Effect of a sulforaphane supplement on muscle soreness and damage induced by eccentric exercise in young adults: A pilot study.

OBJECTIVE: Excessive exercise increases the production of reactive oxygen species in skeletal muscles. Sulforaphane activates nuclear factor erythroid 2-related factor 2 (Nrf2) and induces a protective effect against oxidative stress. In a recent report, sulforaphane intake suppressed exercise-induced oxidative stress and muscle damage in mice. However, the effect of sulforaphane intake on delayed onset muscle soreness after eccentric exercise in humans is unknown. We evaluated the effect of sulforaphane supplement intake in humans regarding the delayed onset muscle soreness (DOMS) after eccentric exercise. RESEARCH METHODS & PROCEDURES: To determine the duration of sulforaphane supplementation, continuous blood sampling was performed and NQO1 mRNA expression levels were analyzed. Sixteen young men were randomly divided into sulforaphane and control groups. The sulforaphane group received sulforaphane supplements. Each group performed six set of five eccentric exercise with the nondominant arm in elbow flexion with 70% maximum voluntary contraction. We assessed muscle soreness in the biceps using the visual analog scale, range of motion (ROM), muscle damage markers, and oxidative stress marker (malondialdehyde; MDA). RESULTS: Sulforaphane supplement intake for 2 weeks increased NQO1 mRNA expression in peripheral blood mononuclear cells (PBMCs). Muscle soreness on palpation and ROM were significantly lower 2 days after exercise in the sulforaphane group compared with the control group. Serum MDA showed significantly lower levels 2 days after exercise in the sulforaphane group compared with the control group. CONCLUSION: Our findings suggest that sulforaphane intake from 2 weeks before to 4 days after the exercise increased NQO1, a target gene of Nrf2, and suppressed DOMS after 2 days of eccentric exercise.

The effect of branched-chain amino acid on muscle damage markers and performance following strenuous exercise: a systematic review and meta-analysis.

This systematic review and meta-analysis determined whether the ergogenic effects of branched-chain amino acids (BCAA) ameliorated markers of muscle damage and performance following strenuous exercise. In total, 25 studies were included, consisting of 479 participants (age 24.3 ± 8.3 years, height 1.73 ± 0.06 m, body mass 70.8 ± 9.5 kg, females 26.3%). These studies were rated as fair to excellent following the PEDro scale. The outcome measures were compared between the BCAA and placebo conditions at 24 and 48 hours following muscle-damaging exercises, using standardised mean differences and associated p-values via forest plots. Our meta-analysis demonstrated significantly lower levels of indirect muscle damage markers (creatine kinase, lactate dehydrogenase and myoglobin) at 48 hours post-exercise (standardised mean difference [SMD] = -0.41; p < 0.05) for the BCAA than placebo conditions, whilst muscle soreness was significant at 24 hours post-exercise (SMD = -0.28 ≤ d ≤ -0.61; p < 0.05) and 48 hours post-exercise (SMD = -0.41 ≤ d≤ -0.92; p < 0.01). However, no significant differences were identified between the BCAA and placebo conditions for muscle performance at 24 or 48 hours post-exercise (SMD = 0.08 ≤ d ≤ 0.21; p > 0.05). Overall, BCAA reduced the level of muscle damage biomarkers and muscle soreness following muscle-damaging exercises. However, the potential benefits of BCAA for muscle performance recovery is questionable and warrants further investigation to determine the practicality of BCAA for ameliorating muscle damage symptoms in diverse populations. PROSPERO registration number: CRD42020191248. Novelty: BCAA reduces the level of creatine kinase and muscle soreness following strenuous exercise with a dose-response relationship. BCAA does not accelerate recovery for muscle performance.

The Effect of Protein Supplementation versus Carbohydrate Supplementation on Muscle Damage Markers and Soreness Following a 15-km Road Race: A Double-Blind Randomized Controlled Trial.

