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

Saliva-derived DNA performs well in large-scale, high-density single-nucleotide polymorphism microarray studies

As of June 2009, 361 genome-wide association studies (GWAS) had been referenced by the HuGE database. GWAS require DNA from many thousands of individuals, relying on suitable DNA collections. We recently performed a multiple sclerosis (MS) GWAS where a substantial component of the cases (24%) had DNA derived from saliva. Genotyping was done on the Illumina genotyping platform using the Infinium Hap370CNV DUO microarray. Additionally, we genotyped 10 individuals in duplicate using both saliva- and blood-derived DNA. The performance of blood- versus saliva-derived DNA was compared using genotyping call rate, which reflects both the quantity and quality of genotyping per sample and the “GCScore,” an Illumina genotyping quality score, which is a measure of DNA quality. We also compared genotype calls and GCScores for the 10 sample pairs. Call rates were assessed for each sample individually. For the GWAS samples, we compared data according to source of DNA and center of origin. We observed high concordance in genotyping quality and quantity between the paired samples and minimal loss of quality and quantity of DNA in the saliva samples in the large GWAS sample, with the blood samples showing greater variation between centers of origin. This large data set highlights the usefulness of saliva DNA for genotyping, especially in high-density single-nucleotide polymorphism microarray studies such as GWAS.

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...

Traffic density estimation of signalised arterials with stop line detector and probe data

This research aims to develop a reliable density estimation method for signalised arterials based on cumulative counts from upstream and downstream detectors. In order to overcome counting errors associated with urban arterials with mid-link sinks and sources, CUmulative plots and Probe Integration for Travel timE estimation (CUPRITE) is employed for density estimation. The method, by utilizing probe vehicles’ samples, reduces or cancels the counting inconsistencies when vehicles’ conservation is not satisfied within a section. The method is tested in a controlled environment, and the authors demonstrate the effectiveness of CUPRITE for density estimation in a signalised section, and discuss issues associated with the method.

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.

Analysis and prediction of the critical current density across [001]-tilt YBa2Cu3O7- grain boundaries of arbitrary misorientation angles

A qualitative analysis of the expected dilatation strain field in the vicinity of an array of grain-boundary (GB) dislocations is presented. The analysis provides a basis for the prediction of the critical current densities (jc) across low-angle YBa2Cu3O7- (YBCO) GBs as a function of their energy. The introduction of the GB energy allows the extension of the analysis to high-angle GBs using established models which predict the GB energy as a function of misorientation angle. The results are compared to published data for jc across [001]-tilt YBCO GBs for the full range of misorientations, showing a good fit. Since the GB energy is directly related to the GB structure, the analysis may allow a generalization of the scaling behavior of jc with the GB energy. © 1995 The American Physical Society.

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.

Nutrient provision increases signalling and protein synthesis in human skeletal muscle after repeated sprints

The effect of nutrient availability on the acute molecular responses following repeated sprint exercise is unknown. The aim of this study was to determine skeletal muscle cellular and protein synthetic responses following repeated sprint exercise with nutrient provision. Eight healthy young male subjects undertook two sprint cycling sessions (10 × 6 s, 0.75 N m torque kg -1, 54 s recovery) with either pre-exercise nutrient (24 g whey, 4.8 g leucine, 50 g maltodextrin) or non-caloric placebo ingestion. Muscle biopsies were taken from vastus lateralis at rest, and after 15 and 240 min post-exercise recovery to determine muscle cell signalling responses and protein synthesis by primed constant infusion of L-[ring- 13C 6] phenylalanine. Peak and mean power outputs were similar between nutrient and placebo trials. Post-exercise myofibrillar protein synthetic rate was greater with nutrient ingestion compared with placebo ( ? 48%, P<0.05) but the rate of mitochondrial protein synthesis was similar between treatments. The increased myofibrillar protein synthesis following sprints with nutrient ingestion was associated with coordinated increases in Akt-mTOR-S6KrpS6 phosphorylation 15 min post-exercise (?200-600%, P<0.05), while there was no effect on these signalling molecules when exercise was undertaken in the fasted state. For the first time we report a beneficial effect of nutrient provision on anabolic signalling and muscle myofibrillar protein synthesis following repeated sprint exercise. Ingestion of protein/carbohydrate in close proximity to high-intensity sprint exercise provides an environment that increases cell signalling and protein synthesis.

