Contrast With Compression Therapy Enhances Muscle Function Recovery and Attenuates Glycogen Disruption After Exercise

Abstract

Background:

Exercise-associated muscle damage (EAMD) temporally impairs muscle function and intramuscular glycogen storage. Contrast with compression (CwC) therapy provides localized EAMD treatment with minimal changes in core/tissue temperature that can impair glycogen resynthesis.

Hypothesis:

CwC will enhance the recovery of strength, power, and joint mobility, reduce markers of EAMD, and attenuate the disruption of glycogen storage observed after damaging exercise.

Study Design:

Randomized controlled trial with crossover design.

Level of Evidence:

Level 2.

Methods:

Ten men completed 2 bouts of eccentric elbow flexor exercise, separated by 1 week, using contralateral arms. After each bout, participants received either CwC therapy (at 0, 24, and 48 h postexercise) or no therapy with intervention order and limb randomly assigned. Prior to (pre-exercise) and 1, 24, 48, and 72 h after each exercise bout, muscular strength, muscular power, intramuscular glycogen, creatine kinase, muscle thickness, muscle soreness, pressure pain threshold, active elbow flexion, passive elbow extension, and dietary intake were assessed. Comparisons were made between conditions over time (interaction effects) using separate repeated-measures analyses of variance/multivariate analyses of variance and effect sizes (Cohen d) to describe treatment effect at each time point.

Results:

Significant interaction effects were observed for muscular strength (d = 0.67-1.12), muscular power (d = 0.20-0.65), intramuscular glycogen (d = 0.29-0.81), creatine kinase (d = 0.01-0.96), muscle thickness (d = 0.35-0.70), muscle soreness (d = 0.18-0.85), and active elbow flexion (d = 0.65-1.17) indicating a beneficial effect of CwC over time (P ≤ 0.05). In contrast, no significant interaction effect was observed for pressure pain threshold or passive elbow extension (P > 0.05).

Conclusion:

These results support the use of CwC for the recovery of muscle function after damaging exercise in male patients and indicate that CwC attenuates, but does not remove, the disruption of intramuscular glycogen stores observed after intense eccentric exercise.

Clinical Relevance:

Glycolysis-dependent athletes may benefit from CwC therapy after training/competition that causes EAMD.

In sports requiring frequent training or competition, therapeutic practices that enhance the rate of recovery from previous exercise bouts can provide athletes with a competitive advantage. As such, various recovery modalities have been developed to mitigate the negative effects of exercise-associated muscle damage (EAMD) such as muscle soreness, inflammation, and the impairment of muscle function during the recovery process. Two common modalities, contrast therapy and compression therapy, reduce EAMD symptoms and improve the recovery of muscular strength after intense exercise.^4,14,18 However, the combined effects of contrast with compression (CwC) therapy on EAMD, inflammation, soreness and the recovery of muscular strength, power, and joint mobility after damaging exercise are unknown. Furthermore, although previous studies have observed that both EAMD and decreased tissue temperature can impair glycogen storage and synthesis rates, no studies have investigated the effects of any recovery modality on intramuscular glycogen storage after damaging exercise.^7,25 As neither contrast nor compression therapy substantially decreases tissue temperature, CwC presents itself as a promising therapy for enhancing glycogen resynthesis after damaging exercise.^13,19

Contrast therapy is the combination of heat and cryotherapies and involves repeated and alternated delivery of hot and cold temperatures to the target tissue. Contrast water therapy, in the form of contrasting hot- and cold-water baths, has been shown to reduce EAMD, inflammation, and delayed onset muscle soreness while enhancing the rate of recovery of muscular strength, power, and joint mobility after damaging exercise.^4,12,19 Contrast water therapy has recently gained popularity over cryotherapy, as the 2 modalities show similar clinical effects, ⁸ whereas cryotherapy has been shown to interfere with anabolic signaling ⁹ and training adaptations ²³ and to reduce glycogen synthesis rate. ²⁵ Unlike cryotherapy, whose therapeutic goal is to reduce intramuscular temperature, metabolism, and blood flow,^8,22 the proposed therapeutic effect of contrast therapy is an alternation in blood flow resulting from peripheral vasoconstriction during the cold portion and vasodilation during the heat portion.^6,8 Therefore, contrast therapy results in a minimal change in mean tissue temperature^13,19 and may avoid negative effects attributed to cryotherapy.^9,23,25 With recent advances in technology, CwC therapy can be delivered to targeted tissues using a pressurized cuff and mobile hot and cold fluid reservoirs. This novel recovery modality also provides several logistical advantages over contrast water therapy such as reduced overhead costs, mobile treatment options, targeted treatment to injured tissue, rapid temperature transitions, improved hygiene, and passive/programable treatment options.