We assessed whether a protein supplementation protocol could attenuate running-induced muscle soreness and other muscle damage markers compared to iso-caloric placebo supplementation. A double-blind randomized controlled trial was performed among 323 recreational runners (age 44 ± 11 years, 56% men) participating in a 15-km road race. Participants received milk protein or carbohydrate supplementation, for three consecutive days post-race. Habitual protein intake was assessed using 24 h recalls. Race characteristics were determined and muscle soreness was assessed with the Brief Pain Inventory at baseline and 1-3 days post-race. In a subgroup (n = 149) muscle soreness was measured with a strain gauge algometer and creatine kinase (CK) and lactate dehydrogenase (LDH) concentrations were measured. At baseline, no group-differences were observed for habitual protein intake (protein group: 79.9 ± 26.5 g/d versus placebo group: 82.0 ± 26.8 g/d, p = 0.49) and muscle soreness (protein: 0.45 ± 1.08 versus placebo: 0.44 ± 1.14, p = 0.96). Subjects completed the race with a running speed of 12 ± 2 km/h. With the Intention-to-Treat analysis no between-group differences were observed in reported muscle soreness. With the per-protocol analysis, however, the protein group reported higher muscle soreness 24 h post-race compared to the placebo group (2.96 ± 2.27 versus 2.46 ± 2.38, p = 0.039) and a lower pressure muscle pain threshold in the protein group compared to the placebo group (71.8 ± 30.0 N versus 83.9 ± 27.9 N, p = 0.019). No differences were found in concentrations of CK and LDH post-race between groups. Post-exercise protein supplementation is not more preferable than carbohydrate supplementation to reduce muscle soreness or other damage markers in recreational athletes with mostly a sufficient baseline protein intake running a 15-km road race.

The Influence of Long-Chain Omega-3 Fatty Acids on Eccentric Exercise-Induced Delayed Muscle Soreness: Reported Outcomes Are Compromised by Study Design Issues.

Delayed onset muscle soreness (DOMS) following eccentric exercise is associated with increased inflammation which can be debilitating. Incorporation of long-chain omega-3 polyunsaturated fatty acids (LC n-3 PUFA), eicosapentaenoic acid, and docosahexaenoic acid into membrane phospholipids provides anti-inflammatory, proresolving, and analgesic effects. This systematic review aims to examine both the quality of studies and the evidence for LC n-3 PUFA in the attenuation of DOMS and inflammation following eccentric exercise, both which of course are empirically linked. The Scopus, Embase, and Web of Science electronic databases were searched to identify studies that supplemented fish oil for a duration of ≥7 days, which included DOMS outcomes following an eccentric exercise protocol. Fifteen (n = 15) studies met inclusion criteria. Eccentric exercise protocols varied from single to multijoint activities. Risk of bias, assessed using either the Cochrane Collaboration tool or the Risk of Bias in Nonrandomized Studies of Interventions tool, was judged as "unclear" or "medium," respectively, for the majority of outcomes. Furthermore, a custom 5-point quality assessment scale demonstrated that only one (n = 1) study satisfied current recommendations for investigating LC n-3 PUFA. In combination, this highlights widespread inappropriate design protocols among studies investigating the role of LC n-3 PUFA in eccentric exercise. Notwithstanding these issues, LC n-3 PUFA supplementation appears to have favorable effects on eccentric exercise-induced DOMS and inflammatory markers. However, the optimal LC n-3 PUFA supplemental dose, duration, and fatty acid composition will only become clear when study design issues are rectified and underpinned by appropriate hypotheses.

Supplementation of Re-Esterified Docosahexaenoic and Eicosapentaenoic Acids Reduce Inflammatory and Muscle Damage Markers after Exercise in Endurance Athletes: A Randomized, Controlled Crossover Trial.