Contraction-induced changes in TNFα and Akt-mediated signalling are associated with increased myofibrillar protein in rat skeletal muscle

Resistance training results in skeletal muscle hypertrophy, but the molecular signalling mechanisms responsible for this altered phenotype are incompletely understood. We used a resistance training (RT) protocol consisting of three sessions [day 1 (d1), day 3 (d3), day 5 (d5)] separated by 48 h recovery (squat exercise, 4 sets × 10 repetitions, 3 min recovery) to determine early signalling responses to RT in rodent skeletal muscle. Six animals per group were killed 3 h after each resistance training session and 24 and 48 h after the last training session (d5). There was a robust increase in TNF? protein expression, and IKKSer180/181 and p38MAPK Thr180/Tyr182 phosphorylation on d1 (P < 0.05), which abated with subsequent RT, returning to control levels by d5 for TNF? and IKK Ser180/181. There was a trend for a decrease in MuRF-1 protein expression, 48 h following d5 of training (P = 0.08). Notably, muscle myofibrillar protein concentration was elevated compared to control 24 and 48 h following RT (P < 0.05). AktSer473 and mTORSer2448 phosphorylation were unchanged throughout RT. Phosphorylation of p70S6k Thr389 increased 3 h post-exercise on d1, d3 and d5 (P < 0.05), whilst phosphorylation of S6Ser235/236 increased on d1 and d3 (P < 0.05). Our results show a rapid attenuation of inflammatory signalling with repeated bouts of resistance exercise, concomitant with summation in translation initiation signalling in skeletal muscle. Indeed, the cumulative effect of these signalling events was associated with myofibrillar protein accretion, which likely contributes to the early adaptations in response to resistance training overload in the skeletal muscle.

Effect of consecutive repeated sprint and resistance exercise bouts on acute adaptive responses in human skeletal muscle

We examined acute molecular responses in skeletal muscle to repeated sprint and resistance exercise bouts. Six men [age, 24.7 ± 6.3 yr; body mass, 81.6 ± 7.3 kg; peak oxygen uptake, 47 ± 9.9 ml·kg -1 ·min -1; one repetition maximum (1-RM) leg extension 92.2 ± 12.5 kg; means ± SD] were randomly assigned to trials consisting of either resistance exercise (8 × 5 leg extension, 80% 1-RM) followed by repeated sprints (10 × 6 s, 0.75 N·m torque·kg -1) or vice-versa. Muscle biopsies from vastus lateralis were obtained at rest, 15 min after each exercise bout, and following 3-h recovery to determine early signaling and mRNA responses. There was divergent exercise order-dependent phosphorylation of p70 S6K (S6K). Specifically, initial resistance exercise increased S6K phosphorylation (?75% P < 0.05), but there was no effect when resistance exercise was undertaken after sprints. Exercise decreased IGF-I mRNA following 3-h recovery (?50%, P = 0.06) independent of order, while muscle RING finger mRNA was elevated with a moderate exercise order effect (P < 0.01). When resistance exercise was followed by repeated sprints PGC-1? mRNA was increased (REX1-SPR2; P = 0.02) with a modest distinction between exercise orders. Repeated sprints may promote acute interference on resistance exercise responses by attenuating translation initiation signaling and exacerbating ubiquitin ligase expression. Indeed, repeated sprints appear to generate the overriding acute exercise-induced response when undertaking concurrent repeated sprint and resistance exercise. Accordingly, we suggest that sprint-activities are isolated from resistance training and that adequate recovery time is considered within periodized training plans that incorporate these divergent exercise modes.

mTOR function in skeletal muscle : a focal point for overnutrition and exercise

The mammalian target of rapamycin (mTOR) is a highly conserved atypical serine-threonine kinase that controls numerous functions essential for cell homeostasis and adaptation in mammalian cells via 2 distinct protein complex formations. Moreover, mTOR is a key regulatory protein in the insulin signalling cascade and has also been characterized as an insulin-independent nutrient sensor that may represent a critical mediator in obesity-related impairments of insulin action in skeletal muscle. Exercise characterizes a remedial modality that enhances mTOR activity and subsequently promotes beneficial metabolic adaptation in skeletal muscle. Thus, the metabolic effects of nutrients and exercise have the capacity to converge at the mTOR protein complexes and subsequently modify mTOR function. Accordingly, the aim of the present review is to highlight the role of mTOR in the regulation of insulin action in response to overnutrition and the capacity for exercise to enhance mTOR activity in skeletal muscle.