Although studies have investigated the effects of various recovery modalities on muscle function after damaging exercise,^4,8 no studies have investigated their effects on intramuscular glycogen stores during recovery.^11,25 This is of particular interest because intramuscular glycogen is the predominant energy source during moderate to high intensity activities and because a muscle’s ability to store glycogen is negatively affected by muscle damage.^3,7,17 However, it is possible that therapeutic treatments may hinder muscle glycogen recovery after exercise. Two studies have investigated the effects of cryotherapy on glycogen synthesis rates after treatment, albeit isolated from exercise, with equivocal results.^11,25 With recent advances in technology, this gap in knowledge can now be addressed because valid and reliable measures of intramuscular glycogen can now be obtained without the need for repeated muscle biopsies, which can interfere with the recovery process.^14,15,20

Given the need to validate CwC as a treatment for EAMD and the lack of understanding of how such treatments affect intramuscular glycogen stores, the purpose of the present study is 3-fold: (1) to determine the effects of CwC on the recovery of muscular strength, power, and joint mobility after a damaging bout of exercise; (2) to determine the effects of CwC on muscle soreness and EAMD after a damaging bout of exercise; and (3) to determine the effects of CwC on the recovery of intramuscular glycogen stores relating to EAMD. We hypothesized that CwC therapy will (1) enhance recovery of strength, power, and joint mobility, (2) reduce muscle soreness and measures of EAMD, and (3) enhance intramuscular glycogen recovery when compared with when no treatment is provided (CON).

Methods

Experimental Approach to the Problem

This study utilized a randomized controlled trial with a repeated-measures crossover (within-within) design. Participants completed a bout of damaging unilateral eccentric elbow flexor exercise and had their recovery from the exercise monitored for 72 h. Then after 1 week of recovery, participants completed a second bout of damaging unilateral eccentric elbow flexor exercise using their contralateral arm and once again had their recovery monitored for 72 h. After each bout of exercise, participants either received either CON or CwC therapy at 0, 24, and 48 h postexercise. The order of interventions, as well as the prescription of each intervention to the participants’ self-reported dominant and nondominant arms, were randomized and counterbalanced using a block randomization table.

Recovery from each eccentric exercise bout was assessed by having participants complete a series of tests in order to determine changes in muscular strength, muscular power, joint mobility, muscle thickness, soreness, creatine kinase (CK), and intramuscular glycogen stores from pre-exercise values at 1, 24, 48, and 72 h after the exercise.^15,20 Tests were performed in the following order: (1) blood measure of CK; (2) ultrasound measures of intramuscular glycogen and muscle thickness; (3) joint mobility testing; (4) soreness measures; and (5) strength and power testing. In the CwC condition, testing was performed immediately prior to the treatment with the exception of the 1-hour postexercise time point, which occurred 45 min after the treatment. During the 1-hour period between the exercise intervention and 1-hour postexercise time point, participants in both conditions rested in a seated position and refrained from performing any physical activity or consuming food or water. Throughout all testing, participants were required to keep dietary logs, which were collected daily, and participants were instructed to replicate their dietary consumption.

