Search

Following dislocation of the glenohumeral joint with an isolated greater tuberosity fracture, closed reduction in the emergency department can lead to fracture propagation or iatrogenic fractures. This article assesses the evidence regarding when anterior dislocations of the shoulder with an isolated fracture of the greater tuberosity can be safely reduced in the emergency department, as there is currently no clear guidance on this. A total of eight articles described 172 cases which underwent closed reduction, which resulted in 22 cases of iatrogenic fractures. Female sex, increased patient age and fragments of the greater tuberosity were associated with an increased risk of iatrogenic fractures. Closed reduction in the emergency department appears to be a safe option in younger patients and those with greater tuberosity fractures less than 40% of the width of the humeral head.

Sport Science is considered the study and application of scientific principles and techniques to improve sporting performance. Thus, a key role of the Sport Scientist is to translate complex information into usable and contextual performance solutions for a range of different stakeholders. These stakeholders consist of athletes, coaches, recruiting, performance support, medical, administration and operations staff and have varying interests and priorities meaning the information required can be vastly different. In addition to these different needs, sport is fast-moving, diverse and complex meaning there are a number of potential translational barriers. Sport Science training programmes entail the development of technical knowledge and practical skills; however, little is considered in view of interpersonal craft skill development and knowledge translation (KT). Given the reported barriers and challenges to effective KT in sport, this lack of specific training may render KT as ineffective and suboptimal. Accordingly, in this article, we propose a framework and work-based training model with the aim of developing the KT process and performance delivery of Sport Scientists operating in professional sport. Firstly, we define the current perspectives and challenges for Sport Scientists in the context of KT, before proposing a framework that focusses on Evidence-Based-Practice, Philosophy, Recipients and Facilitation, in which Sport Scientists can use to develop their interpersonal craft and subsequent KT approach. We finish by presenting a model of sport science practitioner training; the professional sport-doctoral training programme, that combined with the framework, can be effective in developing Sport Scientists.

Context: Exercise in hot environments increases body temperature and thermoregulatory strain. However, little is known regarding the magnitude of effect that ambient temperature (Ta), relative humidity (RH), and solar radiation individually have on team-sport athletes. Purpose: To determine the effect of these individual heat-stress variables on team-sport training performance and recovery. Methods: Professional Australian Rules Football players (N = 45) undertook 8-wk preseason training producing a total of 579 outdoor field-based observations with Ta, RH, and solar radiation recorded at every training session. External load (distance covered, in m/min; percentage high-speed running [%HSR] >14.4 km/h) was collected via a global positioning system. Internal load (ratings of perceived exertion and heart rate) and recovery (subjective ratings of well-being and heart-rate variability [root mean square of the successive differences]) were monitored throughout the training period. Mixed-effects linear models analyzed relationships between variables using standardized regression coefficients. Results: Increased solar-radiation exposure was associated with reduced distance covered (−19.7 m/min, P P P = .019). Greater RH was associated with decreased %HSR (−3.4%, P = .010) but increased percentage duration >85% HRmax (3.9%, P P P = .002). In contrast, higher Ta was associated with increased distance covered (19.7 m/min, P P = .005). Conclusions: The authors show the importance of considering the individual factors contributing to thermal load in isolation for team-sport athletes and that solar radiation and RH reduce work capacity during team-sport training and have the potential to slow recovery between sessions.

Little is known about the effect of preceding endurance-exercise bouts on subsequent resistance-training (RT) performance in team-sport players. Purpose: To examine the effect of prior skills/endurance training and different recovery time periods on subsequent same-day RT performance in professional Australian football players. Methods: Sport-specific endurance-running loads (duration [in minutes], total distance [in meters], mean speed [in meters per minute], high-speed running >15 km·h−1, and relative high-speed running [>75% and >85% of maximal velocity]) were obtained for 46 professional Australian football players for each training session across an entire competitive season. RT was prescribed in 3 weekly mesocycles with tonnage (in kilograms) lifted recorded as RT performance. Endurance and RT sessions were interspersed by different recovery durations: ∼20 min and 1, 2, and 3 h. Fixed- and mixed-effect linear models assessed the influence of skills/endurance-running loads on RT performance. Models also accounted for season period (preseason vs in-season) and recovery duration between concurrent training bouts. Results: An increase in high-speed running and distance covered >75% and >85% of maximal velocity had the greatest reductions on RT performance. In-season total distance covered displayed greater negative effects on subsequent RT performance compared with preseason, while ∼20-min recovery between skills/endurance and RT was associated with greater reductions in RT performance, compared with 1-, 2-, and 3-h recovery. Conclusions: Sport-specific endurance-running loads negatively affect subsequent same-day RT performance, and this effect is greater in-season and with shorter recovery durations between bouts.

This study examined the relationship between dual-energy x-ray absorptiometry (DXA)-derived estimates of energy balance (EB) and changes in body composition across various seasonal phases in team sport athletes. Forty-five Australian rules footballers underwent six DXA scans across a 12-month period (off-season [OS, Week 0-13], early [PS1, Week 13-22] and late pre-season [PS2, Week 22-31] and early [IS1, Week 3-42] and late in-season [IS2, Week 42-51]). EB (kcal·day

Background Little is known about contrast training and post-activation performance enhancement (PAPE) in a same day concurrent training model. The aim of the current study was to examine the use of two short duration (1-min and 4-min) recovery periods on drop jump performance in same day concurrently trained athletes. Methods Ten professional Australian Rules footballers (age, 20.6 ± 1.9 yr; height, 184.8 ± 6.9 cm; body mass, 85.8 ± 8.4 kg) completed two resistance training sessions with different PAPE recovery durations; 1-min and 4-min, 1 h following a field-based endurance session. Baseline (pre) drop jumps were compared to post-test maximal drop jumps, performed after each set of three squats (where each participant was encouraged to lift as heavy as they could), to determine changes between 1-min and 4-min recovery periods. Data were analysed by fitting a mixed model (significance was set at P ≤ 0.05). Corrected Hedges’ g standardised effect sizes ±95% confidence limits were calculated using group means ± SDs. Results There were no significant differences between baseline and experimental sets 1, 2 and 3 for reactive strength index (RSI), flight time, and total and relative impulse for either recovery duration. However, for contact time, 1-min baseline was significantly different from set 2 (mean difference; 95% CI [0.029; 0.000–0.057 s], P = 0.047, ES; 95% CI [−0.27; −1.20 to 0.66]). For RSI and flight time, 1-min was significantly higher than 4-min (RSI: 0.367; 0.091 to 0.642, P = 0.010, ES; 95% CI [0.52; −0.37 to 1.42]; flight time: 0.033; 0.003 to 0.063 s, P = 0.027, ES; 95% CI [0.86; −0.06 to 1.78]). Discussion Short recovery periods of 1-min may be a time-efficient form of prescribing strength-power exercise in contrast loading schemes. Longer recovery periods do not appear to benefit immediate, subsequent performance.

