Impact of Optimal Timing of Intake of Multi-Ingredient Performance Supplements on Sports Performance, Muscular Damage, and Hormonal Behavior across a Ten-Week Training Camp in Elite Cyclists: A Randomized Clinical Trial

Multi-ingredient performance supplements (MIPS), ingested pre- or post-workout, have been shown to increase physiological level effects and integrated metabolic response on exercise. The purpose of this study was to determine the efficacy of pre-and post-training supplementation with its own MIPS, associated with CHO (1 g·kg−1) plus protein (0.3 g·kg−1) on exercise-related benchmarks across a training camp for elite cyclists. Thirty elite male cyclists participated in a randomized non-placebo-controlled trial for ten weeks assigned to one of three groups (n = 10 each): a control group treated with CHO plus protein after training (CG); a group treated with MIPS before training and a CHO plus protein after training, (PRE-MIPS); a group treated with CHO plus protein plus MIPS after training, (POST-MIPS). Performance parameters included (VO2max, peak; median and minimum power (W) and fatigue index (%)); hormonal response (Cortisol; Testosterone; and Testosterone/Cortisol ratio); and muscle biomarkers (Creatine kinase (CK), Lactate dehydrogenase (LDH), and Myoglobin (Mb)) were assessed. MIPS administered before or after training (p ≤ 0.05) was significantly influential in attenuating CK, LDH, and MB; stimulating T response and modulating C; and improved on all markers of exercise performance. These responses were greater when MIPS was administered post-workout.

Vitamin D, Its Role in Recovery after Muscular Damage Following Exercise

Aside from its role in bone metabolism, vitamin D is a key immunomodulatory micronutrient. The active form of vitamin D (1,25(OH)D) seems to modulate the innate immune system through different mechanisms. The vitamin is involved in the differentiation of monocytes into macrophages, increasing the phagocytic and chemotactic functions of these cells. At the same time, vitamin D enables efferocytosis and prevents immunopathology. In addition, vitamin D is involved in other processes related to immune function, such as inflammation. Regarding muscle tissue, vitamin D plays an active role in muscle inflammatory response, protein synthesis, and regulation of skeletal muscle function. Two mechanisms have been proposed: A direct role of 1,25(OH)D binding to vitamin D receptors (VDRs) in muscle cells and the modulation of calcium transport in the sarcoplasmic reticulum. This second mechanism needs additional investigation. In conclusion, vitamin D seems to be effective in cases of deficiency and/or if there is a great muscular commitment, such as in high intensity exercises.

Effect of Glutamine Supplementation on Muscular Damage Biomarkers in Professional Basketball Players

Scientific evidence supports the role of L-glutamine in improving immune function. This could suggest a possible role of L-glutamine in recovery after intense exercise. To this end, the present report aimed to study if oral L-glutamine supplementation could attenuate muscle damage in a group of players of a mainly eccentric sport discipline such as basketball. Participants (n = 12) were supplemented with 6 g/day of glutamine (G group) or placebo (P group) for 40 days in a crossover study design (20 days with glutamine + 20 days with placebo and vice versa). Blood samples were obtained at the beginning and at the end of each period and markers from exercise-induced muscle damage were determined. The glutamine supplemented group displayed significantly low values of aspartate transaminase, creatine kinase and myoglobin in blood, suggesting less muscle damage compared to the placebo. In addition, adrenocorticotropic hormone levels were lower in the glutamine supplemented group than in the placebo. As a result, the circulating cortisol levels did not increase at the end of the study in the glutamine supplemented group. Altogether, the results indicate that glutamine could help attenuate exercise-induced muscle damage in sport disciplines with predominantly eccentric actions.

Pharmacological activation of SERCA ameliorates dystrophic phenotypes in dystrophin-deficient mdx mice

Duchenne muscular dystrophy (DMD) is an X-linked genetic disorder characterized by progressive muscular weakness due to the loss of dystrophin. Extracellular Ca2+ flows into the cytoplasm through membrane tears in dystrophin-deficient myofibers, which leads to muscle contracture and necrosis. Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) takes up cytosolic Ca2+ into the sarcoplasmic reticulum (SR), but its activity is decreased in dystrophic muscle. Here, we show that an allosteric SERCA activator, CDN1163, ameliorates dystrophic phenotypes in dystrophin-deficient mdx mice. Administration of CDN1163 prevented exercise-induced muscular damage and restored mitochondrial function. In addition, treatment with CDN1163 for seven weeks enhanced muscular strength and reduced muscular degeneration and fibrosis in mdx mice. Our findings provide preclinical proof-of-concept evidence that pharmacological activation of SERCA could be a promising therapeutic strategy for DMD. Moreover, CDN1163 improved muscular strength surprisingly in wild-type mice, which may pave the new way for the treatment of muscular dysfunction.

