The aim of this international study was to investigate the prevalence of the use of sports supplements among young athletes, as well as their knowledge and attitudes towards sports supplementation. Organized survey study testing the level of knowledge, attitudes, beliefs and practices concerning the use of sports supplements was administered to 348 athletes, 15–18 year olds from 4 countries competing in 18 sports at the international level. The prevalence rate of the intake of sports supplements was 82.2%, with the protein supplements being predominant (54.5%). Coaches were identified as the primary source of information regarding supplementation (41.4%). The enhancement of athletic performance (35.4%) was the major motivation for the supplements intake. The majority of athletes (72.1%) were aware of associated health risks. The young athletes possess varying levels of knowledge regarding their own supplementation. The obtained data about the level of knowledge were statistically analyzed using the correspondence analysis. Less than 40% of athletes had the knowledge about the proper and intended use of protein, creatine, amino acids, beta alanine and glutamine, while they had greater understanding about vitamins and minerals, sports drinks and caffeine. The athletes in developed countries had greater access and utilization of professional resources such as dieticians. Young athletes are still unfamiliar with WADA regulations (55.5%), and the misuse of sports supplements represents an ethical dilemma for some. These findings indicate the necessity of a comprehensive education of all team members about sports supplements and careful supervision of the athletic development of young athletes.

Molecular oxygen (O₂) is a vital element in human survival and plays a major role in a diverse range of biological and physiological processes. Although normobaric hyperoxia can increase arterial oxygen content ([ ]), it also causes vasoconstriction and hence reduces O₂delivery in various vascular beds, including the heart, skeletal muscle, and brain. Thus, a seemingly paradoxical situation exists in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Nevertheless, with various degrees of effectiveness, and not without consequences, supplemental oxygen is used clinically in an attempt to correct tissue hypoxia (e.g., brain ischemia, traumatic brain injury, carbon monoxide poisoning, etc.) and chronic hypoxemia (e.g., severe COPD, etc.) and to help with wound healing, necrosis, or reperfusion injuries (e.g., compromised grafts). Hyperoxia has also been used liberally by athletes in a belief that it offers performance-enhancing benefits; such benefits also extend to hypoxemic patients both at rest and during rehabilitation. This review aims to provide a comprehensive overview of the effects of hyperoxia in humans from the “bench to bedside.” The first section will focus on the basic physiological principles of partial pressure of arterial O₂, [ ], and barometric pressure and how these changes lead to variation in regional O₂delivery. This review provides an overview of the evidence for and against the use of hyperoxia as an aid to enhance physical performance. The final section addresses pathophysiological concepts, clinical studies, and implications for therapy. The potential of O₂toxicity and future research directions are also considered.

Decompression sickness (DCS) is a systemic disorder, assumed due to gas bubbles, but additional factors are likely to play a role. Circulating microparticles (MPs)—vesicular structures with diameters of 0.1-1.0 μm—have been implicated, but data in human divers have been lacking. We hypothesized that the number of blood-borne, Annexin V-positive MPs and neutrophil activation, assessed as surface MPO staining, would differ between self-contained underwater breathing-apparatus divers suffering from DCS vs. asymptomatic divers. Blood was analyzed from 280 divers who had been exposed to maximum depths from 7 to 105 meters; 185 were control/asymptomatic divers, and 90 were diagnosed with DCS. Elevations of MPs and neutrophil activation occurred in all divers but normalized within 24 h in those who were asymptomatic. MPs, bearing the following proteins: CD66b, CD41, CD31, CD142, CD235, and von Willebrand factor, were between 2.4- and 11.7-fold higher in blood from divers with DCS vs. asymptomatic divers, matched for time of sample acquisition, maximum diving depth, and breathing gas. Multiple logistic regression analysis documented significant associations (P < 0.001) between DCS and MPs and for neutrophil MPO staining. Effect estimates were not altered by gender, body mass index, use of nonsteroidal anti-inflammatory agents, or emergency oxygen treatment and were modestly influenced by divers' age, choice of breathing gas during diving, maximum diving depth, and whether repetitive diving had been performed. There were no significant associations between DCS and number of MPs without surface proteins listed above. We conclude that MP production and neutrophil activation exhibit strong associations with DCS.