O'Connor, FK, Doering, TM, Minett, GM, Reaburn, PR, Bartlett, JD and Coffey, VG. Effect of divergent solar radiation exposure with outdoor versus indoor training in the heat: implications for performance. J Strength Cond Res 36(6): 1622-1628, 2022-The aim of this study was to determine physiological and perceptual responses and performance outcomes when completing high-intensity exercise in outdoor and indoor hot environments with contrasting solar radiation exposure. Seven cyclists and 9 Australian Football League (AFL) players undertook cycling trials in hot conditions (≥30 °C) outdoors and indoors. Cyclists completed 5 × 4 minutes intervals (∼80% peak power output [PPO]) with 2 minutes recovery (∼40% PPO) before a 20-km self-paced ride. Australian Football League players completed a standardized 20 minutes warm-up (∼65% mean 4-minute power output) then 5 × 2 minutes maximal effort intervals. Heart rate (HR), PO, ratings of perceived exertion (RPE), thermal comfort (TC), and thermal sensation (TS) were recorded. Core (Tc) and skin temperature (Tsk) were monitored in cyclists alone. In both studies, ambient temperature, relative humidity, and solar radiation were monitored outdoors and matched for ambient temperature and relative humidity indoors, generating different wet bulb globe temperature (WBGT) for cyclists, but the similar WBGT for AFL players through higher relative humidity indoors. The statistical significance was set at p ≤ 0.05. Cyclists' HR (p = 0.05), Tc (p = 0.03), and Tsk (p = 0.03) were higher outdoors with variable effects for increased RPE, TS, and TC (d = 0.2-1.3). Power output during intervals was not different between trials, but there were small-moderate improvements in cyclists' PO and 20-km time indoors (d = 0.3-0.6). There was a small effect (d = 0.2) for AFL players' mean PO to increase outdoors for interval 4 alone (p = 0.04); however, overall there were small-moderate effects for lower RPE and TS indoors (d = 0.2-0.5). Indoor training in hot conditions without solar radiation may promote modest reductions in physiological strain and improve performance capacity in well-trained athletes.

Background The importance of concurrent exercise order for improving endurance and resistance adaptations remains unclear, particularly when sessions are performed a few hours apart. We investigated the effects of concurrent training (in alternate orders, separated by ~3 hours) on endurance and resistance training adaptations, compared to resistance-only training. Materials and methods Twenty-nine healthy, moderately-active men (mean ± SD; age 24.5 ± 4.7 y; body mass 74.9 ± 10.8 kg; height 179.7 ± 6.5 cm) performed either resistance-only training (RT, n = 9), or same-day concurrent training whereby high-intensity interval training was performed either 3 hours before (HIIT+RT, n = 10) or after resistance training (RT+HIIT, n = 10), for 3 d.wk-1 over 9 weeks. Training-induced changes in leg press 1-repetition maximal (1-RM) strength, countermovement jump (CMJ) performance, body composition, peak oxygen uptake ([Formula: see text]), aerobic power ([Formula: see text]), and lactate threshold ([Formula: see text]) were assessed before, and after both 5 and 9 weeks of training. Results After 9 weeks, all training groups increased leg press 1-RM (~24-28%) and total lean mass (~3-4%), with no clear differences between groups. Both concurrent groups elicited similar small-to-moderate improvements in all markers of aerobic fitness ([Formula: see text] ~8-9%; [Formula: see text] ~16-20%; [Formula: see text] ~14-15%). RT improved CMJ displacement (mean ± SD, 5.3 ± 6.3%), velocity (2.2 ± 2.7%), force (absolute: 10.1 ± 10.1%), and power (absolute: 9.8 ± 7.6%; relative: 6.0 ± 6.6%). HIIT+RT elicited comparable improvements in CMJ velocity only (2.2 ± 2.7%). Compared to RT, RT+HIIT attenuated CMJ displacement (mean difference ± 90%CI, -5.1 ± 4.3%), force (absolute: -8.2 ± 7.1%) and power (absolute: -6.0 ± 4.7%). Only RT+HIIT reduced absolute fat mass (mean ± SD, -11.0 ± 11.7%). Conclusions In moderately-active males, concurrent training, regardless of the exercise order, presents a viable strategy to improve lower-body maximal strength and total lean mass comparably to resistance-only training, whilst also improving indices of aerobic fitness. However, improvements in CMJ displacement, force, and power were attenuated when RT was performed before HIIT, and as such, exercise order may be an important consideration when designing training programs in which the goal is to improve lower-body power.

Context: Team-sport training requires the daily manipulation of intensity, duration, and frequency, with preseason training focusing on meeting the demands of in-season competition and training on maintaining fitness. Purpose: To provide information about daily training in Australian football (AF), this study aimed to quantify session intensity, duration, and intensity distribution across different stages of an entire season. Methods: Intensity (session ratings of perceived exertion; CR-10 scale) and duration were collected from 45 professional male AF players for every training session and game. Each session’s rating of perceived exertion was categorized into a corresponding intensity zone, low (Results: The distribution of the mean session intensity across the season was 29% low intensity, 57% moderate intensity, and 14% high intensity. While 96% of games were high intensity, 44% and 49% of skills training sessions were low intensity and moderate intensity, respectively. Running had the highest proportion of high-intensity training sessions (27%). Preseason displayed higher training-session intensity (effect size [ES] = 0.29–0.91) and duration (ES = 0.33–1.44), while in-season game intensity (ES = 0.31–0.51) and duration (ES = 0.51–0.82) were higher. Conclusions: By using a cost-effective monitoring tool, this study provides information about the intensity, duration, and intensity distribution of all training types across different phases of a season, thus allowing a greater understanding of the training and competition demands of Australian footballers.

Deliberately training with reduced carbohydrate (CHO) availability to enhance endurance-training-induced metabolic adaptations of skeletal muscle (i.e. the 'train low, compete high' paradigm) is a hot topic within sport nutrition. Train-low studies involve periodically training (e.g., 30-50% of training sessions) with reduced CHO availability, where train-low models include twice per day training, fasted training, post-exercise CHO restriction and 'sleep low, train low'. When compared with high CHO availability, data suggest that augmented cell signalling (73% of 11 studies), gene expression (75% of 12 studies) and training-induced increases in oxidative enzyme activity/protein content (78% of 9 studies) associated with 'train low' are especially apparent when training sessions are commenced within a specific range of muscle glycogen concentrations. Nonetheless, such muscle adaptations do not always translate to improved exercise performance (e.g. 37 and 63% of 11 studies show improvements or no change, respectively). Herein, we present our rationale for the glycogen threshold hypothesis, a window of muscle glycogen concentrations that simultaneously permits completion of required training workloads and activation of the molecular machinery regulating training adaptations. We also present the 'fuel for the work required' paradigm (representative of an amalgamation of train-low models) whereby CHO availability is adjusted in accordance with the demands of the upcoming training session(s). In order to strategically implement train-low sessions, our challenge now is to quantify the glycogen cost of habitual training sessions (so as to inform the attainment of any potential threshold) and ensure absolute training intensity is not compromised, while also creating a metabolic milieu conducive to facilitating the endurance phenotype.

Objectives: To develop three different training drill classification systems for Australian Rules football using physical and skill-related data.Methods: Forty professional Australian footballers wore 10 Hz Global Positioning System units for six matches and 17 training sessions including 35 drills. High intensity running per minute, metres per minute and high-intensity running as a percentage of total distance were obtained to represent each drill's physical requirements. Velocity at kick (moving or stationary), time in possession (greater or less than 2 s) and the presence of pressure were coded for each kick to represent the constraints associated with each drill.Results: For the first system, two k-means clustering algorithms were run on physical and skill data separately to identify similarities between drills. For the second system, z-scores were calculated for each physical and skill characteristic to allow direct comparison of each drill with match conditions. For the third system, a “Spec...

Context:Training volume, intensity, and distribution are important factors during periods of return to play.Purpose:To quantify the effect of injury on training load (TL) before and after return to play (RTP) in professional Australian Rules football.Methods:Perceived training load (RPE-TL) for 44 players was obtained for all indoor and outdoor training sessions, while field-based training was monitored via GPS (total distance, high-speed running, mean speed). When a player sustained a competition time-loss injury, weekly TL was quantified for 3 wk before and after RTP. General linear mixed models, with inference about magnitudes standardized by between-players SDs, were used to quantify effects of lower- and upper-body injury on TL compared with the team.Results:While total RPE-TL was similar to the team 2 wk before RTP, training distribution was different, whereby skills RPE-TL was likely and most likely lower for upper- and lower-body injury, respectively, and most likely replaced with small to very large increases in running and other conditioning load. Weekly total distance and high-speed running were most likely moderately to largely reduced for lower- and upper-body injury until after RTP, at which point total RPE-TL, training distribution, total distance, and high-speed running were similar to the team. Mean speed of field-based training was similar before and after RTP compared with the team.Conclusions:Despite injured athletes’ obtaining comparable TLs to uninjured players, training distribution is different until after RTP, indicating the importance of monitoring all types of training that athletes complete.