Utilizing Dynamic Phosphorous-31 Magnetic Resonance Spectroscopy for the Early Detection of Acute Compartment Syndrome: A Pilot Study on Rats

Introduction: Disasters, including terrorism and earthquakes, are significant threats to people and may lead to many people requiring rescue. The longer the rescue takes, the higher the chances of an individual contracting acute compartment syndrome (ACS). ACS is fatal if diagnosed too late, and early diagnosis and treatment are essential. Objective: To assess the ability of dynamic phosphorus magnetic resonance spectroscopy (31P-MRS) in the early detection of muscular damage in ACS. Materials and Methods: Six ACS model rats were used for serial 31P-MRS scanning (9.4 Tesla). Skeletal muscle metabolism, represented by the levels of phosphocreatine (PCr), inorganic phosphate (Pi), and adenosine triphosphate (ATP), was assessed. The PCr/(Pi + PCr) ratio, which decreases with ischemia, was compared with simultaneously sampled plasma creatine phosphokinase (CPK), a muscle damage marker. Results: The PCr/(Pi + PCr) ratio significantly decreased after inducing ischemia (from 0.86 ± 0.10 to 0.18 ± 0.06; p < 0.05), while CPK did not change significantly (from 89 ± 29.46 to 241.50 ± 113.28; p > 0.05). The intracellular and arterial pH index decreased over time, revealing significant differences at 120 min post-ischemia (from 7.09 ± 0.01 to 6.43 ± 0.13, and from 7.47 ± 0.03 to 7.39 ± 0.04, respectively). In the reperfusion state, the spectra and pH did not return to the original values. Conclusions: The dynamic 31P-MRS technique can rapidly detect changes in muscle bioenergetics. This technique is a promising non-invasive method for determining early muscular damage in ACS.

Different Training Methods Cause Similar Muscle Damage in Youth Judo Athletes

It is well known that different factors can contribute to muscle damage in judo matches or training. Previous research analyzed only the effects of simulated judo combat or judo training on biochemical markers of muscle damage without determining its specific causes. Our objective was to identify possible differences in biochemical markers of muscular damage in response to different training methods in youth judo athletes. Twelve high-level male judo athletes were randomly assigned to a standing (SP, n = 6, age = 16.6 ± 1.1 years) or a groundwork (GP, n = 6, age = 17.8 ± 0.8 years) position combat practice group. Both groups had the same protocol of four 4-minute combat practice bouts separated by 1-minute rest intervals. Before and immediately after combat practice blood samples were taken to assess muscle damage markers: creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). There were significant increases in AST, LDH, and CK after the standing and groundwork training sessions compared with resting values in both groups. Additionally, no significant differences in the enzyme's activity between SP and GP groups were found. These results showed that standing and groundwork randori training (free sparring or free practice) causes similar muscle damage in adolescent judo athletes. Future research should assess the effects of the same damage mechanisms over a longer period of time

4-week eicosapentaenoic acid-rich fish oil supplementation partially protects muscular damage following eccentric contractions

Background We previously showed 8-week of fish oil supplementation attenuated muscle damage. However, the effect of a shorter period of fish oil supplementation is unclear. The present study investigated the effect of fish oil, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), for 4 weeks on muscular damage caused by eccentric contractions (ECCs) of the elbow flexors. Methods Twenty-two untrained men were recruited in this double-blind, placebo-controlled, parallel design study and the subjects were randomly assigned to the EPA and DHA group (EPA and DHA, n = 11) and placebo group (PL, n = 11). They consumed either EPA 600 mg and DHA 260 mg per day or placebo supplement for 4 weeks prior to exercise. Subjects performed 60 ECCs at 100 % maximal voluntary contraction (MVC) using a dumbbell. Changes in MVC torque, range of motion (ROM), upper arm circumference, muscle soreness, echo intensity, muscle thickness, serum creatine kinase (CK), and interleukin-6 (IL-6) were assessed before exercise; immediately after exercise; and 1, 2, 3, and 5 days after exercise. Results ROM was significantly higher in the EPA and DHA group than in the PL group immediately after performing ECCs (p < 0.05). No differences between groups were observed in terms of MVC torque, upper arm circumference, muscle soreness, echo intensity, and thickness. A significant difference was observed in serum CK 3 days after ECCs (p < 0.05). Conclusions We concluded that shorter period EPA and DHA supplementation benefits joint flexibility and protection of muscle fiber following ECCs.