Participants

Ten healthy, physically active men aged 18 to 35 years volunteered to take part in this study. This study was approved by the institutional review board of the university at which the study was completed and each participant provided written, informed consent prior to taking part in the study. In order to qualify for the study, participants had to be free from any upper extremity injury in the past 6 months. For the duration of the study, starting 2 days prior to the first day of testing, participants were required to avoid alcohol consumption, the use of anti-inflammatory medications, and non–study related exercise. Participants were instructed to attend all sessions in a euhydrated state. To determine hydration status, prior to the start of each testing session, participants provided a clean, midstream urine sample from which urine specific gravity was measured. Participants were only allowed to take part in testing if their urine specific gravity was less than 1.025. Participant descriptors included height, which was measured using a stadiometer, and body mass, relative body fat percentage, arm circumference, and estimated muscle mass in each arm, which was measured using an 8-polar multifrequency bioelectrical impedance assessment (InBody 770).

Contrast With Compression Therapy Intervention

The CwC intervention was administered to the exercised arm via a 12-inch pressurized cuff, which alternated between flowing hot (42°C) and cold (8°C) fluid (Solid State Cooling Systems Inc). The cuff was strapped around the upper arm firmly (10-20 mmHg) and held in place by 2 Velcro™ straps, which are a part of the cuff’s design (Figure 1). Prior to the start of treatment, the participants sat comfortably with their forearm resting on a table approximately level of their xiphoid process and their arm slightly flexed so that the cuff was not in contact with their body (Figure 1). During the treatment, a temperature-controlled fluid would flow from the CwC device through the bladder network on the cuff, which added additional compressive forces during the cold phase with a target skin pressure of 60 mmHg, but not during the heat phase. The therapy consisted of 10 minutes of treatment where fluid temperature would alternate between hot and cold in 1-minute intervals resulting in 5 1-minute exposures to both heat and cold. The CON condition did not have any type of recovery intervention.

Figure 1.

Depiction of participant positioning (a) while receiving contrast with compression therapy and (b) during elbow flexor strength and power testing.

EAMD Protocol

Eccentric exercise bouts were performed using an isokinetic dynamometer (System 4; Biodex). Each participant had his exercised arm, chest, and hips strapped into position, and the dynamometer’s axis of rotation was positioned in line with the center of his trochlea and capitulum of the humerus. In this position, participants then performed 30 maximal voluntary eccentric contractions consisting of 5 sets of 6 repetitions at a velocity of 30 deg/s⁻¹. Each contraction was performed through 90° of total range of motion with a starting position of 135º of elbow flexion, which resulted in a 3-second contraction duration. Between each repetition, participants were given 10 seconds to passively return their forearm to the starting position before the subsequent repetition and 2 minutes of passive recovery was given between each set. ⁵

Creatine Kinase

Measurements of CK were taken from blood samples obtained from a single digit. After the digit was prepped, lanceted, and the initial blood was removed, a minimum of 60 μL of capillary blood was collected using a capillary blood collection system (Greiner Bio-One MiniCollect). Collected blood was treated with ethylenediamine tetra-acetic acid to prevent clotting, and fresh blood was centrifuged so an aliquot of plasma could be collected. At least 30 μL of nonhemolyzed plasma from each time point was stored in a −80°C freezer until the completion of the study (no more than 3 months) at which time all samples underwent a bioassay to determine CK levels. The bioassay utilized was an enzyme-linked immunosorbent assay, which used colorimetric determination of CK activity at 340 nm with a detection range of 5 to 300 U/L (ECPK007-EnzyChrom; BioAssay Systems USA). During the analysis, nondiluted 10 μL samples from each time point were tested in duplicate with all samples from the same participant tested on the same plate. Assay instructions were followed precisely and measurements were made using a Spectramax plate reader (Molecular Devices) and associated software.

