Contrast water therapy and exercise induced muscle damage : a systematic review and meta-analysis

The aim of this systematic review was to examine the effect of Contrast Water Therapy (CWT) on recovery following exercise induced muscle damage. Controlled trials were identified from computerized literature searching and citation tracking performed up to February 2013. Eighteen trials met the inclusion criteria; all had a high risk of bias. Pooled data from 13 studies showed that CWT resulted in significantly greater improvements in muscle soreness at the five follow-up time points(<6, 24, 48, 72 and 96 hours) in comparison to passive recovery. Pooled data also showed that CWT significantly reduced muscle strength loss at each follow-up time (<6, 24, 48, 72 and 96 hours) in comparison to passive recovery. Despite comparing CWT to a large number of other recovery interventions, including cold water immersion, warm water immersion, compression, active recovery and stretching, there was little evidence for a superior treatment intervention. The current evidence base shows that CWT is superior to using passive recovery or rest after exercise; the magnitudes of these effects may be most relevant to an elite sporting population. There seems to be little difference in recovery outcome between CWT and other popular recovery interventions.

Changes in markers of muscle damage, inflammation and HSP70 after an Ironman triathlon race

We investigated the effects of an Ironman triathlon race on markers of muscle damage, inflammation and heat shock protein 70 (HSP70). Nine well-trained male triathletes (mean +/- SD age 34 +/- 5 years; VO(2peak) 66.4 ml kg(-1) min(-1)) participated in the 2004 Western Australia Ironman triathlon race (3.8 km swim, 180 km cycle, 42.2 km run). We assessed jump height, muscle strength and soreness, and collected venous blood samples 2 days before the race, within 30 min and 14-20 h after the race. Plasma samples were analysed for muscle proteins, acute phase proteins, cytokines, heat shock protein 70 (HSP70), and clinical biochemical variables related to dehydration, haemolysis, liver and renal functions. Muscular strength and jump height decreased significantly (P < 0.05) after the race, whereas muscle soreness and the plasma concentrations of muscle proteins increased. The cytokines interleukin (IL)-1 receptor antagonist, IL-6 and IL-10, and HSP70 increased markedly after the race, while IL-12p40 and granulocyte colony-stimulating factor (G-CSF) were also elevated. IL-4, IL-1beta and tumour necrosis factor-alpha did not change significantly, despite elevated C-reactive protein and serum amyloid protein A on the day after the race. Plasma creatinine, uric acid and total bilirubin concentrations and gamma-glutamyl transferase activity also changed after the race. In conclusion, despite evidence of muscle damage and an acute phase response after the race, the pro-inflammatory cytokine response was minimal and anti-inflammatory cytokines were induced. HSP70 is released into the circulation as a function of exercise duration.

Plasma cytokine changes in relation to exercise intensity and muscle damage

The purpose of this study was to compare the effects of exercise intensity and exercise-induced muscle damage on changes in anti-inflammatory cytokines and other inflammatory mediators. Nine well-trained male runners completed three different exercise trials on separate occasions: (1) level treadmill running at 60% VO2max (moderate-intensity trial) for 60 min; (2) level treadmill running at 85% VO2max (high-intensity trial) for 60 min; (3) downhill treadmill running (-10% gradient) at 60% VO2max (downhill running trial) for 45 min. Blood was sampled before, immediately after and 1 h after exercise. Plasma was analyzed for interleukin-1 receptor antagonist (IL-1ra), IL-4, IL-5, IL-10, IL-12p40, IL-13, monocyte chemotactic protein-1 (MCP-1), prostaglandin E(2), leukotriene B(4) and heat shock protein 70 (HSP70). The plasma concentrations of IL-1ra, IL-12p40, MCP-1 and HSP70 increased significantly (P<0.05) after all three trials. Plasma prostaglandin E(2) concentration increased significantly after the downhill running and high-intensity trials, while plasma IL-10 concentration increased significantly only after the high-intensity trial. IL-4 and leukotriene B(4) did not increase significantly after exercise. Plasma IL-1ra and IL-10 concentrations were significantly higher (P<0.05) after the high-intensity trial than after both the moderate-intensity and downhill running trials. Therefore, following exercise up to 1 h duration, exercise intensity appears to have a greater effect on anti-inflammatory cytokine production than exercise-induced muscle damage