An Early Detection of Acute Compartment Syndrome in Fastened Zip-Tie Rat Model Using Dynamic Phosphorous-31 Magnetic Resonance Spectroscopy at 9.4 Tesla

IntroductionAcute compartment syndrome (ACS) leads to a series of health problems, limb salvage, disability, and even death. In vivo phosphorus-31 magnetic resonance spectroscopy (31P-MRS) provides a unique non-invasive method to assess skeletal muscle metabolisms such as inorganic phosphate (Pi), phosphocreatine (PCr), and adenosine triphosphate (ATP). The study aims to assess the ability of dynamic 31P-MRS in the early detection of muscular damage in ACS.Materials & MethodsThe study induced the fastened zip-tie model of ACS on normotensive Sprague-Dawley rats (n = 6). The spectra were acquired in Bruker 9.4-Tesla preclinical scanner using 1H/31P surface coil. 31P-MRS spectra and blood samples were obtained at time 0 (pre-ischemic phase) and every 15 minutes during the compression (120 minutes) and the reperfusion phase (90 minutes). 31P-MRS spectra findings were compared with plasma creatine phosphokinase (CPK).ResultsPCr/(Pi + PCr) ratio significantly decreased after muscle was compressed (P < 0.05). In contrast to this, CPK did not change significantly (P > 0.05). Both intracellular pH and arterial pH decreased over time. However, intracellular declined significantly (P < 0.05) at 60 minutes of ischemic state, and at 5 minutes and 60 minutes of reperfusion, while arterial pH slightly changed. After 30 minutes of ischemic, phosphomonoesters (PME) peak was detected, which was not seen at the pre-ischemic phase. It gradually increased and reached its highest peak at 120 minutes. At reperfusion state, 31P-MRS spectra and pH did not fully recover to their pre-ischemic state, and PME peak disappeared. There was a correlation between T2-weighted images and CPK from blood tests (R2 = 0.1996, P < 0.05).ConclusionsDynamic 31P-MRS technique is more clearly and rapidly detect the bioenergetic and mitochondrial functions change than blood test in a fastened zip-tie rat model of ACS. This technique is a promising non-invasive method to detect the early ischemic muscular damage in ACS.

The effect of induced training on selected equine blood plasma indicators on treadmill trained horses

The aim of this study was to evaluate the effect of induced training on the horses’ metabolism during an experiment lasting nine weeks where we continually scaled up the load on the horses by three defined stages. Blood was obtained from eighteen horses – two stallions, eight mares and eight geldings. In the experiment, we focused on the biochemical analysis of the blood plasma on multiple mineral profile indicators – Ca, P, Mg, K, Cl and Na, and some other variables (energy, nitrogen, AST, ALT, glucose, urea, creatinine kinase, total proteins). The result showed significant changes between the groups in most indicators. A significant increase in the potassium, phosphorus and calcium and a decrease in the concentrations of magnesium over the course of the experiment were found. For the other indicators, a significant increase in the activities of the AST and ALT out of the other indicators and the fluctuating values in the total proteins were noticed. Summarised, significant changes of multiple indicators were observed in different stages of the experiment. These changes had no visible effect on the horses’ organisms throughout entire duration of the experiment and were most probably caused by the muscular work and possible muscular damage during training.

Duchenne Muscular Dystrophy and Early Onset Hypertrophic Cardiomyopathy associated with Mutations in Dystrophin and Hypertrophic Cardiomyopathy-Associated Genes

Duchenne muscular dystrophy (DMD) is a progressive muscular damage disorder caused by mutations in dystrophin gene. Cardiomyopathy may first be evident after 10 years of age and increases in incidence with age. We present a boy diagnosed at 18 months with a rare phenotype of DMD in association with early-onset hypertrophic cardiomyopathy (HCM). The cause of DMD is a deletion of exons 51–54 of dystrophin gene. The cause of HCM was verified by whole exome sequencing. Novel missense variations in two genes: MAP2K5 inherited from the mother and ACTN2 inherited from the father, or de novo. The combination of MAP2K5, ACTN2, and dystrophin mutations, could be causing the HCM in our patient. This is the second patient diagnosed, at relatively young age, with DMD and HCM, with novel variations in genes known to cause HCM. This study demonstrates the need for genetic diagnosis to elucidate the underlying pathology of HCM.