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The aim of this study was to determine the sensitivity of selected subjective and objective monitoring assessments in detecting changes in group and individual responses to low and high load bouts of high intensity intermittent exercise. In a counterbalanced crossover design, Thirteen Academy Rugby Union players (mean &plusmn, SD: age: 18 &plusmn, 1 years) performed a low load (15 min) and a high load (90 min) bout of high intensity intermittent exercise (Loughborough Intermittent Shuttle Test) one week apart. Monitoring assessments were performed immediately prior to and 20 h following each trial. Subjective self-report Well-being Questionnaire (WQ) items showed small to large deteriorations following the high load compared to low load (d = 0.4&ndash, 1.5, p = 0.03&ndash, 0.57). A very large increase in resting HR (HRrest) (d = 2.1, p = 0.02), moderate decrease in heart rate variability (HRV) indices (d = 0.7, p = 0.04 and d = 0.7, p = 0.01 for the natural logarithm of the standard deviation of R-R intervals (ln SDNN) and the root square of the mean squared differences of successive R-R intervals (rMSSD), respectively) and no change in countermovement jump (d = 0.0, p = 0.97) were evident following the high load compared to low load. Individual WQ responses revealed 7/9, 7/9, 6/9, 6/9, 5/9, 3/9 and 1/9 participants reported deteriorations in recovery, sleep quality, motivation, muscle soreness, fatigue, stress and appetite, respectively, following the high load compared to low load. Individual analysis indicated a negative response following the high load compared to low load in HRrest, ln SDNN and ln rMSSD for 4/6, 2/6 and 1/6 participants, respectively. Selected WQ items detected group and individual responses to high load and low load highlighting their potential utility. However, objective assessments lacked the sensitivity to detect small individual changes.

The 2011 English Elite Player Performance Plan (EPPP) stipulates training volumes that could put elite youth players at high risk of non-functional overreaching. The aim of the study was to assess player perceptions of well-being and physical performance to these high training loads. Fourteen academy football players (mean ± SD: age 17 ± 1 years; stature 179 ± 6 cm; body mass 70.8 ± 8.6 kg, at pre-season) completed a perception of well-being questionnaire 1-4 times per week throughout each training block (pre-season, in-season 1, 2, 3). Physical performance tests were carried out at the end of each training block. Increases in training exposure (P0.05; [Formula: see text] = 0.52) and moderate to large deteriorations in perceptions of well-being (motivation, sleep quality, recovery, appetite, fatigue, stress, muscle soreness P0.05; [Formula: see text] = 0.30-0.53) were evident as the season progressed. A moderate decrease in 30 m sprint performance (P0.05; [Formula: see text] = 0.48), a large improvement in Yo-Yo intermittent recovery test performance (P0.05; [Formula: see text] = 0.93) and small decreases in countermovement jump (P0.05; [Formula: see text] = 0.18) and arrowhead agility (P0.05; [Formula: see text] = 0.24) performance were evident as the season progressed. The present findings show an imbalance between stress and recovery in English elite youth players even when players experience lower training exposure than stipulated by the EPPP.

Motion sickness is common within many forms of transport; it affects most of the population who experience some symptoms at some time. Automated vehicles (AV) offer productivity benefits but also increased incidence of motion sickness. There are mitigation methods with varying degrees of effectiveness to combating motion sickness. Bone conductive vibration (BCV) applied to the head is a proven motion sickness mitigation. It is not known if the level of vibration is important. Twenty-nine participants were subjected to normal urban driving whilst undertaking a 'gaze down' non-driving related task (NDRT) within an AV cabin whilst wearing the BCV device. High and low vibration settings were randomly chosen as were the seating positions in a between participants design. Twenty-five participants successfully completed the experiment. It was found that when the device is applied to the head, the time to nausea increased by up to a factor of 1.6 when set to high over low settings for highly susceptible participants. BCV did not improve task performance.

Prolonged, exhaustive exercise frequently leads to an increased incidence of upper respiratory tract illness (URTI) which is linked to transient immunodepression. We investigated potential biochemical markers of stress and fatigue, and URTI symptoms as a surrogate of immunodepression, in US Marines undergoing intensive winter training at altitude. Selected plasma amino acids and leptin (p[Lep]) were measured as possible markers of fatigue and immunodepression, together with nonesterified fatty acids (p[NEFA]) and total antioxidant capacity (p[TAC]). Changes were observed in plasma free tryptophan (p[FT]), p[Gln], p[Lep], p[NEFA], p[TAC] but not branched chain amino acids (p[BCAA]). p[FT] decreased markedly. Resting p[Gln] decreased overall after one month at altitude. p[Gln] routinely decreases 1-2 hrs after prolonged exercise. Importantly, we observed early morning decreases in p[Gln], suggesting a cumulative effect of prolonged activity, stress, and fatigue. Concomitantly, individuals with highest illness scores had the greatest p[Gln] decrease: low p[Gln] may therefore be associated with a diminished stress tolerance.

Background The aims of this study were to describe the cellular stress response to prolonged endurance exercise in acute heat, hypoxia and the combination of heat and hypoxia and to determine whether prior acute exposure to these stressors improved cellular tolerance to a subsequent exercise bout in hypoxia 24 h later. Methods Twelve males (age 22 ± 4 years, height 1.77 ± 0.05 m, mass 79 ± 12.9 kg, VO2 max 3.57 ± 0.7 L · min-1) completed four trials (30-min rest, 90-min cycling at 50% normoxic VO2 max) in normothermic normoxia (NORM; 18°C, FIO2 = 0.21), heat (HEAT; 40°C, 20% RH), hypoxia (HYP; FIO2 = 0.14) or a combination of heat and hypoxia (COM; 40°C, 20% RH, FIO2 = 0.14) separated by at least 7 days. Twenty-four hours after each trial, participants completed a hypoxic stress test (HST; 15-min rest, 60-min cycling at 50% normoxic VO2 max, FIO2 = 0.14). Monocyte heat shock protein 72 (mHSP72) was assessed immediately before and after each exercise bout. Results mHSP72 increased post exercise in NORM (107% ± 5.5%, p > 0.05), HYP (126% ± 16%, p