This review examines the issues surrounding soccer nutrition, including the nature of the game, training, and how nutrition can play a significant role in improving player performance and recovery. In soccer match-play, a total distance covered of up to 13 km is characterised by an acyclical and intermittent activity profile. The aerobic system is highly taxed, with average heart rates of ~ 85% of maximal values, and the finite muscle glycogen stores represent a key aspect of the interface between training, performance and nutritional support. Diets with high CHO content can optimise muscle glycogen, reduce net glycogen depletion, delay the onset of fatigue, and improve soccer performance. It is more common, however, for players to consume an excessive amount of protein in their daily diet perpetuating the popular belief that additional protein increases strength and enhances performance. More comprehensive recommendations suggest that soccer players should consume a high CHO diet from nutrient-rich complex CHO food sources that ranges from a minimum of 7 to 10 g/kg BM and up to 12 g/kg BM on match or heavy training days. Unfortunately, players often have a low energy intake, which can lead to negative energy balance, especially at times of schedule congestion. In many cases, soccer players often consume diets that are not very different from those of the general public. Therefore, despite a clear understanding of the physiological demands of soccer, and the association between nutritional preparation and performance, the dietary habits of soccer players are often characterised by a lack of education and mis-informed sporting traditions. This review discusses the potential barriers and various nutritional phases that need to be considered for training, pre, on the day of, and post-match to enable players and coaches to be more aware of the need to achieve more optimal macronutrient nutrition.
Recovery from sport injuries commonly involves a muscle disuse situation (i.e., reduction in physical activity levels sometimes preceded by joint immobilization) with subsequent negative effects on muscle mass and function.
To summarize the current body of knowledge on the effectiveness of different physical strategies that are currently available to mitigate the negative effects of muscle disuse during recovery from sports injury.
A narrative review was conducted to summarize the information available on neuromuscular electrical stimulation (NMES), blood flow restriction (BFR) and vibration intervention.
The concomitant application of BFR and low-intensity exercise has shown promising results in the prevention of disuse-induced muscle atrophy. Some benefits might also be obtained with BFR alone (i.e., with no exercise), but evidence is still inconclusive. NMES, which can be applied both passively and synchronously with exercise, can also attenuate most of the negative changes associated with disuse periods. In turn, the mechanical stimulus elicited by vibration seems effective to reduce the loss of bone mineral density that accompanies muscle disuse and could also provide some benefits at the muscle tissue level.
Different physical strategies are available to attenuate disuse-induced negative consequences during recovery from injury. These interventions can be applied passively, which makes them feasible during the first stages of the recovery. However, it would be advisable to apply these strategies in conjunction with low-intensity voluntary exercise as soon as this is feasible.
Physical inactivity is the fourth leading cause of mortality worldwide; regardless of geographic location and income, it is a contributing risk factor to the other three causes. Physical activity is really a drug, a poly-pill; its “regular use” can reduce this risk throughout the activation of a plethora of responses in virtually all the body tissues. The beneficial effects of physical activity on cardiovascular function and hemodynamics are mainly mediated by skeletal muscle, adipose tissue and the immune system via the usage, delivery and distribution of metabolic substrates and improvement in inflammatory status. There is emerging evidence for exercise-dependent changes in bone metabolism as well; with improved bone quality, reduced fracture risk and increased bone endocrine function, the last of which modulates energy metabolism through its effects on pancreatic islet cells, skeletal muscle and adipose tissue. Bone endocrine function relies on the integration of biomechanical stimuli and endocrine signals from other organs and tissues. Here I review current concepts about exercise-dependent modulation of bone endocrine function and its beneficial effects on whole-body metabolism. Several molecular mechanisms have been identified that support this exercise-stimulated bone-mediated metabolic effect and, among these, Wnt signaling, fibroblast growth factor-23, bone morphogenic protein-7, osteocalcin, RANK/RANKL/OPG axis, and lipocalin-2 gave the largest evidences. In conclusion, beside the controversies surrounding technical aspects of the exercise, the efficacy of physical activity in preventing/treating metabolic and inflammatory dysfunctions also passes throughout the bone.
