This study investigated the energy intake and expenditure of professional adolescent academy-level soccer players during a competitive week. Over a seven day period that included four training days, two rest days and a match day, energy intake (self-reported weighed food diary and 24-h recall) and expenditure (tri-axial accelerometry) were recorded in 10 male players from a professional English Premier League club. The mean macronutrient composition of the dietary intake was 318 ± 24 g·day(-1) (5.6 ± 0.4 g·kg(-1) BM) carbohydrate, 86 ± 10 g·day(-1) (1.5 ± 0.2 g·kg(-1) BM) protein and 70 ± 7 g·day(-1) (1.2 ± 0.1 g·kg(-1) BM) fats, representing 55% ± 3%, 16% ± 1%, and 29% ± 2% of mean daily energy intake respectively. A mean daily energy deficit of -1302 ± 1662 kJ (p = 0.035) was observed between energy intake (9395 ± 1344 kJ) and energy expenditure (10679 ± 1026 kJ). Match days (-2278 ± 2307 kJ, p = 0.012) and heavy training days (-2114 ± 2257 kJ, p = 0.016) elicited the greatest deficits between intake and expenditure. In conclusion, the mean daily energy intake of professional adolescent academy-level soccer players was lower than the energy expended during a competitive week. The magnitudes of these deficits were greatest on match and heavy training days. These findings may have both short and long term implications on the performance and physical development of adolescent soccer players.
Taking into account the promising pharmacological actions of (Z)-2,3-bis(4-chlorophenylselanyl) prop-2-en-1-ol) (bis selenide), an organic compound containing the trace element selenium, and the constant search for drugs that improve the cognitive performance, the objective of the present study was to investigate whether bis selenide treatment ameliorates memory deficits induced by reserpine in rats. For this aim, male adult rats received a single subcutaneous injection of reserpine (1 mg/kg), a biogenic amine-depleting agent used to induce memory deficit. After 24 h, bis selenide at doses of 25 and 50 mg/kg was administered to rats by intragastric route, and 1 h later, the animals were submitted to behavior tasks. The effects of acute administration of bis selenide on memory were evaluated by social recognition, step-down passive avoidance, and object recognition paradigms. Exploratory and locomotor activities of rats were determined using the open-field test. Analysis of data revealed that the social memory disruption caused by reserpine was reversed by bis selenide at both doses. In addition, bis selenide, at the highest dose, prevented the memory deficit resulting from reserpine administration to rats in step-down passive avoidance and object recognition tasks. No significant alterations in locomotor and exploratory behaviors were found in animals treated with reserpine and/or bis selenide. Results obtained from distinct memory behavioral paradigms revealed that an acute treatment with bis selenide attenuated memory deficits induced by reserpine in rats.
Caffeine consumption around an exercise bout: effects on energy expenditure, energy intake, and exercise enjoyment
- Journal of applied physiology (Bethesda, Md. : 1985)
- Published almost 6 years ago
Combining an exercise and nutritional intervention is arguably the optimal method of creating energy imbalance for weight loss. This study sought to determine if combining exercise and caffeine supplementation was more effective for promoting acute energy deficits and manipulations to substrate metabolism than exercise alone. Fourteen recreationally-active participants (Mean ± SD BMI: 22.7 ± 2.6 kg∙m(-2)) completed a resting control trial (CON), a placebo exercise trial (EX), and a caffeine exercise trial (EX+CAF, 2x 3 mg∙kg(-1) of caffeine 90 min before and 30 min after exercise) in a randomized, double-blinded design. Trials were 4 h in duration with 1 h of rest, 1 h of cycling at ~65 % power at VO2max or rest, and a 2 h recovery. Gas exchange, appetite perceptions, and blood samples were obtained periodically. Two hours after exercise, participants were offered an ad libitum test meal where energy and macronutrient intake were recorded. EX+CAF resulted in significantly greater energy expenditure and fat oxidation compared to EX (+250 kJ; +10.4 g) and CON (+3126 kJ; +29.7 g) (P < 0.05). A trend for reduced energy and fat intake compared to CON (-718 kJ; -8 g) (P = 0.055) was observed. Consequently, EX+CAF created a greater energy deficit (P < 0.05). Caffeine also led to exercise being perceived as less difficult and more enjoyable (P < 0.05). Combining caffeine with exercise creates a greater energy deficit and the implications of this protocol for weight loss or maintenance over longer time periods in overweight/obese populations require further investigation.
The social skills deficit vulnerability model predicts that people with inadequate social skills are at risk for a range of psychosocial problems, especially when confronted with stress. People with poor social skills often experience stress and loneliness and these two constructs were tested as potential pathways by which the poor social skills confer a risk for compromised mental and physical health. An online survey was completed by 775 adults, aged 18-91. The sample matched national demographics for race/ethnicity and age, among those over 18. Structural equation modeling revealed indirect effects of social skills on both mental and physical health through both stress and loneliness. The models showed that poor social skills were associated with poor mental and physical health through elevated stress and increased loneliness. The findings reveal that social skills deficits are associated with physical as well as mental health problems.