Key points Sleep restriction has previously been associated with the loss of muscle mass in both human and animal models.The rate of myofibrillar protein synthesis (MyoPS) is a key variable in regulating skeletal muscle mass and can be increased by performing high‐intensity interval exercise (HIIE), although the effect of sleep restriction on MyoPS is unknown.In the present study, we demonstrate that participants undergoing a sleep restriction protocol (five nights, with 4 h in bed each night) had lower rates of skeletal muscle MyoPS; however, rates of MyoPS were maintained at control levels by performing HIIE during this period.Our data suggest that the lower rates of MyoPS in the sleep restriction group may contribute to the detrimental effects of sleep loss on muscle mass and that HIIE may be used as an intervention to counteract these effects. Abstract The present study aimed to investigate the effect of sleep restriction, with or without high‐intensity interval exercise (HIIE), on the potential mechanisms underpinning previously‐reported sleep‐loss‐induced reductions to muscle mass. Twenty‐four healthy, young men underwent a protocol consisting of two nights of controlled baseline sleep and a five‐night intervention period. Participants were allocated into one of three parallel groups, matched for age, V˙O2peak, body mass index and habitual sleep duration; a normal sleep (NS) group [8 h time in bed (TIB) each night], a sleep restriction (SR) group (4 h TIB each night), and a sleep restriction and exercise group (SR+EX, 4 h TIB each night, with three sessions of HIIE). Deuterium oxide was ingested prior to commencing the study and muscle biopsies obtained pre‐ and post‐intervention were used to assess myofibrillar protein synthesis (MyoPS) and molecular markers of protein synthesis and degradation signalling pathways. MyoPS was lower in the SR group [fractional synthetic rate (% day–1), mean ± SD, 1.24 ± 0.21] compared to both the NS (1.53 ± 0.09) and SR+EX groups (1.61 ± 0.14) (P, Key points Sleep restriction has previously been associated with the loss of muscle mass in both human and animal models.The rate of myofibrillar protein synthesis (MyoPS) is a key variable in regulating skeletal muscle mass and can be increased by performing high‐intensity interval exercise (HIIE), although the effect of sleep restriction on MyoPS is unknown.In the present study, we demonstrate that participants undergoing a sleep restriction protocol (five nights, with 4 h in bed each night) had lower rates of skeletal muscle MyoPS; however, rates of MyoPS were maintained at control levels by performing HIIE during this period.Our data suggest that the lower rates of MyoPS in the sleep restriction group may contribute to the detrimental effects of sleep loss on muscle mass and that HIIE may be used as an intervention to counteract these effects.

Objective Sleep loss has emerged as a risk factor for the development of impaired glucose tolerance. The mechanisms underpinning this observation are unknown; however, both mitochondrial dysfunction and circadian misalignment have been proposed. Because exercise improves glucose tolerance and mitochondrial function, and alters circadian rhythms, we investigated whether exercise may counteract the effects induced by inadequate sleep. Methods To minimize between-group differences of baseline characteristics, 24 healthy young males were allocated into one of the three experimental groups: a Normal Sleep (NS) group (8 h time in bed (TIB) per night, for five nights), a Sleep Restriction (SR) group (4 h TIB per night, for five nights), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB per night, for five nights and three high-intensity interval exercise (HIIE) sessions). Glucose tolerance, mitochondrial respiratory function, sarcoplasmic protein synthesis (SarcPS), and diurnal measures of peripheral skin temperature were assessed pre- and post-intervention. Results We report that the SR group had reduced glucose tolerance post-intervention (mean change ± SD, P value, SR glucose AUC: 149 ± 115 A.U., P = 0.002), which was also associated with reductions in mitochondrial respiratory function (SR: -15.9 ± 12.4 pmol O2.s−1.mg−1, P = 0.001), a lower rate of SarcPS (FSR%/day SR: 1.11 ± 0.25%, P, Graphical abstract Image 1, Highlights • Sleep loss reduces glucose tolerance with concomitant reductions in mitochondrial function and sarcoplasmic protein synthesis. • Sleep loss leads to reductions in the amplitude of skin temperature diurnal rhythms. • These detrimental effects were not observed when performing exercise during a period of sleep loss.

Sprint capacity is an important attribute for team-sport athletes, yet the most appropriate method to analyze it is unclear. Purpose: To examine the relationship between sprint workloads using relative versus absolute thresholds and lower-body soft-tissue and bone-stress injury incidence in professional Australian rules football. Methods: Fifty-three professional Australian rules football athletes’ noncontact soft-tissue and bone-stress lower-body injuries (N = 62) were recorded, and sprint workloads were quantified over ∼18 months using the global positioning system. Sprint volume (m) and exposures (n) were determined using 2 methods: absolute (>24.9 km·h−1) and relative (≥75%, ≥80%, ≥85%, ≥90%, ≥95% of maximal velocity). Relationships between threshold methods and injury incidence were assessed using logistic generalized additive models. Incidence rate ratios and model performances’ area under the curve were reported. Results: Mean (SD) maximal velocity for the group was 31.5 (1.4), range 28.6 to 34.9 km·h−1. In comparing relative and absolute thresholds, 75% maximal velocity equated to ~1.5 km·h−1 below the absolute speed threshold, while 80% and 85% maximal velocity were 0.1 and 1.7 km·h−1 above the absolute speed threshold, respectively. Model area under the curve ranged from 0.48 to 0.61. Very low and very high cumulative sprint loads ≥80% across a 4-week period, when measured relatively, resulted in higher incidence rate ratios (2.54–3.29), than absolute thresholds (1.18–1.58). Discussion: Monitoring sprinting volume relative to an athlete’s maximal velocity should be incorporated into athlete monitoring systems. Specifically, quantifying the distance covered at >80% maximal velocity will ensure greater accuracy in determining sprint workloads and associated injury risk.

Many studies suggest that performing both endurance and resistance training within the same training program (i.e., concurrent training) can lead to sub-optimal adaptations. However, there are also contrasting and equivocal findings, which may be related to methodological differences between studies. These methodological differences include training program design (e.g., exercise frequency, intensity, volume, order, and recovery duration), as well as other considerations such as participant training status, nutrition, the study design, and statistical analyses used in the research. This chapter will summarize research that has investigated the effects of these methodological considerations on the outcome of concurrent training studies, while also highlighting gaps in the literature and areas requiring further research.

Combining RT with endurance training (i.e., concurrent training) may attenuate skeletal muscle hypertrophy consequent to RT; however, the underlying mechanisms are unclear. We investigated whether markers of ribosome biogenesis, a process linked with skeletal muscle hypertrophy, are attenuated following concurrent training vs. RT alone. Twenty-three males (mean ± SD: age, 29.6 ± 5.5 y; VO2peak, 44 ± 11 mL/kg/min) underwent 8 wk (3 sessions/wk) of either: 1) HIT (high-intensity interval training) combined with RT (HIT+RT group, n=8), 2) work-matched MICT (moderate-intensity continuous training) combined with RT (MICT+RT group, n=7), or 3) RT alone (RT group, n=8). Vastus lateralis biopsies were obtained before training, and immediately before, 1 h and 3 h after the final training session. Type I muscle fibre cross-sectional area (CSA) was further increased by RT vs. HIT+RT (34 ±22%; ES, 1.03 ±0.80), but not vs. MICT+RT (15 ±54%; ES, 0.39 ±1.45). Basal training-induced changes in expression of the 45S ribosomal RNA (rRNA) precursor, and 5.8S and 28S mature rRNAs were greater for concurrent exercise vs. RT, largely because of trends for reduced rRNA expression following RT. During the final training session, RT further increased skeletal muscle mTORC1 signalling (p70S6K1 and rps6 phosphorylation) and signalling related to 45S rRNA transcription (TIF-1A and UBF phosphorylation) vs. concurrent exercise. Thus, when performed in a training-accustomed state, RT preferentially induces mTORC1 and ribosome biogenesis-related signalling in human skeletal muscle vs. concurrent exercise. However, changes in markers of skeletal muscle ribosome biogenesis were more favourable with concurrent training vs. RT.