Intramuscular Glycogen and Muscle Thickness

Ultrasound images taken of the biceps brachii were used to determine changes in intramuscular glycogen as well as changes in muscle thickness. Prior to images being taken, participants lay supine for 20 minutes to allow for any fluid shift to occur. Measurements were taken while the participants lay supine on a padded medical examination table with their arm minimally abducted, so that the arm was not in contact with the body and their elbow fully extended in a relaxed and supported position. In this position, 3 nonconsecutive transverse images were taken by a B-mode ultrasound device (LOGIQ 7; General Electronics) and recorded using a 5.5-cm linear transducer (ML6-15; General Electronics). The same trained researcher took all measurements throughout the study. To standardize the measurement location, a point was marked with indelible ink at 50% of the length between the acromion of the scapula and olecranon process of the ulna on the anterior surface of the arm. Care was taken to be consistent in applying minimal pressure during scanning to avoid the compression of muscle tissue. To enhance acoustic coupling and reduce near-field artifacts, a generous amount of water-soluble transmission gel was applied to the skin. Ultrasound settings (musculoskeletal mode; gain of 58 dB; frequency of 10 MHz) were kept consistent for each scan. To reduce the chance of an imaging error, the depth was adjusted based on each participant’s arm size and then remained unchanged for that participant during subsequent trials.

On the recorded ultrasound images, a rectangular region of interest that included as much of the muscle as possible without including any surrounding fascia was selected in ImageJ (NIH). Within this region of interest, biceps brachii muscle quality was determined from the echo intensity values assessed by computer-aided grayscale analysis using the standard histogram function. The mean pixel intensity was calculated as a value between 0 (black) and 255 (white) arbitrary units. This measured pixel density provided an indirect measurement of the intramuscular water content within a region of interest. Changes in intramuscular glycogen could then be calculated based on the known association of changes in intramuscular water content and intramuscular glycogen.^14,20 This method has been validated previously to muscle biopsy determinations^14,20 and has sufficient test-retest reliability when performed on the biceps brachii for glycogen estimation. ¹⁶

Longitudinal ultrasound images that were obtained at the same location and using the same ultrasound settings described previously were used to measure changes in muscle thickness. Muscle thickness was defined as the distance between the superficial and deep aponeuroses and was measured at 3 locations in each image. The average of the 9 measurements at each time point was recorded.

Joint Mobility

Passive elbow extension was measured with the participant standing in the fundamental position with his arms passively hanging by his sides and forearms unsupported by the body. In this position, a goniometer (Quint Graphics) was placed on the lateral epicondyle of the humerus with the stationary arm placed over the deltoid tuberosity, and the moving arm placed in the center of the wrist with minimal pressure. From this position, participants maximally flexed their forearm while supinating to a neutral position so that maximal active elbow flexion could be measured by placing the goniometer’s axis of rotation over the lateral epicondyle of the humerus, the stationary arm over the deltoid tuberosity, and the moving arm placed directly over the radius. Each measurement was repeated 3 times with the average of the measures reported. All anatomical landmarks used were marked with indelible ink allowing for replication during subsequent testing sessions.

Muscle Soreness

To assess biceps brachii muscle soreness, participants were instructed to indicate their level of soreness during motion on a 10-cm visual analog scale (VAS) where 0 cm indicates no pain and 10 cm indicates the worst pain possible. To take this measurement, participants were seated with their arm flexed to 45° and resting on a firm modeled pad. In this position, participants performed 2 unloaded biceps curls while holding an unloaded dynamometer handle after which they indicated their pain using the VAS. Participants also had their pressure pain threshold measured by application of an external force through the 1-cm² round tip of an algometer (Force Ten; Wagner). The pressure was applied to the midportion of the biceps brachii at a rate of 0.5 kg/cm² until the onset of pain, as indicated by the participant. ²¹ The level of pressure at which the participant first indicated pain was recorded. This measurement was performed 3 times at each time point. The average of the 3 measurements was used for analysis, and the location of measurement was marked with indelible ink in order to remain consistent throughout testing.

Strength and Power

Elbow flexor strength and power were assessed using an isokinetic dynamometer with the participant positioned as described previously. Maximal strength was assessed using a maximal voluntary isometric contraction (MVIC) test at 90° of elbow flexion. Prior to strength testing, participants completed a warm-up consisting of three 5-second isometric contractions at increasing efforts (50%, 70%, and 90% MVIC) with 1 minute between contractions. Afterward, participants completed 3 MVICs with 30 second passive rest between repetitions. The peak torque for each repetition was recorded and the repetition with the greatest value was used for analysis.