Exercise-induced muscle damage, plasma cytokines and markers of neutrophil activation

Introduction: Unaccustomed eccentric exercise often results in muscle damage and neutrophil activation. We examined changes in plasma cytokines stress hormones, creatine kinase activity and myoglobin concentration, neutrophil surface receptor expression, degranulation, and the capacity of neutrophils to generate reactive oxygen species in response to in vitro stimulation after downhill running. Methods: Ten well-trained male runners ran downhill on a treadmill at a gradient of -10% for 45 min at 60% V̇O2max. Blood was sampled immediately before (PRE) and after (POST), 1 h (1 h POST), and 24 h (24 h POST) after exercise. Results: At POST, there were significant increases (P < 0.01) in neutrophil count (32%), plasma interleukin (IL)-6 concentration (460%), myoglobin (Mb) concentration (1100%), and creatine kinase (CK) activity (40%). At 1 h POST, there were further increases above preexercise values for neutrophil count (85%), plasma Mb levels (1800%), and CK activity (56%), and plasma IL-6 concentration remained above preexercise values (410%) (P < 0.01). At 24 h POST, neutrophil counts and plasma IL-6 levels had returned to baseline, whereas plasma Mb concentration (100%) and CK activity (420%) were elevated above preexercise values (P < 0.01). There were no significant changes in neutrophil receptor expression, degranulation and respiratory burst activity, and plasma IL-8 and granulocyte-colony stimulating factor concentrations at any time after exercise. Neutrophil count correlated with plasma Mb concentration at POST (r = 0.64, P < 0.05), and with plasma CK activity at POST (r = 0.83, P < 0.01) and 1 h POST (r = 0.78, P < 0.01). Conclusion: Neutrophil activation remains unchanged after downhill running in well-trained runners, despite increases in plasma markers of muscle damage.

Exercise and Cellular Mechanisms of Muscle Injury

The general aim of this book is to provide a comprehensive summary of the characteristics of exercise-induced muscle damage and the mechanisms of tissue inflammation. The authors present a large amount of our own original data and have summarised the research of others.

Steps toward the validation of the Trendelenburg Test : the effect of experimentally reduced hip abductor muscle function on frontal plane mechanics

Objective: To investigate the validity of the Trendelenburg test (TT) using an ultrasound-guided nerve block (UNB) of the superior gluteal nerve and determine whether the reduction in hip abductor muscle (HABD) strength would result in the theorized mechanical compensatory strategies measured during the TT. Design: Quasi-experimental. Setting: Hospital. Participants: Convenience sample of 9 healthy men. Only participants with no current or previous injury to the lumbar spine, pelvis, or lower extremities, and no previous surgeries were included. Interventions: Ultrasound-guided nerve block. Main Outcome Measures: Hip abductor muscle strength (percent body weight [%BW]), contralateral pelvic drop (cPD), change in contralateral pelvic drop (Delta cPD), ipsilateral hip adduction, and ipsilateral trunk sway (TRUNK) measured in degrees. Results: The median age and weight of the participants were 31 years (interquartile range [IQR], 22-32 years) and 73 kg (IQR, 67-81 kg), respectively. An average 52% reduction of HABD strength (z = 2.36, P = 0.02) resulted after the UNB. No differences were found in cPD or Delta cPD (z = 0.01, P = 0.99, z = 20.67, P = 0.49, respectively). Individual changes in biomechanics showed no consistency between participants and nonsystematic changes across the group. One participant demonstrated the mechanical compensations described by Trendelenburg. Conclusions: The TT should not be used as a screening measure for HABD strength in populations demonstrating strength greater than 30% BW but should be reserved for use with populations with marked HABD weakness. Clinical Relevance: This study presents data regarding a critical level of HABD strength required to support the pelvis during the TT.