We aimed to compare differentiated training loads (TL) between fitness responders and non-responders to an eight-week pre-season training period in a squad of thirty-five professional rugby union players. Differential TL were calculated by multiplying player’s perceptions of breathlessness (sRPE-B) and leg muscle exertion (sRPE-L) with training duration for each completed session. Performance-based fitness measures included the Yo-Yo Intermittent Recovery Test Level 1 (YYIRTL1), 10-, 20-, and 30-m linear sprint times, countermovement jump height (CMJ) and predicted one-repetition maximum back squat (P1RM Squat). The proportion of responders (≥ 75% chance that the observed change in fitness was > typical error and smallest worthwhile change) were 37%, 50%, 52%, 82% and 70% for YYIRTL1, 20/30-m, 10-m, CMJ and P1RM Squat, respectively. Weekly sRPE-B-TL was very likely higher in YYIRTL1 responders (mean difference = 18%; ±90% confidence limits 11%), likely lower in 20/30-m (19%; ±20%) and 10-m (18%; ±17%) responders, and likely higher in CMJ responders (15%; ±16%). All other comparisons were unclear. Weekly sRPE-B discriminate between rugby union players who respond to pre-season training when compared with players who do not. Our findings support the collection of differential ratings of perceived exertion and the use of individual response analysis in team-sport athletes.

The application of guided waves for the testing of plate-type structures has been recently investigated by a number of research groups due to the ability of guided waves to detect corrosion in remote and hidden areas. Guided wave sensors for plate applications can be either directed (i.e., the waves propagate in a single direction) or omnidirectional. Each type has certain advantages and disadvantages. Omnidirectional sensors can inspect large areas from a single location, but it is challenging to define where a feature is located. Conversely, directed sensors can be used to precisely locate an indication, but have no sensitivity to flaws away from the wave propagation direction. This work describes a newly developed sensor that combines the strengths of both sensor types to create a novel omnidirectional transducer. The sensor transduction is based on a custom magnetostrictive transducer (MsT). In this new probe design, a directed, plate-application MsT with known characteristics was incorporated into an automated scanner. This scanner rotates the directed MsT for data collection at regular intervals. Coupling of the transducer to the plate is accomplished using a shear wave couplant. The array of data that is received is used for compiling B-scans and imaging, utilizing a synthetic aperture focusing algorithm (SAFT). The performance of the probe was evaluated on a 0.5-inch thick carbon steel plate mockup with a surface area of over 100 square feet. The mockup had a variety of known anomalies representing localized and distributed pitting corrosion, gradual wall thinning, and notches of different depths. Experimental data was also acquired using the new probe on a retired storage tank with known corrosion damage. The performance of the new sensor and its limitations are discussed together with general directions in technology development.

The aim of the current study was to quantify oxygen uptake, heart rate and molecular responses of human skeletal muscle associated with mitochondrial biogenesis following an acute bout of simulated soccer training. Muscle biopsies (vastus lateralis) were obtained from nine active men immediately pre-completion, post-completion and 3 h post-completion of a laboratory-based soccer-specific training simulation on a motorised treadmill. The soccer-specific simulation was a similar intensity (55 ± 6% [Formula: see text]) and duration (60 min) as that observed in professional soccer training (e.g. standing 41%, walking 37%, jogging 11%, high-speed running 9% and sprinting 2%). Post-exercise, muscle glycogen decreased (Pre; 397 ± 86 mmol∙kg(-1) dw, Post; 344 ± 64 mmol∙kg(-1) dw; P = 0.03), plasma lactate increased (P 0.001) up to ~4-5 mmol∙L(-1), non-esterified fatty acids and glycerol increased (P 0.001) to values of 0.6 ± 0.2 mmol∙L(-1) and 145 ± 54 μmol∙L(-1), respectively. PGC-1α mRNA increased (P = 0.009) fivefold 3 h post-exercise. We provide novel data by demonstrating that soccer-specific training is associated with increases in PGC-1α mRNA. These data may have implications for practitioners in better understanding the metabolic and muscle responses to soccer-specific training protocols in the field.

Sensitization of 5xxx series aluminum alloys is characterized by the gradual precipitation of the alloying element magnesium as a beta phase (Al3Mg2) along the grain boundaries after prolonged exposure to the environment. While the 5xxx alloy is corrosion resistant, these beta phases are corrosive and thus their formation increases the susceptibility of the alloy to intergranular corrosion and stress corrosion cracking. The standardized approach for measuring the degree of sensitization (DoS) is the ASTM G67 test standard. This test, however, is time consuming, difficult to perform, and destructive, as it involves measurement of a mass loss after exposing the alloy to a nitric acid solution. Given the limitations of this test standard, there is a need to develop a nondestructive evaluation (NDE) solution that is easy-to-use, non-intrusive, and faster than current inspection methods while suitable for use outside a laboratory. This paper describes the development of an NDE method for quantifying the DoS value in an alloy using ultrasonic measurements. The work builds upon prior efforts described in the literature that use electromagnetic acoustic transducers (EMATs) to quantify DoS based on velocity measurements. The prior approaches used conventional ultrasonic inspection techniques with short-duration excitation signals (less than 3 cycles) to allow identification of the echo time-of-flight and amplitude decay pattern, but their success was limited by EMAT transducer inefficiency in general, especially at higher frequencies. To overcome these challenges, this paper presents a modified ultrasonic measurement strategy using long-duration excitation signals (greater than 100 cycles), where multiple reverberations in the material overlap. By sweeping through test frequencies, it is possible to establish an acoustic resonance when the wavelength is an integer multiple of twice the material thickness. This approach allows for greatly improved signal to noise ratios as well as higher frequency operation, because the reverberations will constructively interfere at resonance. The measurement approach was evaluated on a large number of 5456-H116 aluminum alloy specimens that were sensitized to varying DoS values and compared to G67 test results. Relationships between DoS values and the ultrasonic velocity were established.

Purpose:To assess the effects of a change in training environment on the sleep characteristics of elite Australian Rules football (AF) players.Methods:In an observational crossover trial, 19 elite AF players had time in bed (TIB), total sleep time (TST), sleep efficiency (SE), and wake after sleep onset (WASO) assessed using wristwatch activity devices and subjective sleep diaries across 8-d home and camp periods. Repeated-measures ANOVA determined mean differences in sleep, training load (session rating of perceived exertion [RPE]), and environment. Pearson product–moment correlations, controlling for repeated observations on individuals, were used to assess the relationship between changes in sleep characteristics at home and camp. Cohen effect sizes (d) were calculated using individual means.Results:On camp TIB (+34 min) and WASO (+26 min) increased compared with home. However, TST was similar between home and camp, significantly reducing camp SE (–5.82%). Individually, there were strong negative correlations for TIB and WASO (r = -.75 and r = -.72, respectively) and a moderate negative correlation for SE (r = -.46) between home and relative changes on camp. Camp increased the relationship between individual s-RPE variation and TST variation compared with home (increased load r = -.367 vs .051, reduced load r = .319 vs –.033, camp vs home respectively).Conclusions:Camp compromised sleep quality due to significantly increased TIB without increased TST. Individually, AF players with higher home SE experienced greater reductions in SE on camp. Together, this emphasizes the importance of individualized interventions for elite team-sport athletes when traveling and/or changing environments.

Decision-support systems are used in team sport for a variety of purposes including evaluating individual performance and informing athlete selection. A particularly common form of decision support is the traffic-light system, where color coding is used to indicate a given status of an athlete with respect to performance or training availability. However, despite relatively widespread use, there remains a lack of standardization with respect to how traffic-light systems are operationalized. This paper addresses a range of pertinent issues for practitioners relating to the practice of traffic-light monitoring in team sports. Specifically, the types and formats of data incorporated in such systems are discussed, along with the various analysis approaches available. Considerations relating to the visualization and communication of results to key stakeholders in the team-sport environment are also presented. In order for the efficacy of traffic-light systems to be improved, future iterations should look to incorporate the recommendations made here.