Peak muscular power during a concentric elbow flexion exercise was measured using the isotonic setting of the dynamometer with resistance set to 30% of MVIC. To perform this test, participants started with a flexed elbow and then extended their forearm 90° in a controlled manner prior to performing a concentric flexion contraction as quickly and forcefully as possible. This test was repeated 5 times and the repetition with the greatest instantaneous power (torque × angular velocity) was used for analysis.

Diet Log

For the duration of the study, participants were instructed to eat a simple diet that could be replicated throughout testing. Each participant completed diet logs for the day preceding his exercise bout as well as throughout the study using the Automated Self-Administered 24-hour Dietary Assessment Tool. During testing sessions related to the second experimental condition, diet logs from the corresponding day from the first experimental condition were given to the participant for replication. Comparisons were made between trials for daily kilocalories and carbohydrate consumption relative to body mass.

Statistical Analysis

Dependent variables were separated into 5 dimensions of recovery for separate analysis. These categories were physical performance (muscular strength and power), joint mobility (active elbow flexion and passive elbow extension), muscle pain (soreness and pressure pain threshold), muscle damage (CK), and muscle glycogen (intramuscular glycogen). Dependent variables within each category were then compared using separate 2 (condition) × 5 (time) analyses of variance (ANOVAs: muscle damage and muscle glycogen) or multivariate analyses of variance (physical performance, joint mobility, and muscle pain) in order to determine whether a condition by time interaction effect was present. When a significant effect was found, differences at specific time points were tested using a Bonferroni post hoc adjustment. Cohen d was calculated to determine the treatment effect sizes at all time points, which are described as marginal (d < 0.2), small (d = 2.0-4.9), medium (d = 0.5-7.9), or large (d ≤ 8.0). Sphericity was tested using a Mauchly test of sphericity, and Greenhouse-Geisser corrections were used when necessary. The present study met the necessary sample size (n = 10) needed to test for an interaction effect for the 2 × 5 repeated measures ANOVA as calculated by an a priori power analysis with statistical power of 0.8 and an alpha of 0.05. The anticipated effect size based on muscle damage of f = 0.4 (small to moderate effect) was based on results from previous studies.^20,24 Comparisons between muscle mass between limbs and work performed in eccentric bouts between conditions were made using a paired t test. The reproducibility of daily caloric and carbohydrate consumption between trials for matched time series data was tested by the calculation of the intraclass correlation coefficient (ICC) test of absolute agreement. Intrarater reliability of ultrasound measurements was tested by the calculation of the ICC of all measurements of the same muscle. Values are reported as means, standard deviations, and percentages of pre-exercise values.

Results

Ten participants (age 21.5 ± 2.7 years; height 181.3 ± 8.1 cm; body mass 87.7 ± 19.2 kg; body fat 18.2% ± 7.2%) completed the study. No differences were observed between lean mass between arms (CwC, 4.13 ± 0.68 kg; CON, 4.11 ± 0.72 kg), arm circumference between arms (CwC, 35.14 ± 2.72 cm; CON, 35.08 ± 3.71 cm) or any dependent variable between conditions at the pre-exercise time point (P > 0.05). The mechanical work performed during the eccentric protocols was similar between conditions (CwC, 1547 ± 276 J·rad; CON, 1636 ± 394 J·rad; P = 0.35). Dietary consumption was sufficiently matched between trials as determined by a significant intraclass correlation of absolute agreement for both caloric consumption (ICC = 0.657; P = 0.00) and carbohydrate consumption (ICC = 0.576; P = 0.01).

Changes in muscular strength and power are reported in Figure 2. A significant interaction effect was observed for both strength (P = 0.00) and power (P = 0.01) indicating enhanced recovery of muscle function in the CwC condition compared with CON. The intervention resulted in a large effect on strength (1 h = 0.67, 24 h = 0.87, 48 h = 0.97, and 72 h = 1.12) and a small to medium effect in power (1 h = 0.20, 24 h = 0.43, 48 h = 0.37, and 72 h = 0.65). With regard to strength recovery, post hoc analysis revealed that strength was reduced from pre-exercise levels in both conditions for the first 24 hours after exercise, but at the 48-hour and 72-hour time points strength had recovered in CwC condition, but not CON. Similarly, power was reduced in both conditions for the first 24 hours postexercise, before returning to pre-exercise values at 48 hours in the CwC condition and 72 hours in CON.