This study aimed to analyse the effect of 10 weeks of a highly concentrated docosahexaenoic acid (DHA) + eicosapentaenoic (EPA) supplementation (ratio 8:1) on strength deficit and inflammatory and muscle damage markers in athletes. Fifteen endurance athletes participated in the study. In a randomized, double-blinded cross-over controlled design, the athletes were supplemented with a re-esterified triglyceride containing 2.1 g/day of DHA + 240 mg/day of EPA or placebo for 10 weeks. After a 4-week wash out period, participants were supplemented with the opposite treatment. Before and after each supplementation period, participants performed one eccentric-induced muscle damage exercise training session (ECC). Before, post-exercise min and 24 and 48 h after exercise, muscle soreness, knee isokinetic strength and muscle damage and inflammatory markers were tested. No significant differences in strength deficit variables were found between the two conditions in any of the testing sessions. However, a significant effect was observed in IL1ß (p = 0.011) and IL6 (p = 0.009), which showed significantly lower values after DHA consumption than after placebo ingestion. Moreover, a significant main effect was observed in CPK (p = 0.014) and LDH-5 (p = 0.05), in which significantly lower values were found after DHA + EPA consumption. In addition, there was a significant effect on muscle soreness (p = 0.049), lower values being obtained after DHA + EPA consumption. Ten weeks of re-esterified DHA + EPA promoted lower concentrations of inflammation and muscle damage markers and decreased muscle soreness but did not improve the strength deficit after an ECC in endurance athletes.

Supplementation with a Mango Leaf Extract (Zynamite®) in Combination with Quercetin Attenuates Muscle Damage and Pain and Accelerates Recovery after Strenuous Damaging Exercise.

Prolonged or unusual exercise may cause exercise-induced muscle damage (EIMD). To test whether Zynamite®, a mango leaf extract rich in the natural polyphenol mangiferin, administered in combination with quercetin facilitates recovery after EIMD, 24 women and 33 men were randomly assigned to two treatment groups matched by sex and 5 km running performance, and ran a 10 km race followed by 100 drop jumps to elicit EIMD. One hour before the competition, and every 8 hours thereafter for 24 hours, they ingested placebo (728 mg of maltodextrin) or 140 mg of Zynamite® combined with 140 mg of quercetin (double-blind). Although competition times were similar, polyphenol supplementation attenuated the muscle pain felt after the competition (6.8 ± 1.5 and 5.7 ± 2.2 a.u., p = 0.035) and the loss of jumping performance (9.4 ± 11.5 and 3.9 ± 5.2%, p = 0.036; p = 0.034) and mechanical impulse (p = 0.038) 24 hours later. The polyphenols attenuated the increase of serum myoglobin and alanine aminotransferase in men, but not in women (interaction p < 0.05). In conclusion, a single dose of 140 mg Zynamite® combined with 140 mg of quercetin, administered one hour before competition, followed by three additional doses every eight hours, attenuates muscle pain and damage, and accelerates the recovery of muscle performance.

Effect of Branched-Chain Amino Acid Supplementation on Recovery Following Acute Eccentric Exercise.

This study investigated the effect of branched-chain amino acid (BCAA) supplementation on recovery from eccentric exercise. Twenty males ingested either a BCAA supplement or placebo (PLCB) prior to and following eccentric exercise. Creatine kinase (CK), vertical jump (VJ), maximal voluntary isometric contraction (MVIC), jump squat (JS) and perceived soreness were assessed. No significant (p > 0.05) group by time interaction effects were observed for CK, soreness, MVIC, VJ, or JS. CK concentrations were elevated above baseline (p < 0.001) in both groups at 4, 24, 48 and 72 hr, while CK was lower (p = 0.02) in the BCAA group at 48 hr compared to PLCB. Soreness increased significantly from baseline (p < 0.01) in both groups at all time-points; however, BCAA supplemented individuals reported less soreness (p < 0.01) at the 48 and 72 hr time-points. MVIC force output returned to baseline levels (p > 0.05) at 24, 48 and 72 hr for BCAA individuals. No significant difference between groups (p > 0.05) was detected for VJ or JS. BCAA supplementation may mitigate muscle soreness following muscle-damaging exercise. However, when consumed with a diet consisting of ~1.2 g/kg/day protein, the attenuation of muscular performance decrements or corresponding plasma CK levels are likely negligible.

Protein Supplementation During or Following a Marathon Run Influences Post-Exercise Recovery.