Lonely adolescents report that they have poor social skills, but it is unknown whether this is due to an accurate perception of a social skills deficit, or a biased negative perception. This is an important distinction, as actual social skills deficits require different treatments than biased negative perceptions. In this study, we compared self-reported social skills evaluations with peer-reported social skills and meta-evaluations of social skills (i.e., adolescents' perceptions of how they believe their classmates evaluate them). Based on the social skills view, we expected negative relations between loneliness and these three forms of social skills evaluations. Based on the bias view, we expected lonely adolescents to have more negative self- and meta-evaluations compared to peer-evaluations of social skills. Participants were 1342 adolescents (48.64 % male, M age = 13.95, SD = .54). All classmates rated each other in a round-robin design to obtain peer-evaluations. Self- and meta-evaluations were obtained using self-reports. Data were analyzed using polynomial regression analyses and response surface modeling. The results indicated that, when self-, peer- and meta-evaluations were similar, a greater sense of loneliness was related to poorer social skills. Loneliness was also related to larger discrepancies between self- and peer-evaluations of loneliness, but not related to the direction of these discrepancies. Thus, for some lonely adolescents, loneliness may be related to an actual social skills deficit, whereas for others a biased negative perception of one’s own social skills or a mismatch with the environment may be related to their loneliness. This implies that different mechanisms may underlie loneliness, which has implications for interventions.
Simultanagnosia is a disorder of visual attention that leaves a patient’s world unglued: scenes and objects are perceived in a piecemeal manner. It is generally agreed that simultanagnosia is related to an impairment of attention, but it is unclear whether this impairment is object- or space-based in nature. We first consider the findings that support a concept of simultanagnosia as deficit of object-based attention. We then examine the evidence suggesting that simultanagnosia results from damage to a space-based attentional system, and in particular a model of simultanagnosia as a narrowed spatial window of attention. We ask whether seemingly object-based deficits can be explained by space-based mechanisms, and consider the evidence that object processing influences spatial deficits in this condition. Finally, we discuss limitations of a space-based attentional explanation.
A selective deficit in processing the global (overall) motion, but not form, of spatially extensive objects in the visual scene is frequently associated with several neurodevelopmental disorders, including preterm birth. Existing theories that proposed to explain the origin of this visual impairment are, however, challenged by recent research. In this review, we explore alternative hypotheses for why deficits in the processing of global motion, relative to global form, might arise. We describe recent evidence that has utilised novel tasks of global motion and global form to elucidate the underlying nature of the visual deficit reported in different neurodevelopmental disorders. We also examine the role of IQ and how the sex of an individual can influence performance on these tasks, as these are factors that are associated with performance on global motion tasks, but have not been systematically controlled for in previous studies exploring visual processing in clinical populations. Finally, we suggest that a new theoretical framework is needed for visual processing in neurodevelopmental disorders and present recommendations for future research.
. Spatial neglect is a debilitating disorder for which there is no agreed on course of rehabilitation. The lack of consensus on treatment may result from systematic differences in the syndrome’s characteristics, with spatial cognitive deficits potentially affecting perceptual-attentional “Where” or motor-intentional “ AIM: ing” spatial processing. Heterogeneity of response to treatment might be explained by different treatment impacts on these dissociated deficits: prism adaptation, for example, might reduce Aiming deficits without affecting Where spatial deficits.
All the current frailty measures count deficits. They differ chiefly in which items, and how many, they consider. These differences are related: if a measure considers only a few items, to define broad risks those items need to integrate across several systems (e.g. mobility or function). If many items are included, the cumulative effect of small deficits can be considered. Even so, it is not clear just how small deficits can be. To better understand how the scale of deficit accumulation might impact frailty measurement, we consider how age-related, subcellular deficits might become macroscopically visible and so give rise to frailty. Cellular deficits occur when subcellular damage has neither been repaired nor cleared. With greater cellular deficit accumulation, detection becomes more likely. Deficit detection can be done by either subclinical (e.g. laboratory, imaging, electrodiagnostic) or clinical methods. Not all clinically evident deficits need cross a disease threshold. The extent to which cellular deficit accumulation compromises organ function can reflect not just what is happening in that organ system, but deficit accumulation in other organ systems too. In general, frailty arises in relation to the number of organ systems in which deficits accumulate. This understanding of how subcellular deficits might scale has implications for understanding frailty as a vulnerability state. Considering the cumulative effects of many small deficits appears to allow important aspects of the behaviour of systems close to failure to be observed. It also suggests the potential to detect frailty with less reliance on clinical observation than current methods employ.
Is acute in-hospital physiotherapy with additional progressive knee-extension strength training (ST) of the fractured limb more effective in reducing knee-extension strength deficit at follow-up compared to physiotherapy without strength training in patients with a hip fracture?