Figure 2.

Changes in (a) muscular strength and (b) power after participants (n = 10) received contrast with compression therapy (CwC) and no therapy (CON) during separate trials. Values are presented as mean ± SD, with significant effects of treatment over time indicated with *. Pre, pre-exercise.

For intramuscular glycogen, an interaction effect of condition by time was observed (P = 0.02) (Figure 3). The effect size of the intervention on intramuscular glycogen ranged from small to large depending on the time point examined (1 h = 0.36, 24 h = 0.29, 48 h = 0.81, and 72 h = 0.35). Furthermore, a significant main effect of time was observed for both CwC (P < 0.00; f = 7.60) and CON (P < 0.00; f = 13.78), indicating an increase in pixel intensity or decrease in glycogen content of the muscle after the exercise intervention. In the CwC trial, glycogen levels did not differ from baseline (pre-exercise) at 1 hour (P = 0.12) or 24 hours (P = 0.28), but were significantly lower at 48 hours (P = 0.02) and 72 hours (P = 0.02). In the CON, trial glycogen levels were significantly lower at all time points (P = 0.00-0.04) compared with pre-exercise values. Measurements of intramuscular glycogen were found to be reliable over time (ICC = 0.880; P < 0.00).

Figure 3.

Changes in intramuscular glycogen as measured by echo intensity from ultrasound images of the biceps brachii. An example of measurement of echo intensity of a damaged muscle is depicted (left) as well as changes in echo intensity after participants (n = 10) received contrast with compression therapy (CwC) and no therapy (CON) during separate trials. Values are presented as mean ± SD, with significant effects of treatment over time indicated with *. Pre, pre-exercise.

For both muscle thickness and CK, a significant interaction effect of condition over time was observed (muscle thickness, P = 0.05; CK, P = 0.04) (Figure 4). The intervention resulted in a small to medium effect on muscle thickness (1 h = 0.35, 24 h = 0.45, 48 h = 0.60, and 72 h = 0.70). For muscle thickness, although a main effect of time was observed for both conditions (P < 0.00). Post hoc analysis failed to identify any specific time points where muscle thickness was different than baseline values for CwC and only 48 hours postexercise was significantly different from baseline for CON. Measurements of muscle thickness were found to be reliable over time (ICC = 0.950; P < 0.00).

Figure 4.

Changes in (a) creatine kinase (CK), (b) muscle thickness, (c) soreness while moving, and (d) pressure pain threshold after participants (n = 10) received contrast with compression therapy (CwC) and no therapy (CON) during separate trials. Values are presented as mean ± SD, with significant effects of treatment over time indicated with *. Pre, pre-exercise; VAS, visual analog scale.

For CK, the differences between conditions were trivial at 1 hour (d = 0.01), small at 24 hours (d = 0.46), medium at 48 hours (d = 0.76), and large at 72 hours (d = 0.96). In addition, for CK, a main effect of time was observed for CON (P = 0.02) but not for CwC (P = 0.52) trial; and post hoc analysis revealed that the difference between trials only reached significance at the 72-hour time point and not at the 1-hour (P = 0.60), 24-hour (P = 0.06), or 48-hour (P = 0.12) time points.