© 2016 Informa UK Limited, trading as Taylor & Francis Group. ABSTRACT: Despite the perceived importance of sleep for elite footballers, descriptions of the duration and quality of sleep, especially following match play, are limited. Moreover, recovery responses following sleep loss remain unclear. Accordingly, the present study examined the subjective sleep and recovery responses of elite footballers across training days (TD) and both day and night matches (DM and NM). Sixteen top division European players from three clubs completed a subjective online questionnaire twice a day for 21 days during the season. Subjective recall of sleep variables (duration, onset latency, time of wake/sleep, wake episode duration), a range of perceptual variables related to recovery, mood, performance and internal training loads and non-exercise stressors were collected. Players reported significantly reduced sleep durations for NM compared to DM (−157 min) and TD (−181 min). In addition, sleep restfulness (SR; arbitrary scale 1 = very restful, 5 = not at all restful) and perceived recovery (PR; acute recovery and stress scale 0 = not recovered at all, 6 = fully recovered) were significantly poorer following NM than both TD (SR: +2.0, PR: −2.6), and DM (SR: +1.5; PR: −1.5). These results suggest that reduced sleep quantity and quality and reduced PR are mainly evident following NM in elite players.

Purpose:The aim of this study was to quantify and predict relationships between rating of perceived exertion (RPE) and GPS training-load (TL) variables in professional Australian football (AF) players using group and individualized modeling approaches.Methods:TL data (GPS and RPE) for 41 professional AF players were obtained over a period of 27 wk. A total of 2711 training observations were analyzed with a total of 66 ± 13 sessions/player (range 39–89). Separate generalized estimating equations (GEEs) and artificial-neural-network analyses (ANNs) were conducted to determine the ability to predict RPE from TL variables (ie, session distance, high-speed running [HSR], HSR %, m/min) on a group and individual basis.Results:Prediction error for the individualized ANN (root-mean-square error [RMSE] 1.24 ± 0.41) was lower than the group ANN (RMSE 1.42 ± 0.44), individualized GEE (RMSE 1.58 ± 0.41), and group GEE (RMSE 1.85 ± 0.49). Both the GEE and ANN models determined session distance as the most important predictor of RPE. Furthermore, importance plots generated from the ANN revealed session distance as most predictive of RPE in 36 of the 41 players, whereas HSR was predictive of RPE in just 3 players and m/min was predictive of RPE in just 2 players.Conclusions:This study demonstrates that machine learning approaches may outperform more traditional methodologies with respect to predicting athlete responses to TL. These approaches enable further individualization of load monitoring, leading to more accurate training prescription and evaluation.

Summary Sleep loss has emerged as a risk factor comparable to that of physical inactivity for the development of insulin resistance, impaired glucose tolerance and type 2 diabetes mellitus. This is a concern as it was estimated in 2012 that approximately 70 million adults in the United States are sleeping less than 6 h each night, and the average nightly sleep duration of a representative sample of the U.S. adult population is reported to be significantly less than in previous decades. The underlying mechanisms responsible for chronic sleep loss induced insulin resistance include modifications in the regulation of hormone secretion, peripheral clock gene regulation, and the cellular signaling processes associated with regulating mitochondrial respiratory function. Emerging evidence shows these mechanisms share similar biochemical signaling pathways to those underpinning exercise-induced adaptations, which together suggest exercise might be a viable, suitable, and potent treatment alternative to alleviate sleep loss induced insulin resistance and glucose intolerance. In this theoretical review, we provide a summary of the impact of reduced sleep duration and quality on mitochondrial function and insulin resistance, before detailing the possible underlying mechanisms. Finally, we propose how and why regular exercise may be a therapeutic intervention to mitigate sleep loss induced mitochondrial dysfunction and insulin resistance.

The aim of the present study was to examine the effects of ageing and training status on (1) markers of skeletal muscle mitochondrial content and (2) the ability to activate the acute signalling pathways associated with regulating exercise-induced mitochondrial biogenesis. Muscle biopsies were obtained from the vastus lateralis muscle of young untrained (24 ± 4 years, n = 6; YU), young trained (22 ± 3 years, n = 6; YT), old untrained (65 ± 6 years, n = 6; OU) and old trained (64 ± 3 years, n = 6; OT) healthy males before and after (3 h and 3 days post-exercise) completion of high-intensity interval cycling exercise. In resting muscle, lifelong training preserved mtDNA, PGC-1α and COXIV protein content such that muscles from OT individuals were comparable to muscles from both YU and YT individuals, whereas lifelong sedentary behaviour reduced such markers of mitochondrial content. Regardless of age or training status, acute exercise induced comparable increases in p38MAPK phosphorylation immediately post-exercise, PGC-1α and COXIV mRNA expression at 3 h post-exercise and COXIV protein at 3 days post-exercise. Data demonstrate that lifelong endurance training preserves skeletal muscle PGC-1α content and that despite the mitochondrial dysfunction typically observed with sedentary ageing, muscles from sedentary elderly individuals retain the capacity to activate the acute signalling pathways associated with regulating the early processes of mitochondrial biogenesis. We consider our data to have immediate translational potential as they highlight the potential therapeutic effects of exercise to induce skeletal muscle mitochondrial biogenesis persist late in adulthood, even after a lifetime of physical inactivity.

The aim of the present study was to test the hypothesis that acute high-intensity interval (HIT) running induces greater activation of signaling pathways associated with mitochondrial biogenesis compared with moderate-intensity continuous (CONT) running matched for work done. In a repeated-measures design, 10 active men performed two running protocols consisting of HIT [6 × 3-min at 90% maximal oxygen consumption (V̇o2max) interspersed with 3-min recovery periods at 50% V̇o2maxwith a 7-min warm-up and cool-down period at 70% V̇o2max] or CONT (50-min continuous running at 70% V̇o2max). Both protocols were matched, therefore, for average intensity, duration, and distance run. Muscle biopsies (vastus lateralis) were obtained preexercise, postexercise, and 3 h postexercise. Muscle glycogen decreased ( P < 0.05) similarly in HIT and CONT (116 ± 11 vs. 111 ± 17 mmol/kg dry wt, respectively). Phosphorylation (P-) of p38MAPKThr180/Tyr182(1.9 ± 0.1- vs. 1.5 ± 0.2-fold) and AMPKThr172(1.5 ± 0.3- vs. 1.5 ± 0.1-fold) increased immediately postexercise ( P < 0.05) in HIT and CONT, respectively, and returned to basal levels at 3 h postexercise. P-p53Ser15(HIT, 2.7 ± 0.8-fold; CONT, 2.1 ± 0.8-fold), PGC-1α mRNA (HIT, 4.2 ± 1.7-fold; CONT, 4.5 ± 0.9-fold) and HSP72 mRNA (HIT, 4.4 ± 2-fold; CONT, 3.5 ± 1-fold) all increased 3 h postexercise ( P < 0.05) although neither parameter increased ( P > 0.05) immediately postexercise. There was no difference between trials for any of the above signaling or gene expression responses ( P > 0.05). We provide novel data by demonstrating that acute HIT and CONT running (when matched for average intensity, duration, and work done) induces similar activation of molecular signaling pathways associated with regulation of mitochondrial biogenesis. Furthermore, this is the first report of contraction-induced p53 phosphorylation in human skeletal muscle, thus highlighting an additional pathway by which exercise may initiate mitochondrial biogenesis.