The effects of protein supplementation on the ratings of energy/fatigue, muscle soreness [ascending (A) and descending (D) stairs], and serum creatine kinase levels following a marathon run were examined. Variables were compared between recreational male and female runners ingesting carbohydrate + protein (CP) during the run (CPDuring, n = 8) versus those that were consuming carbohydrate (CHODuring,n = 8). In a second study, outcomes were compared between subjects who consumed CP or CHO immediately following exercise [CPPost (n = 4) versus CHOPost (n = 4)]. Magnitude-based inferences revealed no meaningful differences between treatments 24 h post-marathon. At 72 h, recovery [Δ(72 hr-Pre)] was likely improved with CPDuring versus CHODuring, respectively, for Physical Energy (+14 ± 64 vs -74 ± 70 mm), Mental Fatigue (-52 ± 59 vs +1 ± 11 mm), and Soreness-D (+15 ± 9 vs +21 ± 70 mm). In addition, recovery at 72 h was likely-very likely improved with CPPost versus CHOPost for Physical Fatigue, Mental Energy, and Soreness-A. Thus, protein supplementation did not meaningfully alter recovery during the initial 24 h following a marathon. However, ratings of energy/fatigue and muscle soreness were improved over 72 h when CP was consumed during exercise, or immediately following the marathon.

Effects of lymphatic drainage and cryotherapy on indirect markers of muscle damage.

BACKGROUND: Muscle enzymes are cleared from the extracellular space by the lymphatic system, while smaller proteins enter the bloodstream directly. We investigated if manual lymphatic drainage (MLD), local cryotherapy (CRY), and rest (RST) differently affect the time course of creatine kinase (CK, 84 kDa) and heart-type fatty acid binding protein (h-FABP, 15 kDa) in the blood. METHODS: Randomized controlled trial. After 4x20 unilateral, eccentric accentuated knee extensions (with one-third of the maximal isometric force) 30 sports students randomly received either a 30 min MLD, CRY or they rested (RST) for the same amount of time. CK, h-FABP, neutrophil granulocytes, and the perceived muscle soreness were assessed before, immediately after, and 1 hour, 4 hours, and 24 hours after the exercise. RESULTS: All measures increased significantly (P<0.001) after the protocol indicating that muscle damage was induced. However, the responses did not differ between the treatments. CONCLUSIONS: Large and small damage markers were not affected differently by MLD, CRY, or RST, when applied for 30 min and no beneficial effects on inflammation or muscle soreness could be found for MLD and CRY when compared to RST. This information is particularly important for those sports physicians and conditioning specialists who use biochemical muscle damage markers to adjust the training load and volume of athletes.

A low-dose, 6-week bovine colostrum supplementation maintains performance and attenuates inflammatory indices following a Loughborough Intermittent Shuttle Test in soccer players.

PURPOSE: The aim of the study was to investigate the effect of a 6-week, low-dose bovine colostrum (BC) supplementation on exercise-induced muscle damage (EIMD) and performance decline in soccer players following the Loughborough Intermittent Shuttle Test (LIST) during a competitive season period. METHODS: In a double-blind, randomized, placebo-controlled design, two groups of soccer players were allocated to a 3.2 g/day of whey protein (WP, N = 8) or BC (N = 10) and performed a pre- and a post-supplementation LIST. Maximum isometric voluntary contraction, squat jump (SQJ), countermovement jump, muscle soreness, blood cell counts, creatine kinase (CK), C-reactive protein (CRP) and interleukin-6 (IL-6) were monitored for 2, 24, 48, 72 h post-LIST. RESULTS: LIST induced transient increases in leukocytes, granulocytes, CK, muscle soreness, CRP, IL-6 and declines in lymphocytes and performance indices. Supplementation resulted in a faster recovery of SQJ, CK and CRP compared to pre-supplementation kinetics (trial × time: p = 0.001, 0.056, 0.014, respectively) and lower incremental area under the curve (iAUC) for IL-6, only in the BC group [pre-: 31.1 (6.78-46.9), post-: 14.0 (-0.16 to 23.5) pg h/ml, p = 0.034]. Direct comparison of the two groups after supplementation demonstrated higher iAUC of SQJ [WP: -195.2 (-229.0 to (-52.5)), BC: -15.8 (-93.2 to 16.8) cm h, p = 0.034], a trend for lower iAUC of CK in the BC group [WP: 18,785 (4651-41,357), BC: 8842 (4807-14,802) U h/L, p = 0.081] and a significant intervention × time interaction for CRP (p = 0.038) in favor of BC. CONCLUSIONS: Post-exercise EIMD may be reduced and performance better maintained by a low dose of BC administration following LIST in soccer players.

