Purpose The aim of this study was to quantify and predict relationships between RPE and GPS training load variables in professional Australian Football (AF) players using group and individualised modelling approaches. Methods Training load data (GPS and RPE) for 41 professional AF players was obtained over a period of 27 weeks. A total of 2711 training observations were analysed with a total of 66 13 sessions per player (range; 39 to 89).Separate generalised estimating equations (GEE) and artificial neural network analyses (ANN) were conducted to determine the ability to predict RPE from training load variables (i.e. session distance, high-speed running (HSR), high-speed running %, m·min Further, importance plots generated from the ANN revealed session distance was most predictive of RPE in 36 of the 41 players, whereas, HSR was predictive of RPE in just 3 players and m . min -1 as predictive as session distance in just 2 players. Conclusions This study demonstrates that machine learning approaches may outperform more traditional methodologies with respect to predicting athlete responses to training load. These approaches enable further individualisation of load monitoring, leading to more accurate training prescription and evaluation.
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, V̇normalO2peak, 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 < 0.05). However, there were no changes in the purported regulators of protein synthesis (i.e. p‐AKTser473 and p‐mTORser2448) and degradation (i.e. Foxo1/3 mRNA and LC3 protein) in any group. These data suggest that MyoPS is acutely reduced by sleep restriction, although MyoPS can be maintained by performing HIIE. These findings may explain the sleep‐loss‐induced reductions in muscle mass previously reported and also highlight the potential therapeutic benefit of HIIE to maintain myofibrillar remodelling in this context.
Sleep quality and quantity may be compromised during training camps; however, daytime naps may be beneficial for athletes due to their known benefits, without being detrimental to nighttime sleep.
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.
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 O 2 .s −1 .mg −1 , P = 0.001), a lower rate of SarcPS (FSR%/day SR: 1.11 ± 0.25%, P < 0.001), and reduced amplitude of diurnal rhythms. These effects were not observed when incorporating three sessions of HIIE during this period (SR+EX: glucose AUC 67 ± 57, P = 0.239, mitochondrial respiratory function: 0.6 ± 11.8 pmol O 2 .s −1 .mg −1 , P = 0.997, and SarcPS (FSR%/day): 1.77 ± 0.22%, P = 0.971). Conclusions A five-night period of sleep restriction leads to reductions in mitochondrial respiratory function, SarcPS, and amplitude of skin temperature diurnal rhythms, with a concurrent reduction in glucose tolerance. We provide novel data demonstrating that these same detrimental effects are not observed when HIIE is performed during the period of sleep restriction. These data therefore provide evidence in support of the use of HIIE as an intervention to mitigate the detrimental physiological effects of sleep loss.
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.
Lee, NA, Fell, JW, Pitchford, NW, Hall, AH, Leveritt, MD, and Kitic, CM. Combined carbohydrate and protein ingestion during Australian rules football matches and training sessions does not reduce fatigue or accelerate recovery throughout a weeklong junior tournament. J Strength Cond Res 32(2): 344-355, 2018-Australian rules football (ARF) is a physically demanding sport that can induce high levels of fatigue. Fatigue may be intensified during periods where multiple matches are played with limited recovery time. Combined carbohydrate and protein (CHO + PRO) intake during physical activity may provide performance and recovery benefits. The aim of this study was to investigate whether CHO + PRO ingestion during ARF matches and training sessions throughout a tournament would enhance performance or recovery in comparison with CHO-only ingestion. Australian rules football players (n = 21) competing in a 7-day national tournament participated in this randomized and double-blinded study. Beverages containing either CHO (n = 10) or CHO + PRO (n = 11) were provided during matches (day 1, day 4, and day 7) and training sessions (day 2 and day 3). Countermovement jumps (CMJs), ratings of muscle soreness, and autonomic function were assessed throughout the tournament. Gastrointestinal tract (GI) discomfort was measured after matches. Countermovement jump peak velocity increased in the CHO + PRO group (p = 0.01) but not in the CHO group. There were no differences in the other CMJ variables. In both groups, muscle soreness increased from days 0 and 1 to day 2 (p ≤ 0.05) but did not remain elevated. R-R intervals (time elapsed between successive peaks in QRS complexes) increased in both groups from day 1 to day 7 (mean difference = 59.85 ms, p < 0.01). Postmatch GI discomfort was not different (p > 0.05) between groups. When daily dietary protein is adequate (>1.8 g·kg·d), the ingestion of CHO + PRO during matches and training sessions throughout a tournament does not reduce muscle soreness nor have clear benefits for neuromuscular recovery or modulate autonomic function in junior ARF athletes, compared with that of CHO alone.
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