This aims of this study were to investigate the effects of carbohydrate availability during endurance training on the plasma interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α response to a subsequent acute bout of high-intensity interval exercise. Three groups of recreationally active males performed 6 weeks of high-intensity interval running. Groups 1 (LOW+GLU) and 2 (LOW+PLA) trained twice per day, 2 days per week, and consumed a 6.4% glucose or placebo solution, respectively, before every second training session and at regular intervals throughout exercise. Group 3 (NORM) trained once per day, 4 days per week, and consumed no beverage during training. Each group performed 50 min of high-intensity interval running at the same absolute workloads before and after training. Muscle glycogen utilization in the gastrocnemius muscle during acute exercise was reduced (p < 0.05) in all groups following training, although this was not affected by training condition. Plasma IL-6 concentration increased (p < 0.05) after acute exercise in all groups before and after training. Furthermore, the magnitude of increase was reduced (p < 0.05) following training. This training-induced attenuation in plasma IL-6 increase was similar among groups. Plasma IL-8 concentration increased (p < 0.05) after acute exercise in all groups, although the magnitude of increase was not affected (p > 0.05) by training. Acute exercise did not increase (p > 0.05) plasma TNF-α when undertaken before or after training. Data demonstrate that the exercise-induced increase in plasma IL-6 concentration in response to customary exercise is attenuated by previous exercise training, and that this attenuation appears to occur independent of carbohydrate availability during training.

The primary aim of the present study was to test the hypothesis that training with reduced carbohydrate availability from both endogenous and exogenous sources provides an enhanced stimulus for training-induced heat shock protein (HSP) adaptations of skeletal muscle. A secondary aim was to investigate the influence of reduced carbohydrate availability on oxidative adaptations and exercise performance. Three groups of recreationally active men performed 6 wk of high-intensity intermittent running occurring four times per week. Group 1 ( n = 8; Low + Glu) and 2 ( n = 7; Low + Pla) trained twice per day, 2 days/wk, and consumed a 6.4% glucose or placebo solution, respectively, immediately before every second training session and at regular intervals throughout exercise. Group 3 ( n = 8; Norm) trained once per day, 4 days/wk, and consumed no beverage throughout training. Training induced significant improvements in maximal oxygen uptake (V̇o2max) ( P = 0.001) and distance covered on Yo-Yo Intermittent Recovery Test 2 ( P = 0.001) in all groups, with no difference between conditions. Similarly, training resulted in significant increases in HSP70, HSP60, and αB-crystallin in the gastrocnemius ( P = 0.03, 0.02, and 0.01, respectively) and vastus lateralis ( P = 0.01, 0.02, and 0.003, respectively) muscles in all groups, with no difference between conditions. In contrast, training resulted in significant increases in succinate dehydrogenase (SDH) activity of the gastrocnemeius (Low + Glu, Low + Pla, and Norm: 27, 76, and 53% increases, respectively; P = 0.001) and vastus lateralis muscles (Low + Glu, Low + Pla, and Norm: 17, 70, and 19% increases, respectively; P = 0.001) where the magnitude of increase in SDH activity was significantly larger for both muscles ( P = 0.03 and 0.04 for gastrocnemius and vastus lateralis, respectively) for subjects training in the Low + Pla condition. Data provide the first evidence that in whole body exercise conditions, carbohydrate availability appears to have no modulating effect on training-induced increases of the HSP content of skeletal muscle. In contrast, training under conditions of reduced carbohydrate availability from both endogenous and exogenous sources provides an enhanced stimulus for inducing oxidative enzyme adaptations of skeletal muscle although this does not translate to improved performance during high-intensity exercise.

Sleep is fundamental to normal physiological and cognitive function. Sleep promotion strategies have been used extensively in clinical settings, as a treatment for various ailments (ie, insomnia). However, sleep problems are prevalent outside these realms, with 56% of American, 31% of Western European and 29% of Japanese people suffering from sleep problems the previous year. The global public health concern over sleep has increased the demand for sleep promotion interventions, but the efficacy of these strategies is unclear in otherwise healthy and athletic populations. One possibility is due to the presentation and analysis of grouped data, despite sleep naturally being a highly variable and inherent trait. We argue the case for (1) presenting sleep data at the individual level and (2) individualising sleep promotion interventions.

Purpose:Load monitoring in Australian football (AF) has been widely adopted, yet team-sport periodization strategies are relatively unknown. The authors aimed to quantify training and competition load across a season in an elite AF team, using rating of perceived exertion (RPE) and GPS tracking.Methods:Weekly totals for RPE and GPS loads (including accelerometer data; PlayerLoad) were obtained for 44 players across a full season for each training modality and for competition. General linear mixed models compared mean weekly load between 3 preseason and 4 in-season blocks. Effects were assessed with inferences about magnitudes standardized with between-players SD.Results:Total RPE load was most likely greater during preseason, where the majority of load was obtained via skills and conditioning. There was a large reduction in RPE load in the last preseason block. During in-season, half the total load came from games and the remaining half from training, predominantly skills and upper-body weights. Total distance, high-intensity running, and PlayerLoad showed large to very large reductions from preseason to in-season, whereas changes in mean speed were trivial across all blocks. All these effects were clear at the 99% level.Conclusions:These data provide useful information about targeted periods of loading and unloading across different stages of a season. The study also provides a framework for further investigation of training periodization in AF teams.

The relationships between team performance indicators and match outcome have been examined in many team sports, however are limited in Australian Rules football. Using data from the 2013 and 2014 Australian Football League (AFL) regular seasons, this study assessed the ability of commonly reported discrete team performance indicators presented in their relative form (standardised against their opposition for a given match) to explain match outcome (Win/Loss). Logistic regression and decision tree (chi-squared automatic interaction detection (CHAID)) analyses both revealed relative differences between opposing teams for "kicks" and "goal conversion" as the most influential in explaining match outcome, with two models achieving 88.3% and 89.8% classification accuracies, respectively. Models incorporating a smaller performance indicator set displayed a slightly reduced ability to explain match outcome (81.0% and 81.5% for logistic regression and CHAID, respectively). However, both were fit to 2014 data with reduced error in comparison to the full models. Despite performance similarities across the two analysis approaches, the CHAID model revealed multiple winning performance indicator profiles, thereby increasing its comparative feasibility for use in the field. Coaches and analysts may find these results useful in informing strategy and game plan development in Australian Rules football, with the development of team-specific models recommended in future.

Traditional nutritional approaches to endurance training have typically promoted high carbohydrate (CHO) availability before, during and after training sessions to ensure adequate muscle substrate to meet the demands of high daily training intensities and volumes. However, during the past decade, data from our laboratories and others have demonstrated that deliberately training in conditions of reduced CHO availability can promote training-induced adaptations of human skeletal muscle (i.e. increased maximal mitochondrial enzyme activities and/or mitochondrial content, increased rates of lipid oxidation and, in some instances, improved exercise capacity). Such data have led to the concept of ‘training low, but competing high’ whereby selected training sessions are completed in conditions of reduced CHO availability (so as to promote training adaptation), but CHO reserves are restored immediately prior to an important competition. The augmented training response observed with training-low strategies is likely regulated by enhanced activation of key cell signalling kinases (e.g. AMPK, p38MAPK), transcription factors (e.g. p53, PPARδ) and transcriptional co-activators (e.g. PGC-1α), such that a co-ordinated up-regulation of both the nuclear and mitochondrial genomes occurs. Although the optimal practical strategies to train low are not currently known, consuming additional caffeine, protein, and practising CHO mouth-rinsing before and/or during training may help to rescue the reduced training intensities that typically occur when ‘training low’, in addition to preventing protein breakdown and maintaining optimal immune function. Finally, athletes should practise ‘train-low’ workouts in conjunction with sessions undertaken with normal or high CHO availability so that their capacity to oxidise CHO is not blunted on race day.

