressure instead of pain receptors, thereby lowering soreness intensity."21
The Final Score
The whole point of research is to start with what we know and hopefully move to a new level, adding to the base from which we began. It appears there is still much to learn about DOMS. Researchers believe that by pinpointing the cause, we will be closer to identifying an effective treatment.
In their review of DOMS treatment strategies, Cheung et al. pose a number of interesting questions yet to be answered: Is the combination of models a valid explanation for the mechanism of DOMS? (A clarification of the specific timing of biochemical and mechanical events, from injury to full-blown symptoms, is essential to treatment.) Is DOMS preventable and what prophylactic strategies should we be using? And if we assume "that DOMS induces temporary alterations in joint kinematics and muscle activation patterns," what are the implications for a return to exercise activity?22
Once again we hark to the old refrain, "More research needed." As flawed and small as these studies are, they provide the building blocks for larger, more solid attempts to establish what is and what isn't valid in the field of massage therapy and bodywork.
Shirley Vanderbilt is a staff writer for Massage Bodywork magazine.
References
1 Cheung, Karoline et al. Delayed onset muscle soreness: Treatment strategies and performance factors. Sports Medicine 2003;33(2):146-7.
2 Hilbert, J.E. et al. The effects of massage on delayed onset muscle soreness. British Journal of Sports Medicine 2003 Feb;37(1):72.
3 Cheung, 150-3.
4 Ibid., 147, 149.
5 Hilbert, 72.
6 Ibid.
7 Cheung, 149-50.
8 Ibid., 147-8.
9 Ibid., 153-60.
10 Ernst, E. Does post-exercise massage treatment reduce delayed onset muscle soreness? A systematic review. British Journal of Sports Medicine 1998 Sep;32(3):212-4
11 Hilbert, 72.
12 Ibid.
13 Ibid.
14 Ibid., 72-73.
15 Ibid., 73.
16 Ibid.
17 Ibid.
18 Ibid.
19 Ibid., 74.
20 Ibid.
21 Ibid., 75.
22 Cheung, 160-1.