Minimal muscle damage after a marathon and no influence of beetroot juice on inflammation and recovery.

This study examined whether beetroot juice (BTJ) would attenuate inflammation and muscle damage following a marathon. Using a double blind, independent group design, 34 runners (each having completed ca. ∼16 previous marathons) consumed either BTJ or an isocaloric placebo (PLA) for 3 days following a marathon. Maximal isometric voluntary contractions (MIVC), countermovement jumps (CMJ), muscle soreness, serum cytokines, leucocytosis, creatine kinase (CK), high sensitivity C-reactive protein (hs-CRP), and aspartate aminotransferase (AST) were measured pre, post, and 2 days after the marathon. CMJ and MIVC were reduced after the marathon (P < 0.05), but no group differences were observed (P > 0.05). Muscle soreness was increased in the day after the marathon (BTJ; 45 ± 48 vs. PLA; 46 ± 39 mm) and had returned to baseline by day 2, irrespective of supplementation (P = 0.694). Cytokines (interleukin-6; IL-6, interleukin-8, tumour necrosis factor-α) were increased immediately post-marathon but apart from IL-6 had returned to baseline values by day 1 post. No interaction effects were evident for IL-6 (P = 0.213). Leucocytes increased 1.7-fold after the race and remained elevated 2 days post, irrespective of supplement (P < 0.0001). CK peaked at 1 day post marathon (BTJ: 965 ± 967, and PLA: 1141 ± 979 IU·L-1) and like AST and hs-CRP, was still elevated 2 days after the marathon (P < 0.05); however, no group differences were present for these variables. Beetroot juice did not attenuate inflammation or reduce muscle damage following a marathon, possibly because most of these indices were not markedly different from baseline values in the days after the marathon.

The effects of a multi-ingredient supplement on markers of muscle damage and inflammation following downhill running in females.

BACKGROUND: The effects of a multi-ingredient performance supplement (MIPS) on markers of inflammation and muscle damage, perceived soreness and lower limb performance are unknown in endurance-trained female athletes. The purpose of this study was to determine the impact of MIPS (NO-Shotgun®) pre-loaded 4 weeks prior to a single-bout of downhill running (DHR) on hsC-Reactive Protein (hsCRP), interleukin (IL)-6, creatine kinase (CK), muscle soreness, lower limb circumferences and performance. METHOD: Trained female runners (n = 8; 29 ± 5.9 years) (VO2max: ≥ 50 ml-1.kg-1.min-1, midfollicular phase (7-11 days post-menses) were randomly assigned in a double-blind manner into two groups: MIPS (n = 4) ingested one serving of NO Shotgun daily for 28 days prior to DHR and 30 min prior to all post-testing visits; Control (CON) (n = 4) consumed an isocaloric maltodextrin placebo in an identical manner to MIPS. hsCRP, IL-6, CK, perceived soreness, limb circumferences, and performance measures (flexibility, squat jump peak power) were tested on 5 occasions; immediately before (PRE), immediately post-DHR, 24, 48 and 72 h post-DHR. RESULTS: There were main effects of time for CK (p = 0.05), pain pressure threshold (right tibialis anterior (p = 0.010), right biceps femoris (p = 0.01), and left iliotibial band (ITB) (p = 0.05) across all time points), and maximum squat jump power (p = 0.04). Compared with 24 h post-DHR, maximum squat jump power was significantly lower at 48 h post-DHR (p = 0.05). Lower body perceived soreness was significantly increased at 24 h (p = 0.02) and baseline to 48 h (p = 0.02) post DHR. IL-6 peaked immediately post-DHR (p = 0.03) and hsCRP peaked at 24 h post-DHR (p = 0.06). Calculation of effect sizes indicated a moderate attenuation of hsCRP in MIPS at 72 h post-DHR. CONCLUSIONS: Consumption of MIPS for 4 weeks prior to a single bout of DHR attenuated inflammation three days post, but did not affect perceived soreness and muscle damage markers in endurance trained female runners following a single bout of DHR.