Muscle soreness during motion and pressure pain threshold are reported in Figure 3. The intervention resulted in a large effect on soreness at 1 hour (d = 0.85), 48 hours (d = 0.80), and 72 hours (d = 0.84), but a negligible effect at 24 hours (d = 0.18) and a negligible to small effect on pressure pain threshold (1 h = 0.16, 24 h = 0.10, 48 h = 0.21, and 72 h = 0.25). Both conditions experienced an increase in muscle soreness while moving at 24 and 48 hours postexercise; however, pain was greater in the CON than CwC at the 48-hour time point. At 72 hours postexercise, muscle soreness was significantly different from pre-exercise values in CON but not CwC. At 1 hour postexercise, pain was greater than pre-exercise values in CON but not CwC; however, for the CwC condition, this time point was only 45 minutes removed from treatment, indicating transient effects of the treatment may have still been present during this time point. Pressure pain threshold failed to show any significant differences over time or between trials.

Changes in passive elbow extension and active elbow flexion are depicted in Figure 5. A significant interaction effect was observed for active elbow flexion (P < 0.00) but not passive elbow extension. The intervention resulted in a medium to large effect on active elbow flexion (1 h = 0.82, 24 h = 0.65, 48 h = 1.17, and 72 h = 1.00) and a negligible to small effect on passive elbow extension at all time points except for 1 hour postexercise where a medium effect was observed (1 h = 0.79, 24 h = 0.16, 48 h = 0.18, and 72 h = 0.34). Significant time effects were observed for both active flexion and passive extension indicating loss of joint mobility in both directions of motion.

Figure 5.

Changes in (a) passive elbow extension and (b) active elbow flexion (right) after participants (n = 10) received contrast with compression therapy (CwC) and no therapy (CON) during separate trials. Values are presented as mean ± SD, with significant effects of treatment over time indicated with *. Pre, pre-exercise.

Discussion

The present study is novel for 2 reasons. First, this is the first study to investigate the effects of CwC on recovery after damaging exercise. In this regard, our results showed that CwC provided significant benefits to recovering muscular strength, muscular power, joint mobility, and intramuscular glycogen stores, as well as reducing muscle soreness, muscle swelling, and muscle damage after damaging exercise compared with when no therapy is given. Second, this is the first study to examine the effects of any therapeutic recovery modality on intramuscular glycogen recovery after a damaging bout of exercise. As such, this study provides contextual information regarding the efficacy of using CwC for athletes who rely on strength, power, or the glycolytic energy system for their sport.

The results from the present study, which found CwC enhanced the recovery of strength, power, and joint mobility and reduced soreness and muscle swelling, are in line with those reported previously for traditional contrast water therapy. ⁴ Unfortunately, direct comparison of CwC with contrast water therapy that is performed without compression is not possible within the present study design. Therefore, although the present study is the first to validate the efficacy of CwC for recovery of muscle function and reduction of EAMD, soreness, and muscle swelling, comparisons with other recovery modalities for these purposes is not possible. However, the contrast water therapy used in previous studies required the submersion of large portions of the body into prepared baths, ⁴ whereas the CwC device used in the present study is a mobile unit in which the therapy is applied locally to the target tissue through a pressurized cuff. Given this difference, CwC used in the present study may be an attractive alternative to contrast water therapy because of its mobility, portability, ease of use, limited cleanup, and ability to target specific tissues.

The results from the present study also indicate that CwC therapy significantly reduces the impairment of intramuscular glycogen stores experienced at 72 hours following a bout of damaging exercise compared with when no treatment is given. Improved glycogen storage is likely related to reduced muscle damage response and/or altered chemotaxis response resulting from eccentric exercise. In addition, a main effect of time was observed for CK in the CON trial, indicating the exercise damaged the muscle to an extent that impaired glycogen resynthesis could be observed. However, as no significant time effect was observed in the CwC study, it can be concluded that this damage was largely mitigated by the CwC therapy. Despite this, both trials experienced a time effect of decreased intramuscular glycogen levels from pre-exercise. Furthermore, as CwC experienced decreased glycogen at 48 and 72 hours postexercise, it can be assumed that this decrease was not related to depleted glycogen stores from the exercise itself. Therefore, it is possible that factors other than those included in the present study may have affected intramuscular glycogen stores such as a differing altered leukocyte response between conditions. ²² Alternatively, CK may not have been reflective of muscle damage in a manner that would affect the muscle’s ability to store glycogen.^1,2 However, this is unlikely, as concurrent decreases in muscle function, soreness, and muscle swelling were observed.