Ciplines and to compare them in relation to specific demands of each sport. Wingate anaerobic tests were conducted on 145 elite athletes (14 boxers, 17 wrestlers, 27 hockey players, 23 volleyball players, 20 handball players, 25 basketball players, and 19 soccer players). Three variables were measured as markers of anaerobic capacity: peak power, mean power, and explosive power. The highest values of peak power were measured in volleyball 11.71 ± 1.56 W·kg−1 and basketball players 10.69 ± 1.67 W·kg−1, and the difference was significant compared with the other athletes (p ≤ 0.05). The lowest value of peak power (8.58 ± 1.56 W·kg−1) was registered in handball players. The mean power variable showed a similar distribution as peak power among groups. The highest values of explosive power were also registered in volleyball 1.75 ± 0.33 W·s−1·kg−1 and basketball players 1.64 ± 0.35 W·s−1·kg−1, but there was no significant difference in values between volleyball players and wrestlers, between boxers and wrestlers, between boxers and basketball players, and between volleyball and hockey players (p > 0.05). The measured results show the influence of anaerobic capacity in different sports and the referral values of these variables for the elite male athletes. Explosive power presented a new dimension of anaerobic power, i.e., how fast maximal energy for power development can be obtained, and its values are high in all sports activities that demand explosiveness and fast maximal energy production. Coaches or other experts in the field could, in the future, find useful to follow and improve, through training process, one of the variables that is most informative for that sport....

To evaluate the connection between menstrual disorders and body fat mass, we examined a group of 30 ballet dancers and a group of 30 non-athletic girls (controls). Body mass index (BMI) was calculated and percent body fat (FAT%) was measured using the bioelectrical impedance method. A questionnaire was used to obtain age at menarche and duration of menstrual cycles. Ballet dancers had significantly lower values of BMI (18.56 +/- 1.53 vs. 19.96 +/- 2.12 kg/m2) and FAT% (18.85 +/- 4.50 vs. 23.41 +/- 4.34%) compared with controls. According to BMI, 50.0% of ballet dancers and 23.3% of the control group were underweight. Of underweight ballet dancers, 66.7% had lower values of body fat, while most underweight girls from the control group had normal body fat. Normal-weight obesity was registered in 40.9% of the control group and in 6.7% of ballet dancers. Amenorrhea was found in 20.0% and oligomenorrhea in 10.0% of ballet dancers. Ballet dancers more frequently had later appearance of menarche and menstrual cycles of longer duration than did non-athletic girls. A significant negative correlation was found between menstrual cycle duration and FAT% among ballet dancers (r = -0.415). To prevent complications caused by changes of body fat mass, we conclude that body composition assessment in ballet dancers is very important.

Key points: The present study describes the cerebral oxidative and non‐oxidative metabolism in man during a prolonged apnoea (ranging from 3 min 36 s to 7 min 26 s) that generates extremely low levels of blood oxygen and high levels of carbon dioxide. The cerebral oxidative metabolism, measured from the product of cerebral blood flow and the radial artery‐jugular venous oxygen content difference, was reduced by ∼29% at the termination of apnoea, although there was no change in the non‐oxidative metabolism. A subset study with mild and severe hypercapnic breathing at the same level of hypoxia suggests that hypercapnia can partly explain the cerebral metabolic reduction near the apnoea breakpoint. A hypercapnia‐induced oxygen‐conserving response may protect the brain against severe oxygen deprivation associated with prolonged apnoea. Prolonged apnoea in humans is reflected in progressive hypoxaemia and hypercapnia. In the present study, we explore the cerebral metabolic responses under extreme hypoxia and hypercapnia associated with prolonged apnoea. We hypothesized that the cerebral metabolic rate for oxygen (CMRO₂) will be reduced near the termination of apnoea, attributed in part to the hypercapnia. Fourteen elite apnoea‐divers performed a maximal apnoea (range 3 min 36 s to 7 min 26 s) under dry laboratory conditions. In a subset study with the same divers, the impact of hypercapnia on cerebral metabolism was determined using varying levels of hypercapnic breathing, against the background of similar hypoxia. In both studies, the CMRO₂ was calculated from the product of cerebral blood flow (ultrasound) and the radial artery‐internal jugular venous oxygen content difference. Non‐oxidative cerebral metabolism was calculated from the ratio of oxygen and carbohydrate (lactate and glucose) metabolism. The CMRO₂ was reduced by ∼29% (P < 0.01, Cohen's d = 1.18) near the termination of apnoea compared to baseline, although non‐oxidative metabolism remained unaltered. In the subset study, in similar backgrounds of hypoxia (arterial O₂ tension: ∼38.4 mmHg), severe hypercapnia (arterial CO₂ tension: ∼58.7 mmHg), but not mild‐hypercapnia (arterial CO₂ tension: ∼46.3 mmHg), depressed the CMRO₂ (∼17%, P = 0.04, Cohen's d = 0.87). Similarly to the apnoea, there was no change in the non‐oxidative metabolism. These data indicate that hypercapnia can partly explain the reduction in CMRO₂ near the apnoea breakpoint. This hypercapnic‐induced oxygen conservation may protect the brain against severe hypoxaemia associated with prolonged apnoea.