The use of thermal imaging to assess the effectiveness of ice massage and cold-water immersion as methods for supporting post-exercise recovery.

Cold water immersion (CWI) and ice massage (IM) are commonly used treatments to prevent the delay onset of muscle soreness (DOMS); however, little is known on their relative benefits and effectiveness to lower tissue temperature. This study was designed to evaluate the effectiveness of IM and CMI on tissue temperature and potential benefit to preventing DOMS. The research encompassed 36 subjects divided into three groups of twelve depending on the form of recovery: ice massage (IM), cold-water immersion (CWI), or passive recovery (PAS). All the participants were asked to jump as high as possible from a full squat for one minute. Thermal imaging was conducted at rest, immediately following the exercise, immediately after the trial, following the recovery treatment, and after 30min of rest. Their pain levels were assessed using the Visual Analogue Scale (VAS). After applying the selected method for supporting recovery, the LA level decreased by 4.25mmol/L in the IM group, and by 4.96mmol/L in the CWI group (IM vs. CWI p>0.05). The 2.75mmol/L decrease in lactate concentration in the PAS group was significantly lower than in the other groups (IM vs. PAS p<0.05/ CWI vs. PAS p<0.01). In both groups, Tsk after 30min was significantly lower (ΔTsk~0.5°C) than at rest (p<0.05). In turn, Tsk in the PAS group returned to the resting values (p>0.05). Seventy-two hours after the exercise, a clear decrease in discomfort was observed in the IM and CWI groups compared to the PAS group. The two applied treatments have proven to be effective both in utilizing lactate and preventing DOMS. Depending on training requirements, we recommend the use of IM when athletes experience localized muscle fatigue. One the other hand, CWI is recommended in situations of global or generalized muscle injury or fatigue.

Effects of Light-Emitting Diode Therapy on Muscle Hypertrophy, Gene Expression, Performance, Damage, and Delayed-Onset Muscle Soreness: Case-control Study with a Pair of Identical Twins.

OBJECTIVE: The aim of this study was to verify how a pair of monozygotic twins would respond to light-emitting diode therapy (LEDT) or placebo combined with a strength-training program during 12 weeks. DESIGN: This case-control study enrolled a pair of male monozygotic twins, allocated randomly to LEDT or placebo therapies. Light-emitting diode therapy or placebo was applied from a flexible light-emitting diode array (λ = 850 nm, total energy = 75 J, t = 15 seconds) to both quadriceps femoris muscles of each twin immediately after each strength training session (3 times/wk for 12 weeks) consisting of leg press and leg extension exercises with load of 80% and 50% of the 1-repetition maximum test, respectively. Muscle biopsies, magnetic resonance imaging, maximal load, and fatigue resistance tests were conducted before and after the training program to assess gene expression, muscle hypertrophy and performance, respectively. Creatine kinase levels in blood and visual analog scale assessed muscle damage and delayed-onset muscle soreness, respectively, during the training program. RESULTS: Compared with placebo, LEDT increased the maximal load in exercise and reduced fatigue, creatine kinase, and visual analog scale. Gene expression analyses showed decreases in markers of inflammation (interleukin 1ß) and muscle atrophy (myostatin) with LEDT. Protein synthesis (mammalian target of rapamycin) and oxidative stress defense (SOD2 [mitochondrial superoxide dismutase]) were up-regulated with LEDT, together with increases in thigh muscle hypertrophy. CONCLUSIONS: Light-emitting diode therapy can be useful to reduce muscle damage, pain, and atrophy, as well as to increase muscle mass, recovery, and athletic performance in rehabilitation programs and sports medicine.