The major tumour suppressor protein, p53, is one of the most well-studied proteins in cell biology. Often referred to as the Guardian of the Genome, the list of known functions of p53 include regulatory roles in cell cycle arrest, apoptosis, angiogenesis, DNA repair and cell senescence. More recently, p53 has been implicated as a key molecular player regulating substrate metabolism and exercise-induced mitochondrial biogenesis in skeletal muscle. In this context, the study of p53 therefore has obvious implications for both human health and performance, given that impaired mitochondrial content and function is associated with the pathology of many metabolic disorders such as ageing, type 2 diabetes, obesity and cancer, as well as reduced exercise performance. Studies on p53 knockout (KO) mice collectively demonstrate that ablation of p53 content reduces intermyofibrillar (IMF) and subsarcolemmal (SS) mitochondrial yield, reduces cytochrome c oxidase (COX) activity and peroxisome proliferator-activated receptor gamma co-activator 1-α protein content whilst also reducing mitochondrial respiration and increasing reactive oxygen species production during state 3 respiration in IMF mitochondria. Additionally, p53 KO mice exhibit marked reductions in exercise capacity (in the magnitude of 50 %) during fatiguing swimming, treadmill running and electrical stimulation protocols. p53 may regulate contractile-induced increases in mitochondrial content via modulating mitochondrial transcription factor A (Tfam) content and/or activity, given that p53 KO mice display reduced skeletal muscle mitochondrial DNA, Tfam messenger RNA and protein levels. Furthermore, upon muscle contraction, p53 is phosphorylated on serine 15 and subsequently translocates to the mitochondria where it forms a complex with Tfam to modulate expression of mitochondrial-encoded subunits of the COX complex. In human skeletal muscle, the exercise-induced phosphorylation of p53(Ser15) is enhanced in conditions of reduced carbohydrate availability in association with enhanced upstream signalling through 5'adenosine monophosphate-activated protein kinase but not p38 mitogen-activated protein kinase. In this way, undertaking regular exercise in carbohydrate restricted states may therefore be a practical approach to achieve the physiological benefits of consistent p53 signalling. Although our knowledge of p53 in exercise metabolism has advanced considerably, much of our current understanding of p53 regulation and associated targets is derived from various non-muscle cells and tissues. As such, many fundamental questions remain unanswered in contracting skeletal muscle. Detailed studies concerning the time-course of p53 activation (including additional post-translational modifications and subsequent subcellular translocation), as well as the effects of exercise modality (endurance versus resistance), intensity, duration, fibre type, age, training status and nutrient availability, must now be performed so that we can optimise exercise prescription guidelines to strategically target p53 signalling. The emerging role of p53 in skeletal muscle metabolism therefore represents a novel and exciting research area for exercise and muscle physiologists.

The mechanisms that regulate the enhanced skeletal muscle oxidative capacity observed when training with reduced carbohydrate (CHO) availability are currently unknown. The aim of the present study was to test the hypothesis that reduced CHO availability enhances p53 signaling and expression of genes associated with regulation of mitochondrial biogenesis and substrate utilization in human skeletal muscle. In a repeated-measures design, muscle biopsies (vastus lateralis) were obtained from eight active males before and after performing an acute bout of high-intensity interval running with either high (HIGH) or low CHO availability (LOW). Resting muscle glycogen (HIGH, 467 ± 19; LOW, 103 ± 9 mmol/kg dry wt) was greater in HIGH compared with LOW ( P < 0.05). Phosphorylation (P-) of ACCSer79(HIGH, 1.4 ± 0.4; LOW, 2.9 ± 0.9) and p53Ser15(HIGH, 0.9 ± 0.4; LOW, 2.6 ± 0.8) was higher in LOW immediately postexercise and 3 h postexercise, respectively ( P < 0.05). Before and 3 h postexercise, mRNA content of pyruvate dehydrogenase kinase 4, mitochondrial transcription factor A, cytochrome- c oxidase IV, and PGC-1α were greater in LOW compared with HIGH ( P < 0.05), whereas carnitine palmitoyltransferase-1 showed a trend toward significance ( P = 0.09). However, only PGC-1α expression was increased by exercise ( P < 0.05), where three-fold increases occurred independently of CHO availability. We conclude that the exercise-induced increase in p53 phosphorylation is enhanced in conditions of reduced CHO availability, which may be related to upstream signaling through AMPK. Given the emergence of p53 as a molecular regulator of mitochondrial biogenesis, such nutritional modulation of contraction-induced p53 activation has implications for both athletic and clinical populations.

The aim of the present study was to test the hypothesis that consuming protein does not attenuate AMPK signalling when exercise is commenced in a glycogen-depleted state. After performing a glycogen-depleting protocol the evening before, the subsequent morning ten active men performed 45 min steady-state cycling at 50 % of peak power output (PPO) followed by an exercise capacity test (1-min intervals at 80 % PPO interspersed with 1-min periods at 40 % PPO). In a repeated measures design, subjects consumed 20 g of a casein hydrolysate solution (PRO) 45 min before exercise, 10 g during and a further 20 g immediately post-exercise, or an equivalent volume of a non-calorie taste matched placebo (PLA). Resting (PRO = 134 ± 29; PLA = 136 ± 28 mmol kg(-1)) and post-exercise muscle glycogen (PRO = 43 ± 16; PLA = 47 ± 18 mmol kg(-1)) was not different (P0.05) between trials nor was exercise capacity (PRO = 26 ± 9; PLA = 25 ± 10 min, P0.05). Phosphorylation of AMPK(Thr172) increased threefold immediately post-exercise (P0.05) and PGC1-mRNA increased sixfold at 3 h post-exercise (P0.05), though there were no differences between conditions (P0.05). In contrast, there was a trend (P = 0.08) for a divergent response in eEF2(Thr56) phosphorylation such that 1.5 fold increases post- and 3 h post-exercise in PLA were blunted with PRO, thus indicative of greater eEF2 activation. We conclude that athletes who deliberately incorporate training phases with reduced muscle glycogen into their training programmes may consume protein before, during and after exercise without negating signalling through the AMPK cascade.

The aim of this study was to objectively quantify ratings of perceived enjoyment using the Physical Activity Enjoyment Scale following high-intensity interval running versus moderate-intensity continuous running. Eight recreationally active men performed two running protocols consisting of high-intensity interval running (6 × 3 min at 90% VO(2max) interspersed with 6 × 3 min active recovery at 50% VO(2max) with a 7-min warm-up and cool down at 70% VO(2max)) or 50 min moderate-intensity continuous running at 70% VO(2max). Ratings of perceived enjoyment after exercise were higher (P0.05) following interval running compared with continuous running (88 ± 6 vs. 61 ± 12) despite higher (P0.05) ratings of perceived exertion (14 ± 1 vs. 13 ± 1). There was no difference (P0.05) in average heart rate (88 ± 3 vs. 87 ± 3% maximum heart rate), average VO(2) (71 ± 6 vs. 73 ± 4%VO(2max)), total VO(2) (162 ± 16 vs. 166 ± 27 L) or energy expenditure (811 ± 83 vs. 832 ± 136 kcal) between protocols. The greater enjoyment associated with high-intensity interval running may be relevant for improving exercise adherence, since running is a low-cost exercise intervention requiring no exercise equipment and similar relative exercise intensities have previously induced health benefits in patient populations.