Normative and critical criteria for iliotibial band and iliopsoas muscle flexibility

Context: The Ober and Thomas tests are subjective and involve a "negative" or "positive" assessment, making them difficult to apply within the paradigm of evidence-based medicine. No authors have combined the subjective clinical assessment with an objective measurement for these special tests. Objective: To compare the subjective assessment of iliotibial band and iliopsoas flexibility with the objective measurement of a digital inclinometer, to establish normative values, and to provide an evidence-based critical criterion for determining tissue tightness. Design: Cross-sectional study. Setting: Clinical research laboratory. Patients or Other Participants: Three hundred recreational athletes (125 men, 175 women; 250 in injured group, 50 in control group). Main Outcome Measure(s): Iliotibial band and iliopsoas muscle flexibility were determined subjectively using the modified Ober and Thomas tests, respectively. Using a digital inclinometer, we objectively measured limb position. lnterrater reliability for the subjective assessment was compared between 2 clinicians for a random sample of 100 injured participants, who were classified subjectively as either negative or positive for iliotibial band and iliopsoas tightness. Percentage of agreement indicated interrater reliability for the subjective assessment. Results: For iliotibial band flexibility, the average inclinometer angle was -24.59 degrees +/- 7.27 degrees. A total of 432 limbs were subjectively assessed as negative (-27.13 degrees +/- 5.53 degrees) and 168 as positive (-16.29 degrees +/- 6.87 degrees). For iliopsoas flexibility, the average inclinometer angle was -10.60 degrees +/- 9.61 degrees. A total of 392 limbs were subjectively assessed as negative (-15.51 degrees +/- 5.82 degrees) and 208 as positive (0.34 degrees +/- 7.00 degrees). The critical criteria for iliotibial band and iliopsoas flexibility were determined to be -23.16 degrees and -9.69 degrees, respectively. Between-clinicians agreement was very good, ranging from 95.0% to 97.6% for the Thomas and Ober tests, respectively. Conclusions: Subjective assessments and instrumented measurements were combined to establish normative values and critical criterions for tissue flexibility for the modified Ober and Thomas tests.

Steps towards the validation of the Trendelenburg test : The effect of experimentally reduced hip abductor muscle function on frontal plane mechanics

Introduction: The Trendelenburg Test (TT) is used to assess the functional strength of the hip abductor muscles (HABD), their ability to control frontal plane motion of the pelvis, and the ability of the lumbopelvic complex to transfer load into single leg stance. Rationale: Although a standard method to perform the test has been described for use within clinical populations, no study has directly investigated Trendelenburg’s hypotheses. Purpose: To investigate the validity of the TT using an ultrasound guided nerve block (UNB) of the superior gluteal nerve and determine whether the reduction in HABD strength would result in the theorized mechanical compensatory strategies measured during the TT. Methods: Quasi-experimental design using a convenience sample of nine healthy males. Only subjects with no current or previous injury to the lumbar spine, pelvis, or lower extremities, and no previous surgeries were included. Force dynamometry was used to evaluation HABD strength (%BW). 2D mechanics were used to evaluate contralateral pelvic drop (cMPD), change in contralateral pelvic drop (∆cMPD), ipsilateral hip adduction (iHADD) and ipsilateral trunk sway (TRUNK) measured in degrees (°). All measures were collected prior to and following a UNB on the superior gluteal nerve performed by an interventional radiologist. Results: Subjects’ age was median 31yrs (IQR:22-32yrs); and weight was median 73kg (IQR:67-81kg). An average 52% reduction of HABD strength (z=2.36,p=0.02) resulted following the UNB. No differences were found in cMPD or ∆cMPD (z=0.01,p= 0.99, z=-0.67,p=0.49). Individual changes in biomechanics show no consistency between subjects and non-systematic changes across the group. One subject demonstrated the mechanical compensations described by Trendelenburg. Discussion: The TT should not be used as screening measure for HABD strength in populations demonstrating strength greater than 30%BW but reserved for use with populations with marked HABD weakness. Importance: This study presents data regarding a critical level of HABD strength required to support the pelvis during the TT.

The relationship between hip abductor muscle strength and magnitude of pelvic drop following a 3 week strengthening protocol in non-specific low back pain patients.