When interpreting the results of the present study, it is important to note that the exercise intervention given (multiple low-repetition sets of eccentric-only contractions with 1:3 work-to-rest ratio) was designed to elicit muscle damage with a relatively small utilization of intramuscular glycogen as an energy source. This design was adopted in order to isolate the effects of EAMD in a realistic manner in order to provide construct validity in the study. ¹⁰ However, as CON experienced a decrease in intramuscular glycogen 1 hour postexercise before a measurable change in CK occurred, it can be concluded that a sufficient amount of glycogen was utilized either during the exercise or as part of the initial recovery from the exercise. As pixel density assessment using ultrasound images provides information on the relative changes in glycogen and not absolute measures of glycogen, the use of this energy store^15,16,20 is unclear. Regardless, it is of interest to determine whether similar results would be observed if the exercise prescription was intended to fully deplete intramuscular glycogen or if minimal muscle damage was present, both of which are common scenarios in sport training. ³

In the present study, the effect of CwC therapy on intramuscular stores was compared with a control condition; and mitigation of the disruption of intramuscular glycogen stores was attributed to decreased muscle damage from the therapy. For the present study design, CwC therapy was chosen over other common therapeutic modalities, as both contrast and compression therapies have been shown to reduce EAMD ⁸ by increasing intramuscular blood flow and decreasing edema, ¹⁷ which should not adversely affect glycogen synthesis rates. However, as other therapeutic modalities that reduce EAMD after damaging exercise (eg, cryotherapy) also result in different physiological effects that may adversely affect glycogen synthesis rates (eg, decreased tissue temperature), additional research is needed to determine whether similar results would be seen with other modalities.^12,25

Complete recovery of several variables (strength, CK, soreness, and glycogen) was not achieved in the 72-hour observation window, which is a limitation of the present study. As CK had continued to increase in the CON condition between the final 2 time points (48 and 72 h), it is likely that the greatest effect of muscle damage on intramuscular glycogen stores was not observed in the present study. ⁷ Another limitation of the present study was the use of ultrasound as a measurement of muscle glycogen. Although this method has been validated by 2 independent lab groups,^15,20 a recent study by a third lab group has questioned the use of this technique when they failed to find a significant relationship between changes in muscle glycogen when measured by biopsy and ultrasound (P = 0.11) in a euhydrated state. ²³ However, the more recent study had a smaller sample size (N = 16) than the previous studies (N = 22 and N = 20) with no power analysis performed to justify the sample size. In addition, several vital control criteria were not reported in this study, such as measurement of hydration to ensure similar hydration between testing (eg, urine-specific gravity), adequate time given for fluid shift to occur before ultrasound measurements, or restriction of exercise during the evaluation period. ²⁴ Another limitation of the present study was that only men were tested. By intent, women were excluded from this present study due to potentially confounding effects of the menstrual cycle on pain sensation, fluid retention, joint mobility, and muscle function. Due to the aforementioned limitations, the restriction of testing on the elbow flexors, and relatively small sample size of the present study, conclusions based on our results should be viewed as preliminary data. As such, additional research is needed to compare the effects of CwC over longer time periods, to determine whether gender of muscle-specific effects of CwC are present, and to substantiate the results of the present study in a larger athletic cohort.

In conclusion, this study found that CwC therapy was effective at enhancing recovery of muscle function and reducing markers of muscle damage, muscle swelling, and soreness after a damaging bout of exercise. Although these results validate the use of CwC for these purposes, additional research is needed to compare CwC with other recovery therapies to determine whether compression provides additive effects to contrast therapy. In addition, CwC significantly reduced the impairment of intramuscular glycogen stores experienced after a damaging bout of exercise. Intramuscular glycogen stores are important for athletes who train or compete in moderate- to high-intensity sports with prolonged durations. This is the first study to provide evidence that any therapeutic modality can improve performance in such tasks, however, more research is needed to determine the effects CwC over the full period of recovery, in the absence of muscle damage and when glycogen stores are fully depleted.