Risk identification and possible countermeasures for muscle adverse effects during statin therapy.

The use of statins for cardiovascular disease prevention is clearly supported by clinical evidence. However, in January 2014 the U.S. Food and Drug Administration released an advice on statin risk reporting that "statin benefit is indisputable, but they need to be taken with care and knowledge of their side effects". Among them the by far most common complication is myopathy, ranging from common but clinically benign myalgia to rare but life-threatening rhabdomyolysis. This class side effect appears to be dose dependent, with more lipophilic statin (i.e., simvastatin) carrying a higher overall risk. Hence, to minimize statin-associated myopathy, clinicians should take into consideration a series of factors that potentially increase this risk (i.e., drug-drug interactions, female gender, advanced age, diabetes mellitus, hypothyroidism and vitamin D deficiency). Whenever it is appropriate to stop statin treatment, the recommendations are to stay off statin until resolution of symptoms or normalization of creatine kinase values. Afterwards, clinicians have several options to treat dyslipidemia, including the use of a lower dose of the same statin, intermittent non-daily dosing of statin, initiation of a different statin, alone or in combination with nonstatin lipid-lowering agents, and substitution with red yeast rice.

Berberis aristata combined with Silybum marianum on lipid profile in patients not tolerating statins at high doses.

AIM: To evaluate the effects of Berberis aristata combined with Silybum marianum in dyslipidemic patients intolerant to statins at high doses. METHODS: 137 euglycemic, dyslipidemic subjects, with previous adverse events to statins at high doses, were enrolled. Statins were stopped for 1 month (run-in), then they were re-introduced at the half of the previously taken dose. At randomization, patients tolerating the half dose of statin, were assigned to add placebo or B. aristata/S. marianum 588/105 mg, 1 tablet during the lunch and 1 tablet during the dinner, for six months. We evaluated lipid profile and safety parameters variation at randomization, and after 3, and 6 months. RESULTS: B. aristata/S. marianum reduced fasting plasma glucose (-9 mg/dl), insulin (-0.7 µU/ml), and HOMA-index (-0.35) levels compared to baseline and also to placebo. Lipid profile did not significantly change after 6 months since the reduction of statin dosage and the introduction of B. aristata/S. marianum, while it worsened in the placebo group both compared to placebo and with active treatment (+23.4 mg/dl for total cholesterol, +19.6 mg/dl for LDL-cholesterol, +23.1 mg/dl for triglycerides with placebo compared to B. aristata/S. marianum). We did not record any variations of safety parameters in nether of groups. CONCLUSIONS: B. aristata/S. marianum can be considered as addition to statins in patients not tolerating high dose of these drugs.

Analysis of vitamin D levels in patients with and without statin-associated myalgia - a systematic review and meta-analysis of 7 studies with 2420 patients.

INTRODUCTION: Vitamin D (vit D) deficiency may be associated with an increased risk of statin-related symptomatic myalgia in statin-treated patients. The aim of this meta-analysis was to substantiate the role of serum vitamin D levels in statin-associated myalgia. METHODS: The search included PUBMED, Cochrane Library, Scopus, and EMBASE from January 1, 1987 to April 1, 2014 to identify studies that investigated the impact of vit D levels in statin-treated subjects with and without myalgia. Two independent reviewers extracted data on study characteristics, methods and outcomes. Quantitative data synthesis was performed using a fixed-effect model. RESULTS: The electronic search yielded 437 articles; of those 20 were scrutinized as full texts and 13 studies were considered unsuitable. The final analysis included 7 studies with 2420 statin-treated patients divided into subgroups of patients with (n=666 [27.5%]) or without (n=1754) myalgia. Plasma vit D concentrations in the symptomatic and asymptomatic subgroups were 28.4±13.80ng/mL and 34.86±11.63ng/mL, respectively. The combination of data from individual observational studies showed that vit D plasma concentrations were significantly lower in patients with statin-associated myalgia compared with patients not manifesting this side effect (weighted mean difference -9.41ng/mL; 95% confidence interval: -10.17 to -8.64; p<0.00001). CONCLUSIONS: This meta-analysis provides evidence that low vit D levels are associated with myalgia in patients on statin therapy. Randomized controlled trials are necessary to establish whether vitamin D supplementation reduces the risk for statin-associated myalgia.

Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials.

OBJECTIVE: To evaluate the efficacy of coenzyme Q10 (CoQ10) supplementation on statin-induced myopathy. PARTICIPANTS AND METHODS: We searched the MEDLINE, Cochrane Library, Scopus, and EMBASE databases (November 1, 1987, to May 1, 2014) to identify randomized controlled trials investigating the impact of CoQ10 on muscle pain and plasma creatine kinase (CK) activity as 2 measures of statin-induced myalgia. Two independent reviewers extracted data on study characteristics, methods, and outcomes. RESULTS: We included 6 studies with 302 patients receiving statin therapy: 5 studies with 226 participants evaluated the effect of CoQ10 supplementation on plasma CK activity, and 5 studies (4 used in the CK analysis and 1 other study) with 253 participants were included to assess the effect of CoQ10 supplementation on muscle pain. Compared with the control group, plasma CK activity was increased after CoQ10 supplementation, but this change was not significant (mean difference, 11.69 U/L [to convert to µkat/L, multiply by 0.0167]; 95% CI, -14.25 to 37.63 U/L; P=.38). Likewise, CoQ10 supplementation had no significant effect on muscle pain despite a trend toward a decrease (standardized mean difference, -0.53; 95% CI, -1.33 to 0.28; P=.20). No dose-effect association between changes in plasma CK activity (slope, -0.001; 95% CI, -0.004 to 0.001; P=.33) or in the indices of muscle pain (slope, 0.002; 95% CI, -0.005 to 0.010; P=.67) and administered doses of CoQ10 were observed. CONCLUSION: The results of this meta-analysis of available randomized controlled trials do not suggest any significant benefit of CoQ10 supplementation in improving statin-induced myopathy. Larger, well-designed trials are necessary to confirm the findings from this meta-analysis.

The impact of neuromuscular electrical stimulation on recovery after intensive, muscle damaging, maximal speed training in professional team sports players.

OBJECTIVES: During congested fixture periods in team sports, limited recovery time and increased travel hinder the implementation of many recovery strategies; thus alternative methods are required. We examined the impact of a neuromuscular electrical stimulation device on 24-h recovery from an intensive training session in professional players. DESIGN: Twenty-eight professional rugby and football academy players completed this randomised and counter-balanced study, on 2 occasions, separated by 7 days. METHODS: After baseline perceived soreness, blood (lactate and creatine kinase) and saliva (testosterone and cortisol) samples were collected, players completed a standardised warm-up and baseline countermovement jumps (jump height). Players then completed 60 m × 50 m maximal sprints, with 5 min recovery between efforts. After completing the sprint session, players wore a neuromuscular electrical stimulation device or remained in normal attire (CON) for 8 h. All measures were repeated immediately, 2 and 24-h post-sprint. RESULTS: Player jump height was reduced from baseline at all time points under both conditions; however, at 24-h neuromuscular electrical stimulation was significantly more recovered (mean±SD; neuromuscular electrical stimulation -3.2±3.2 vs. CON -7.2±3.7%; P<0.001). Creatine kinase concentrations increased at all time points under both conditions, but at 24-h was lower under neuromuscular electrical stimulation (P<0.001). At 24-h, perceived soreness was significantly lower under neuromuscular electrical stimulation, when compared to CON (P=0.02). There was no effect of condition on blood lactate, or saliva testosterone and cortisol responses (P>0.05). CONCLUSIONS: Neuromuscular electrical stimulation improves recovery from intensive training in professional team sports players. This strategy offers an easily applied recovery strategy which may have particular application during sleep and travel.