Purpose: To examine the relationship between hip abductor muscle (HABD) strength and the magnitude of pelvic drop (MPD) for patients with non-specific low back pain (NSLBP) and controls (CON) prior to and following a 3-week HABD strengthening protocol. At baseline, we hypothesized that NSLBP patients would exhibit reduced HABD strength and greater MPD compared to CON. Following the protocol, we hypothesized that strength would increase and MPD would decrease. Relevance: The Trendelenburg test (TT) is a common clinical test used to examine the ability of the HABD to maintain horizontal pelvic position during single limb stance. However, no study has specifically tested this theory. Moreover, no study has investigated the relationship between HABD strength and pelvic motion during walking or tested whether increased HABD strength would reduce the MPD. Methods: Quasi-experimental with 3-week exercise intervention. Fifteen NSLBP patients (32.5yrs,range 21-51yrs; VAS baseline: 5.3cm) and 10 CON (29.5yrs,range 22-47yrs) were recruited. Isometric HABD strength was measured using a force dynamometer and the average of three maximal voluntary contractions were normalized to body mass (N/kg). Two-dimensional MPD (degrees) was measured using a 60 Hz camera and was derived from two retroreflective-markers placed on the posterior superior iliac spines. MPD was measured while performing the static TT and while walking and averaged over 10 consecutive footfalls. NSLBP patients completed a 3-week HABD strengthening protocol consisting of 2 open-kinetic-chain exercises then all measures were repeated. Non-parametric analysis was used for group comparisons and correlation analysis. Results: At baseline, the NSLBP patients demonstrated 31% reduced HABD strength (mean=6.6 N/kg) compared to CON (mean=9.5 N/kg: p=0.03) and no significant differences in maximal pelvic frontal plane excursion while walking (NSLBP:mean=8.1°, CON:mean=7.1°: p=0.72). No significant correlations were measured between left HABD strength and right MPD (r=-0.37, p=0.11), or between right HABD strength and left MPD (r=-0.04, p=0.84) while performing the static TT. Following the 3-week strengthening protocol, NSLBP patients demonstrated a 12% improvement in strength (Post:mean=7.4 N/kg: p=0.02), a reduction in pain (VAS followup: 2.8cm), but no significant decreases in MPD while walking (p=0.92). Conclusions: NSLBP patients demonstrated reduced HABD strength at baseline and were able to increase strength and reduce pain in a 3-week period. However, despite increases in HABD strength, the NSLBP group exhibited similar MPD motion during the static TT and while walking compared to baseline and controls. Implications: The results suggest that the HABD alone may not be primarily responsible for controlling a horizontal pelvic position during static and dynamic conditions. Increasing the strength of the hip abductors resulted in a reduction of pain in NSLBP patients providing evidence for further research to identify specific musculature responsible for controlling pelvic motion.

Cerebral cortex activation mapping upon electrical muscle stimulation by 32-channel time-domain functional near-infrared spectroscopy

The application of different EMS current thresholds on muscle activates not only the muscle but also peripheral sensory axons that send proprioceptive and pain signals to the cerebral cortex. A 32-channel time-domain fNIRS instrument was employed to map regional cortical activities under varied EMS current intensities applied on the right wrist extensor muscle. Eight healthy volunteers underwent four EMS at different current thresholds based on their individual maximal tolerated intensity (MTI), i.e., 10 % < 50 % < 100 % < over 100 % MTI. Time courses of the absolute oxygenated and deoxygenated hemoglobin concentrations primarily over the bilateral sensorimotor cortical (SMC) regions were extrapolated, and cortical activation maps were determined by general linear model using the NIRS-SPM software. The stimulation-induced wrist extension paradigm significantly increased activation of the contralateral SMC region according to the EMS intensities, while the ipsilateral SMC region showed no significant changes. This could be due in part to a nociceptive response to the higher EMS current intensities and result also from increased sensorimotor integration in these cortical regions.

Whole-body cryotherapy (extreme cold air exposure) for preventing and treating muscle soreness after exercise in adults (Protocol)

"This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the effects (benefits and harms) of whole-body cryotherapy (cold air exposure) for preventing and treating muscle soreness after exercise in adults." -- publisher website

What do we know about recovery interventions used in the management of delayed onset muscle soreness?

