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Single bouts of land-based exercise suppress appetite and do not typically alter energy intake in the short-term, whereas it has been suggested that water-based exercise may evoke orexigenic effects. The primary aim was to systematically review the available literature investigating the influence of water-based exercise on energy intake in adults (PROSPERO ID number CRD42022314349). PubMed, Medline, Sport-Discus, Academic Search Complete, CINAHL and Public Health Database were searched for peer-reviewed articles published in English from 1900 to May 2022. Included studies implemented a water-based exercise intervention versus a control or comparator. Risk of bias was assessed using the revised Cochrane 'Risk of bias tool for randomised trials' (RoB 2.0). We identified eight acute (same day) exercise studies which met the inclusion criteria. Meta-analysis was performed using a fixed effects generic inverse variance method on energy intake (8 studies (water versus control), 5 studies (water versus land) and 2 studies (water at two different temperatures)). Appetite and appetite-related hormones are also examined but high heterogeneity did not allow a meta-analysis of these outcome measures. We identified one chronic exercise training study which met the inclusion criteria with findings discussed narratively. Meta-analysis revealed that a single bout of exercise in water increased ad-libitum energy intake compared to a non-exercise control (mean difference [95% CI]: 330 [118, 542] kJ, P = 0.002). No difference in ad libitum energy intake was identified between water and land-based exercise (78 [-176, 334] kJ, P = 0.55). Exercising in cold water (18-20 °C) increased energy intake to a greater extent than neutral water (27-33 °C) temperature (719 [222, 1215] kJ; P 0.005). The one eligible 12-week study did not assess whether water-based exercise influenced energy intake but did find that cycling and swimming did not alter fasting plasma concentrations of total ghrelin, insulin, leptin or total PYY but contributed to body mass loss 87.3 (5.2) to 85.9 (5.0) kg and 88.9 (4.9) to 86.4 (4.5) kg (P 0.05) respectively. To conclude, if body mass management is a person's primary focus, they should be mindful of the tendency to eat more in the hours after a water-based exercise session, particularly when the water temperature is cold (18-20 °C).

Exercise can induce numerous health benefits that can reduce the risk of chronic diseases and all-cause mortality, yet a significant percentage of the population do not meet minimal physical activity guidelines. Several recent studies have shown that passive heating can induce numerous health benefits, many of which are comparable with exercise, such as improvements to cardiorespiratory fitness, vascular health, glycemic control, and chronic low-grade inflammation. As such, passive heating is emerging as a promising therapy for populations who cannot perform sustained exercise or display poor exercise adherence. There appears to be some overlap between the cellular signaling responses that are regulated by temperature and the mechanisms that underpin beneficial adaptations to exercise, but detailed comparisons have not yet been made. Therefore, the purpose of this mini review is to assess the similarities and distinctions between adaptations to passive heating and exercise. Understanding the potential shared mechanisms of action between passive heating and exercise may help to direct future studies to implement passive heating more effectively and identify differences between passive heating and exercise-induced adaptations.

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.

Four compounds derived from 2-aminothiazole and 2-amino-2-thiazoline were prepared by coupling the respective bases with the acid chlorides of either 3- or 4-(N,N-dimethylamino)benzoic acid. Products were identified using infrared spectroscopy, 1H NMR spectroscopy and electrospray mass spectroscopy and in two cases by single-crystal X-ray diffraction. Of the four, N-(thiazol-2-yl)-3-(N,N-dimethylamino)-benzamide (1), N-(thiazolin-2-yl)-4-(N,N-dimethylamino)benzamide (2), N-(thiazolin-2-yl)-3-(N,N-dimethylamino) benzamide (3) and N-(thiazolin-2-yl)-4-(N,N-dimethylamino)benzamide (4), the hydrochloride salts of compounds 3 and 4 showed anti-inflammatory activity across a concentration range of 10−2−5 × 10−4 M while 3 (at a concentration of 10−5 M) was found to have no adverse effect on myocardial function. The X-ray crystal structure of 2 and the 1:1 adduct structure of 3 with 3-(N,N-dimethylamino)benzoic acid are reported.

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

Oxygen delivery (DO2) calculated from cardiac output, haematocrit (Hct) and arterial oxygen saturation (SaO2), has been obtained on six subjects at sea level (London) and after slow ascent to 5000 meters (Chamlang base camp) at rest and during mild exercise (25 watts and 50 watts). Haematocrit was increased in all six subjects at 5000 m and expressed as haemoglobin (Hb) rose from a mean (+/- standard error; SEM) of 13.8 +/- 0.1 g (100 ml)(-1) to 15.8 +/-0.3 g (100 ml)(-1) (t = 6.3, p = 0.0014). SaO2 was almost constant with exercise at sea level (rest 98.5%, 25 w 98.3% and 50 w 98.3%) but declined more steeply with exercise at 5000 m (rest 88.8 +/-0.6%, 25 w 85.4 +/-0.4% and 50 w 84.4 +/- 0.5%). Arterial oxygen content (CaO2) was very similar for 25 watts exercise at altitude (5000 m, 18.1 ml per decilitre--dl) as at sea level (London, CaO2 18.2 ml dl(-1)). At rest CaO2 was higher at altitude (18.8 +/-0.2 ml dl(-1)) than at sea level (18.3 +/- 0.4 ml dl(-1)) and at 50 w CaO2 was lower at altitude (17.9 +/- 0.4 ml dl(-1)) than at sea level (18.2 +/- 0.2 ml dl(-1)). Hence, similar cardiac output values at rest (sea level, 5.0 +/- 0.4 litres min(-1) l min(-1); altitude, 5.6 +/- 0.31 min(-1)-) and at 25 w exercise (sea level, 8.2 +/-0.7 1 min(-1); altitude, 8.3 +/-0 .9 1 min'(-1) resulted in similar values for DO2 at rest (sea level, 0.9 +/-0.1 l min(-1) altitude, 1.0 +/-0.1 l min(-1) and 25 w exercise (sea level, 1.5 +/-0.1 l min(-1) altitude, 1.5 +/- 0.2 l min(-1). For 50 w exercise cardiac output and oxygen delivery were greater at altitude in one subject but were significantly reduced for the remaining five (cardiac output mean difference 3.0 +/- 0.91 min(-1), p = 0.015; DO2 mean difference, 0.56 +/- 0.21 l min(-1) p = 0.028). Acclimatization was therefore adequate to sustain a normal value for oxygen delivery for rest and 25 watts exercise (via compensatory erythropoiesis) but insufficient for 50-watt exercise in five of the six subjects.