Passive and active stretching techniques have been shown to increase both chronic and acute range of motion (ROM). Acute ROM improvements can be countered by decreases in muscle performance, primarily after prolonged static stretching (SS) and proprioceptive neuromuscular facilitation (PNF) techniques when not incorporated into a full warm up procedure. In contrast, ballistic stretching and dynamic stretching techniques typically induce either an increase or no change in muscular force and power. This review explores studies that have investigated stretching responses on ROM, muscle functionality and performance. Collectively, the literature demonstrates that prolonged acute SS and PNF stretching can elicit the greatest changes in flexibility, but without additional dynamic activities (i.e. full warm up) can induce neuromuscular force and power output impairments, while increasing ROM and some sports specific performance. Muscle response to stretching may be determined by the manipulation of confounding variables such as duration, population, volume, test specificity and frequency. An increased dosage of some of these variables during stretching in isolation, augments ROM increases while attenuating muscle force output, except for stretching intensity which may lead to similar responses. Populations with high flexibility may have positive effects from stretching when tested on their sport specific performance, while general population may suffer greater negative effects. Not controlling these variables during stretching protocols may lead to misleading information regarding its effects on muscle performance.
To summarize current non-exercise prediction models to estimate cardiorespiratory fitness (CRF), cross-validate these models, and apply them to predict health outcomes.
PubMed search was up to August 2018 for eligible publications. The current review was comprised of three steps. The first step was to search the literature on non-exercise prediction models. The key words combined non-exercise, CRF and one among prediction, prediction model, equation, prediction equation and measurement. The second step was to search the literature about cross-validation of non-exercise equations. The key words included non-exercise, CRF and one among validation, cross-validation and validity. The last step was to search for application of CRF assessed from non-exercise equations. The key words were non-exercise, CRF, mortality, all-cause mortality, cardiovascular disease (CVD) mortality and cancer mortality.
Sixty non-exercise equations were identified. Age, gender, percent body fat, body mass index, weight, height and physical activity status were commonly used in the equations. Several researchers cross-validated non-exercise equations and proved their validity. In addition, non-exercise estimated CRF was significantly associated with all-cause mortality and fatal and nonfatal CVD.
Measurement of CRF from non-exercise models is practical and viable when exercise testing is not feasible. Despite the limitations of equations, application of CRF from non-exercise methods showed accuracy and predictive ability.
Exercise inevitably induces damages and triggers a brief inflammation in challenged tissues of the human body. Nevertheless, regular exercise is associated with improved physical fitness and lower all-cause mortality among adults in a dose-dependent manner. The paradox between destructive nature of exercise and its anti-aging benefit can be best explained by decreasing aged cell population of the human body in a Darwinian natural selection fashion, resulting in tissue renewal. In this concept, the unfit-to-fit cell ratio of a multicellular system increases during growth (expansion of cell population and size) and decreases after exercise challenges. Inflammation serves as an innate mechanism to recognize cells in danger and triggers clearance mechanism to eliminate unhealthy cells followed by regeneration. A recent finding of decreased p16INK4a+ senescent cells together with CD68+ macrophage infiltration in human skeletal muscle after resistance exercise supports this concept. The senescent cells are mostly stem cells located in capillaries surrounding myofibers, functioning to replace short-lived endothelial cells. They can be found in young men aged 20–25 years. In this context, exercise controls weight gain (i.e. cell number and size) and decrease senescent cell proportion in capillaries of the human body, providing benefits in physical fitness and increasing life expectancy.
Declines in muscle mass and function are inevitable during the aging process. However, what is the “normal age appropriate” decline of muscle mass and function? Further, is this decline uniform for muscle mass versus functions or between different functional abilities? Using recognized Sarcopenia criteria [i.e. skeletal muscle mass index (SMI) defined as appendicular skeletal muscle mass/height (kg/m2), handgrip strength, gait velocity], the aim of the present project was to determine corresponding changes in community-dwelling men 70 years+ with low SMI over a 2-year period.
One hundred and seventy-seven (177) men within the lowest SMI quartile of a recent epidemiologic study (n = 965) were included in the 2-year follow-up analysis. Muscle mass was determined via direct-segmental, multi-frequency Bio-Impedance-Analysis, handgrip strength was tested with a Jamar hand-dynamometer and habitual gait speed was assessed with photo sensors applying the 10 m protocol.
SMI, handgrip strength and gait velocity all declined significantly ( P< 0.001; effect size, d′ 0.39–1.17), however, with significantly higher reductions (P< 0.001) in functional compared with morphologic Sarcopenia criteria (P ≤ 0.006). Less expected, handgrip strength featured a fourfold higher decline compared with gait velocity (− 12.8 ± 10.9% versus − 3.5 ± 9.0%).
We provided evidence for significant non-uniform changes of Sarcopenia criteria in a cohort of community dwelling men 70 years+ with low SMI. We doubt that this result might be a particularity of the selected cohort; however, studies with other (older) cohorts should address this issue in more depth. Of practical relevance, our data further give implications for the prioritization of interventions that address Sarcopenia criteria in older community-dwelling men.