As the so-called ‘Guardian of the Genome’, p53 is one of the most well-characterised proteins in cell biology. Although most widely recognised for its role as a tumour suppressor, the list of known functions of p53 include regulatory roles in substrate metabolism, autophagy, DNA repair, cell senescence, angiogenesis and oxidative stress (Vousden & Lane, 2007). More recently, the study of p53 has revealed a potential role as a key molecular regulator of exercise-induced skeletal muscle mitochondrial biogenesis. Indeed, evidence suggestive of a role for p53 in regulating mitochondrial content and function has been provided by a number of studies employing p53 knock-out (KO) animal models. For example, Saleem et al. (2009) observed that p53 KO mice exhibit reduced subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondrial content as well as reduced cytochrome c oxidase (COX) activity and PGC-1α expression when compared with wild-type animals. Additionally, ablation of p53 also reduces state 3 respiration in IMF mitochondria and impaired exercise performance, as evidenced by an increased rate of fatigue during acute contractile activity. In this issue of The Journal of Physiology, Saleem & Hood (2013) advance our understanding of the potential role of p53 in modulating exercise-induced mitochondrial biogenesis by examining the subcellular translocation of p53 in response to an acute exercise stimulus. Wild-type and p53 KO mice were subjected to an acute bout of treadmill exercise (90 min at approximately 75%) and were sacrificed immediately post-exercise or after 3 h of recovery. The authors observed that exercise reduced the nuclear abundance of p53 (in contrast, PGC-1α showed increased nuclear translocation in accordance with previous findings) whereas p53 abundance in both the SS and IMF mitochondria significantly increased at 3 h post-exercise. This increase in mitochondrial abundance of total p53 protein content also occurred concomitantly with an increased p53Ser15 phosphorylation in the SS fraction, a modification that is associated with increased protein stability and activity. Furthermore, despite no apparent increase in mitochondrial transcription factor A (Tfam) content, it was observed that p53 forms a complex with Tfam and mitochondrial (mt) DNA (within the D-loop region) at 3 h post-exercise. When taken together, these findings suggest that p53 may preferentially function to co-ordinate regulation of the mitochondrial genome either directly or indirectly through modulation of Tfam activity. Supporting evidence for this hypothesis was also provided by the observation that the exercise-induced expression of COX-I mRNA (a mtDNA-encoded protein) was abolished in p53 KO mice compared with wild-type animals. The authors also present an intriguing hypothesis that the apparent exodus of p53 from the nucleus upon muscle contraction may be a deliberate strategy to offset any negative regulation on PGC-1α, thereby allowing the master regulator to continue its work in regulating the nuclear genome. The identification of p53 as a molecular regulator of the mitochondrial genome represents a significant development in our understanding of p53 function in skeletal muscle, one that has obvious implications for both human health and physical performance. Indeed, reduced p53 function is associated with tumour development, insulin resistance, reduced longevity and impaired exercise performance (Vousden & Lane, 2007; Saleem et al. 2009). If p53 does indeed have therapeutic potential for the exercising human, it follows that we should now increase our basic understanding of the molecular regulation of p53 activation in skeletal muscle. At present, contraction-induced post-translational modifications of p53 have been limited to the study of phosphorylation on serine 15, though as noted by the authors, there are many other potential modifications that may assist in the subcellular trafficking of nuclear and mitochondrial p53. Additionally, the upstream kinases regulating p53 activity upon muscle contraction are not currently well known. In this regard, we recently observed that AMPK (but probably not p38MAPK) may be a possible upstream signalling candidate given that exercise-induced p53Ser15 phosphorylation in human skeletal muscle (Bartlett et al. 2012) is completely attenuated when the exercise is completed with high carbohydrate availability before, during and after exercise (Bartlett et al. 2013). As such, our data suggest that there may be an initial glycogen threshold that is required to initiate p53 signalling. Such a hypothesis is particularly attractive given the widely recognised role of p53 in regulating glucose metabolism in cell lines (Vousden & Lane, 2007). Undertaking regular exercise in a carbohydrate-restricted state may therefore be an effective strategy to achieve the physiological benefits of p53 signalling, especially in relation to reduced risk of metabolic disease. Longitudinal training studies would therefore now seem warranted. At a fundamental level, however, there are also many basic questions that remain unanswered in relation to exercise-induced p53 signalling. Indeed, similar to other key molecular players (such as AMPK and PGC-1α), detailed studies concerning the time-course of p53 activation (and subsequent translocation) as well as the effects of exercise intensity and duration, fibre type, age, training status and nutrient availability now need to be performed so that we can optimise exercise prescription guidelines to strategically target p53 signalling. Additional downstream gene targets of p53 must also be identified so as to provide direct evidence for a crucial regulatory role in modulating mitochondrial biogenesis. With the integration of both animal and human exercise-related studies, it is hoped that in the coming years exercise scientists will continue to advance our understanding of how p53 may unlock the gateway to the mitochondrial genome.

Data from cycling based protocols demonstrate that high-intensity interval training (HIT) is a more efficient mode of exercise training compared with traditional moderate-intensity continuous (CONT) approaches. The use of cycling based protocols is methodologically advantageous as total work done can be quantified by measuring subject9s power output while pedalling on a cycle ergometer. However, examining the efficacy of HIT vs CONT running is more challenging as measurements of heart rate per se may not always reflect energy production. It may therefore be more accurate to prescribe, quantify and match exercise intensity during HIT and CONT running by matching protocols for average velocity corresponding to a particular %VO 2max . The aim of the current study was to develop and match laboratory-based HIT and CONT running protocols for energy expenditure, average intensity, duration and distance run. Eight recreationally active men performed two running protocols consisting of HIT (6×3 min 90% VO 2max interspersed with 6×3 min active recovery at 50% VO 2max with 7-min warm-up and cool-down at 70% VO 2max ) and CONT (50 min continuous running exercise at 70% VO 2max ). Protocols were matched for average intensity (70% VO 2max ), duration (50 min) and distance run (9843±494 m). There was no difference (p>0.05) in average heart rate (88±3% HRmax vs 87±3% HRmax), average VO 2 (71±6% VO 2max vs 73±4% VO 2max ), total VO 2 (162±16 litres vs 166±27 litres) or energy expenditure (811±83 kcal vs 832±136 kcal) between HIT and CONT protocols, respectively. Although ratings of perceived exertion were higher (p

Given that the enhanced oxidative adaptations observed when training in carbohydrate (CHO) restricted states are potentially regulated through free fatty acid (FFA) mediated signalling and that leucine rich protein elevates muscle protein synthesis, the present study aimed to test the hypothesis that leucine enriched protein feeding enhances circulating leucine concentration but does not impair FFA availability nor whole body lipid oxidation 56 during exercise. Nine males cycled for 2 h at 70% VO2peak when fasted (PLACEBO) or having consumed a whey protein solution (WHEY) or a leucine enriched whey protein gel (GEL), administered as 22 g 1 hour pre-exercise, 11 g/h during and 22 g thirty minutes post-exercise. Total leucine administration was 14.4 g and 6.3 in GEL and WHEY, respectively. Mean plasma leucine concentrations were elevated in GEL (P= 0.001) compared 60 with WHEY and PLACEBO (375 ± 100, 272 ± 51, 146 ± 14 μmol.L-1 respectively). No differences (P= 0.153) in plasma FFA (WHEY 0.53 ± 0.30, GEL 0.45 ± 0.25, PLACEBO 0.65 ± 0.30, mmol.L-1) or whole body lipid oxidation during exercise (WHEY 0.37 ± 0.26, GEL 0.36 ± 0.24, PLACEBO 0.34 ± 0.24 g/min) were apparent between trials, despite elevated (P= 0.001) insulin in WHEY and GEL compared with PLACEBO (38 ± 16, 35 ± 16, 22 ± 11 pmol.L-1 respectively). We conclude that leucine enriched protein feeding does not impair FFA availability nor whole body lipid oxidation during exercise, thus having practical applications for athletes who deliberately train in CHO restricted states to promote skeletal muscle adaptations.

Purpose We tested the hypothesis that both post-exercise and passive cold water immersion (CWI) increases PGC-1α and VEGF mRNA expression in human skeletal muscle. Method Study 1 Nine males completed an intermittent running protocol (8 × 3-min bouts at 90 % \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\dot{V}{\text{O}}_{2} \hbox{max}$$\end{document}V˙O2max, interspersed with 3-min active recovery (1.5-min at 25 % and 1.5-min at 50 % \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\dot{V}{\text{O}}_{2} \hbox{max}$$\end{document}V˙O2max) before undergoing CWI (10 min at 8 °C) or seated rest (CONT) in a counterbalanced, randomised manner. Study 2 Ten males underwent an identical CWI protocol under passive conditions. Results Study 1 PGC-1α mRNA increased in CONT (~3.4-fold; P