Oxygen delivery (DO 2 ) calculated from cardiac output, haematocrit (Hct) and arterial oxygen saturation (SaO 2 ), has been obtained on six subjects at sea level (London) and after slow ascent to 5000 meters (Chamlang base camp) at rest and during mild exercise (25 watts and 50 watts). Haematocrit was increased in all six subjects at 5000 m and expressed as haemoglobin (Hb) rose from a mean (+/- standard error; SEM) of 13.8 +/-0.1 g (100 ml) -1 to 15.8 +/-0.3 g (100 ml) -1 (t = 6.3, p = 0.0014). SaO 2 was almost constant with exercise at sea level (rest 98.5%, 25 w 98.3% and 50 w 98.3%) but declined more steeply with exercise at 5000 m (rest 88.8 +/-0.6%, 25 w 85.4 +/-0.4% and 50 w 84.4 +/-0.5%). Arterial oxygen content (CaO 2 ) was very similar for 25 watts exercise at altitude (5000 m, 18.1 ml per decilitre - dl) as at sea level (London, CaO 2 18.2 ml dl -1 ). At rest CaO 2 was higher at altitude (18.8 +/-0.2 ml dl -1 ) than at sea level (18.3 +/-0.4 ml dl -1 ) and at 50 w CaO 2 was lower at altitude (17.9 +/-0.4 ml dl -1 ) than at sea level (18.2 +/-0.2 ml dl -1 ). Hence, similar cardiac output values at rest (sea level, 5.0 +/-0.4 litres min -1 l min -1 ; altitude, 5.6 +/-0.3 l min -1 ) and at 25 w exercise (sea level, 8.2 +/-0.7 l min -1 ; altitude, 8.3 +/-0.9 l min -1 ) resulted in similar values for DO 2 at rest (sea level, 0.9 +/-0.1 I min -1 ; altitude, 1.0 +/-0.1 I min -1 ) and 25 w exercise (sea level, 1.5 +/-0.1 l min -1 ; altitude, 1.5 +/-0.2 l min -1 ). For 50 w exercise cardiac output and oxygen delivery were greater at altitude in one subject but were significantly reduced for the remaining five (cardiac output mean difference 3.0 +/-0.9 1 l min -1 , p = 0.015; DO 2 mean difference, 0.56 +/-0.2 1 1 min -1 , p = 0.028). Acclimatization was therefore adequate to sustain a normal value for oxygen delivery for rest and 25 watts exercise (via compensatory erythropoiesis) but insufficient for 50―watt exercise in five of the six subjects.

Symptoms and signs of infectious disease are increased in subjects at altitude. Most infections at altitude are diagnosed clinically and do not have objective data to support the diagnosis. Since in vivo innate immune responses to hypoxia have not been thoroughly characterized, we investigated the effect of acute systemic hypocapnic hypoxia on leukocyte trafficking and neutrophil activity in healthy humans at rest.Sixteen male subjects [mean +/- SD age 28.3 +/- 6.5 yrs, body mass 80.9 +/- 15.9 kg, Vo2peak 4.10 +/- 0.76 L x min(-1)] breathed a hypoxic gas mixture (F(IO)2 = 12.2%, equivalent to 4000 m; H) or normoxic room air (F(IO)2 = 20.9%; N) for 240 min, via a mouthpiece, followed by 60 min of normal breathing.H induced a differential response in peripheral venous blood neutrophils (p0.05), lymphocytes (p0.01), and eosinophils (p0.01; 60-240 min), resulting in a relative lymphopenia (H 1.88 +/- 0.48 and N 2.14 +/- 0.45 x 10(9) L(-1)) and neutrophilia (H 5.2 +/- 1.8 and N 3.9 +/- 1.1 x 10(9) L(-1)) by 240 and 300 min, respectively. Unstimulated leukocyte oxidative activity, as determined by luminol enhanced chemiluminescence; plasma elastase, a marker of in vivo neutrophil degranulation; and sP-selectin, a marker of endothelial cell activation, did not change throughout.Differences in immune cell numbers showed a marked similarity to changes previously reported in response to intense short- and long-duration exercise and were attributed to the physiological responses induced by acute hypoxia that are known to mediate immune cell trafficking. These findings could be relevant to the etiology of conditions where hypoxia and immune cells are implicated.