Consecutive bouts of diverse contractile activity alter acute responses in human skeletal muscle

We examined acute molecular responses in skeletal muscle to divergent exercise stimuli by combining consecutive bouts of resistance and endurance exercise. Eight men [22.9 ± 6.3 yr, body mass of 73.2 ± 4.5 kg, peak O2 uptake (V?O2peak) of 54.0 ± 5.7 ml·kg-1·min-1] were randomly assigned to complete trials consisting of either resistance exercise (8 x 5 leg extension, 80% 1 repetition maximum) followed by a bout of endurance exercise (30 min cycling, 70% V?O2peak) or vice versa. Muscle biopsies were obtained from the vastus lateralis at rest, 15 min after each exercise bout, and after 3 h of passive recovery to determine early signaling and mRNA responses. Phosphorylation of Akt and Akt1Ser473 were elevated 15 min after resistance exercise compared with cycling, with the greatest increase observed when resistance exercise followed cycling (?55%; P < 0.01). TSC2-mTOR-S6 kinase phosphorylation 15 min after each bout of exercise was similar regardless of the exercise mode. The cumulative effect of combined exercise resulted in disparate mRNA responses. IGF-I mRNA content was reduced when cycling preceded resistance exercise (-42%), whereas muscle ring finger mRNA was elevated when cycling was undertaken after resistance exercise (?52%; P < 0.05). The hexokinase II mRNA level was higher after resistance cycling (?45%; P < 0.05) than after cycling-resistance exercise, whereas modest increases in peroxisome proliferator-activated receptor gamma coactivator-1? mRNA did not reveal an order effect. We conclude that acute responses to diverse bouts of contractile activity are modified by the exercise order. Moreover, undertaking divergent exercise in close proximity influences the acute molecular profile and likely exacerbates acute "interference".

Global gene expression in skeletal muscle from well-trained strength and endurance athletes

PURPOSE: We used gene microarray analysis to compare the global expression profile of genes involved in adaptation to training in skeletal muscle from chronically strength-trained (ST), endurance-trained (ET), and untrained control subjects (Con). METHODS: Resting skeletal muscle samples were obtained from the vastus lateralis of 20 subjects (Con n = 7, ET n = 7, ST n = 6; trained [TR] groups >8 yr specific training). Total RNA was extracted from tissue for two color microarray analysis and quantative (Q)-PCR. Trained subjects were characterized by performance measures of peak oxygen uptake V?O 2peak) on a cycle ergometer and maximal concentric and eccentric leg strength on an isokinetic dynamometer. RESULTS: Two hundred and sixty-three genes were differentially expressed in trained subjects (ET + ST) compared with Con (P < 0.05), whereas 21 genes were different between ST and ET (P < 0.05). These results were validated by reverse transcriptase polymerase chain reaction for six differentially regulated genes (EIFSJ, LDHB, LMO4, MDH1, SLC16A7, and UTRN. Manual cluster analyses revealed significant regulation of genes involved in muscle structure and development in TR subjects compared with Con (P < 0.05) and expression correlated with measures of performance (P < 0.05). ET had increased whereas ST had decreased expression of gene clusters related to mitochondrial/oxidative capacity (P ?‰Currency sign 0.05). These mitochondrial gene clusters correlated with V?O2peak (P < 0.05). V?O2peak also correlated with expression of gene clusters that regulate fat and carbohydrate oxidation (P < 0.05). CONCLUSION: We demonstrate that chronic training subtly coregulates numerous genes from important functional groups that may be part of the long-term adaptive process to adapt to repeated training stimuli.