Since the pioneering work of Hough in 1902 (1) the term ‘delayed onset muscle soreness (DOMS)’ has dominated the field of athletic recovery. DOMS typically occurs after exercise induced muscle damage (EIMD), particularly if the exercise is unaccustomed or involves a large amount of eccentric (muscle lengthening) contractions. The symptoms of EIMD manifest as a temporary reduction in muscle force, disturbed proprioceptive acuity, increases in inflammatory markers both within the injured muscle and in the blood as well as increased muscle soreness, stiffness and swelling. The intensity of discomfort and soreness associated with DOMS increases within the first 24 hours, peaks between 24 and 72 hours, before subsiding and eventually disappearing 5-7 days after the exercise. Consequently, DOMS may interfere with athletic training or competition and several recovery interventions have been utilised by athletes and coaches in an attempt to offset the negative effects...

Caffeine ingestion and cycling power output in a low or normal muscle glycogen state

Purpose Commencing selected workouts with low muscle glycogen availability augments several markers of training adaptation compared with undertaking the same sessions with normal glycogen content. However, low glycogen availability reduces the capacity to perform high-intensity (>85% of peak aerobic power (V·O2peak)) endurance exercise. We determined whether a low dose of caffeine could partially rescue the reduction in maximal self-selected power output observed when individuals commenced high-intensity interval training with low (LOW) compared with normal (NORM) glycogen availability. Methods Twelve endurance-trained cyclists/triathletes performed four experimental trials using a double-blind Latin square design. Muscle glycogen content was manipulated via exercise–diet interventions so that two experimental trials were commenced with LOW and two with NORM muscle glycogen availability. Sixty minutes before an experimental trial, subjects ingested a capsule containing anhydrous caffeine (CAFF, 3 mg-1·kg-1 body mass) or placebo (PLBO). Instantaneous power output was measured throughout high-intensity interval training (8 × 5-min bouts at maximum self-selected intensity with 1-min recovery). Results There were significant main effects for both preexercise glycogen content and caffeine ingestion on power output. LOW reduced power output by approximately 8% compared with NORM (P < 0.01), whereas caffeine increased power output by 2.8% and 3.5% for NORM and LOW, respectively, (P < 0.01). Conclusion We conclude that caffeine enhanced power output independently of muscle glycogen concentration but could not fully restore power output to levels commensurate with that when subjects commenced exercise with normal glycogen availability. However, the reported increase in power output does provide a likely performance benefit and may provide a means to further enhance the already augmented training response observed when selected sessions are commenced with reduced muscle glycogen availability. It has long been known that endurance training induces a multitude of metabolic and morphological adaptations that improve the resistance of the trained musculature to fatigue and enhance endurance capacity and/or exercise performance (13). Accumulating evidence now suggests that many of these adaptations can be modified by nutrient availability (9–11,21). Growing evidence suggests that training with reduced muscle glycogen using a “train twice every second day” compared with a more traditional “train once daily” approach can enhance the acute training response (29) and markers representative of endurance training adaptation after short-term (3–10 wk) training interventions (8,16,30). Of note is that the superior training adaptation in these previous studies was attained despite a reduction in maximal self-selected power output (16,30). The most obvious factor underlying the reduced intensity during a second training bout is the reduction in muscle glycogen availability. However, there is also the possibility that other metabolic and/or neural factors may be responsible for the power drop-off observed when two exercise bouts are performed in close proximity. Regardless of the precise mechanism(s), there remains the intriguing possibility that the magnitude of training adaptation previously reported in the face of a reduced training intensity (Hulston et al. (16) and Yeo et al.) might be further augmented, and/or other aspects of the training stimulus better preserved, if power output was not compromised. Caffeine ingestion is a possible strategy that might “rescue” the aforementioned reduction in power output that occurs when individuals commence high-intensity interval training (HIT) with low compared with normal glycogen availability. Recent evidence suggests that, at least in endurance-based events, the maximal benefits of caffeine are seen at small to moderate (2–3 mg·kg-1 body mass (BM)) doses (for reviews, see Refs. (3,24)). Accordingly, in this study, we aimed to determine the effect of a low dose of caffeine (3 mg·kg-1 BM) on maximal self-selected power output during HIT commenced with either normal (NORM) or low (LOW) muscle glycogen availability. We hypothesized that even under conditions of low glycogen availability, caffeine would increase maximal self-selected power output and thereby partially rescue the reduction in training intensity observed when individuals commence HIT with low glycogen availability.