We sought to describe and examine the interrelationships between energy intake, body composition, and estimated energy balance.
Using self-reported hourly food intake and formula-based energy expenditure (EE) protocols, 19 female professional cheerleaders (mean age 25.4 years) were assessed to obtain energy balance (EB) for a typical training day. Energy intake (EI) was predicted using the USDA Food Composition Database SR27, and EE was predicted using the Harris-Benedict equation plus a MET-based relative intensity activity scale. Body composition was predicted using a multi-current, 8-mode segmental bioelectrical impedance analysis system. Hourly and daily EB was calculated from EI and EE data.
Subjects reported a 24 h EI significantly below (P < 0.001) the unadjusted predicted energy requirement (1482 kcal vs. 2199 kcal, respectively), resulting in an average negative net EB of − 720 kcal. Carbohydrate intake was significantly below the minimum recommended level (3.1 g/kg vs. 6 g/kg, P < 0.001) while protein and fat intakes met the recommended levels. Higher fat intake (g/kg) was significantly associated with a higher EI kcal/kg (r = 0.726; P < 0.001), which was significantly associated (r = − 0.55; P = 0.01) with a lower body fat percent (BF%). Using the median of BF% (20.9) as the cut point, participants with fewer hours in a negative EB had lower BF% (P = 0.043) and those with lower BF% spent more time in an EB of ± 300 kcal (P = 0.013).
These athletes reported low energy intakes that resulted in large EB deficits and/or more hours in a negative EB, which could be counterproductive for achieving a lean body composition overtime.
The aim of this study was to investigate whether skeletal muscle-derived follistatin-like 1 (FSTL1) reaches the heart and exerts the angiogenetic function in rats suffering myocardial infarctions (MI) after exercise intervention.
Forty-eight male adult Sprague–Dawley rats were randomly divided into four groups. MI was provoked by ligation of left anterior descending coronary artery. MI rats underwent adeno-associated virus injection of FST1 in tibialis anterior muscle and 4 weeks of resistance exercise via a tail-suspended incremental weight-climbing method (0–75% body weight, daily load increased by 10%; 1 h/day, 5 day/w). Heart function was evaluated by hemodynamics including LVSP, LVEDP and ± dP/dt max; the cross-sectional area of muscle cells and myocardium fibrosis were analyzed by DiI and Masson’s staining, respectively; the FSTL1 expression, endothelial cell proliferation and angiogenesis were visualized by immunofluorescence staining; and protein expression was quantified by Western blotting.
Resistance exercise reverted MI-induced skeletal muscle atrophy, increased muscle FSTL1 expression and stimulated skeletal muscle derived FSTL1 entering into the MI heart via blood circulation. The overexpression of skeletal muscle FSTL1 improved myocardial endothelial cell proliferation, increased small vessel density in the fibrotic border, inhibited myocardial fibrosis and improved heart function in the MI rats after the exercise intervention. Meanwhile, DIP2A-PI3K-Akt-mTOR, Erk1/2 and TGFβ-Smad2/3 pathways were activated in the myocardium.
Resistance exercise stimulates skeletal muscle derived FSTL1 to reach the myocardium which makes a positive contribution to cardioprotection in MI rat.
To evaluate the effects of acute moderate-intensity exercise on ecological memory, as assessed from a face-name memory task.
A two-arm, parallel-group, randomized controlled intervention was employed. Participants (N = 40; Mage = 20.8 years) were randomized into a seated control task or a bout of acute moderate-intensity treadmill exercise (15-min). Thereafter, participants completed a 3-phase face-name memory task, involving a study phase and two test phases (immediate and delayed recall, with the delay occurring 15 min after the immediate recall).
For the immediate memory recall, the mean (SD) scores for the exercise and control conditions, respectively, were 6.60 (2.5) and 6.20 (2.5). For the 15-min delayed assessment, the respective scores were 6.25 (2.6) and 5.75 (1.9). There was a significant main effect for time (F = 4.06, P = 0.05, $ \eta^{2}_{{p}} $ = 0.10). However, there were no main effects for group (F = 0.33, P = 0.56, $ \eta^{2}_{{p}} $ = 0.01) or time by group interactions (F = 0.12, P = 0.72, $ \eta^{2}_{{p}} $ = 0.003).
Despite the exercise group having slightly higher immediate and delayed face-name memory scores, we did not observe robust evidence of acute exercise enhancing face-name memory performance.