Preexercise aminoacidemia and muscle protein synthesis after resistance exercise

PURPOSE We have previously shown that the aminoacidemia caused by the consumption of a rapidly digested protein after resistance exercise enhances muscle protein synthesis (MPS) more than the amino acid (AA) profile associated with a slowly digested protein. Here, we investigated whether differential feeding patterns of a whey protein mixture commencing before exercise affect postexercise intracellular signaling and MPS. METHODS Twelve resistance-trained males performed leg resistance exercise 45 min after commencing each of three volume-matched nutrition protocols: placebo (PLAC, artificially sweetened water), BOLUS (25 g of whey protein + 5 g of leucine dissolved in artificially sweetened water; 1× 500 mL), or PULSE (15× 33-mL aliquots of BOLUS drink every 15 min). RESULTS The preexercise rise in plasma AA concentration with PULSE was attenuated compared with BOLUS (P < 0.05); this effect was reversed after exercise, with two-fold greater leucine concentrations in PULSE compared with BOLUS (P < 0.05). One-hour postexercise, phosphorylation of p70 S6K and rpS6 was increased above baseline with BOLUS and PULSE, but not PLAC (P < 0.05); furthermore, PULSE > BOLUS (P < 0.05). MPS throughout 5 h of recovery was higher with protein ingestion compared with PLAC (0.037 ± 0.007), with no differences between BOLUS or PULSE (0.085 ± 0.013 vs. 0.095 ± 0.010%•h, respectively, P = 0.56). CONCLUSIONS Manipulation of aminoacidemia before resistance exercise via different patterns of intake of protein altered plasma AA profiles and postexercise intracellular signaling. However, there was no difference in the enhancement of the muscle protein synthetic response after exercise. Protein sources producing a slow AA release, when consumed before resistance exercise in sufficient amounts, are as effective as rapidly digested proteins in promoting postexercise MPS.

Low muscle glycogen concentration does not suppress the anabolic response to resistance exercise

We determined the effect of muscle glycogen concentration and postexercise nutrition on anabolic signaling and rates of myofibrillar protein synthesis after resistance exercise (REX). Sixteen young, healthy men matched for age, body mass, peak oxygen uptake (VO2peak) and strength (one repetition maximum; 1RM) were randomly assigned to either a nutrient or placebo group. After 48 h diet and exercise control, subjects undertook a glycogen-depletion protocol consisting of one-leg cycling to fatigue (LOW), whereas the other leg rested (NORM). The next morning following an overnight fast, a primed, constant infusion of L-[ring-13C6] phenylalanine was commenced and subjects completed 8 sets of 5 unilateral leg press repetitions at 80% 1RM. Immediately after REX and 2 h later, subjects consumed a 500 ml bolus of a protein/CHO (20 g whey + 40 g maltodextrin) or placebo beverage. Muscle biopsies from the vastus lateralis of both legs were taken at rest and 1 and 4 h after REX. Muscle glycogen concentration was higher in the NORM than LOW at all time points in both nutrient and placebo groups (P < 0.05). Postexercise Akt-p70S6K-rpS6 phosphorylation increased in both groups with no differences between legs (P < 0.05). mTORSer2448 phosphorylation in placebo increased 1 h after exercise in NORM (P < 0.05), whereas mTOR increased ?4-fold in LOW (P < 0.01) and ?11 fold in NORM with nutrient (P < 0.01; different between legs P < 0.05). Post-exercise rates of MPS were not different between NORM and LOW in nutrient (0.070 ± 0.022 vs. 0.068 ± 0.018 %/h) or placebo (0.045 ± 0.021 vs. 0.049 ± 0.017 %/h). We conclude that commencing high-intensity REX with low muscle glycogen availability does not compromise the anabolic signal and subsequent rates of MPS, at least during the early (4 h) postexercise recovery period.