The current manuscript sets out a position stand for blood flow restriction (BFR) exercise, focusing on the methodology, application and safety of this mode of training. With the emergence of this technique and the wide variety of applications within the literature, the aim of this position stand is to set out a current research informed guide to BFR training to practitioners. This covers the use of BFR to enhance muscular strength and hypertrophy via training with resistance and aerobic exercise and preventing muscle atrophy using the technique passively. The authorship team for this article was selected from the researchers focused in BFR training research with expertise in exercise science, strength and conditioning and sports medicine.

Physical activity has been reported to improve cognitive function in humans and rodents, possibly via a brain-derived neurotrophic factor (BDNF)-regulated mechanism. In this study of human subjects, we have assessed the effects of acute and chronic exercise on performance of a face-name matching task, which recruits the hippocampus and associated structures of the medial temporal lobe, and the Stroop word-colour task, which does not, and have assessed circulating concentrations of BDNF and IGF-1 in parallel. The results show that a short period of high-intensity cycling results in enhancements in performance of the face-name matching, but not the Stroop, task. These changes in cognitive function were paralleled by increased concentration of BDNF, but not IGF-1, in the serum of exercising subjects. 3 weeks of cycling training had no effect on cardiovascular fitness, as assessed by VO2 scores, cognitive function, or serum BDNF concentration. Increases in fitness, cognitive function and serum BDNF response to acute exercise were observed following 5 weeks of aerobic training. These data indicate that both acute and chronic exercise improve medial temporal lobe function concomitant with increased concentrations of BDNF in the serum, suggesting a possible functional role for this neurotrophic factor in exercise-induced cognitive enhancement in humans.

Objectives To characterise the sleep of elite athletes and to identify factors associated with training and competition that negatively affect sleep. Design Prognosis systematic review. Data sources Three databases (PubMed, SCOPUS and SPORTDiscus) were searched from inception to 26 February 2018. Eligibility criteria for selecting studies Included studies objectively reported total sleep time (TST) and/or sleep efficiency (SE) in elite athletes. Studies were required to be observational or to include an observational trial. Results Fifty-four studies were included. During training, many studies reported athletes were unable to achieve TST (n=23/41) and/or SE (n=16/37) recommendations. On the night of competition, most studies reported athletes were unable to achieve TST (n=14/18) and/or SE (n=10/16) recommendations. TST was shorter (60 min) the night of competition compared with previous nights. SE was lower (1%) the night of competition compared with the previous night. TST was shorter the night of night competition (start ≥18:00; 80 min) and day competition (20 min) compared with the previous night. SE was lower (3%–4%) the night of night competition but unchanged the night of day competition compared with previous nights. Early morning training (start 25%), late night/early morning travel departure times, eastward air travel and altitude ascent impaired sleep. Conclusion Athletes were often unable to achieve sleep recommendations during training or competition periods. Sleep was impaired the night of competition compared with previous nights. Early morning training, increases in training load, travel departure times, jet lag and altitude can impair athletes’ sleep. PROSPERO registration number CRD42017074367.

Patients with end-stage kidney disease on dialysis have increased mortality and reduced physical activity, contributing to impaired physical function. Although exercise programs have demonstrated a positive effect on physiological outcomes such as cardiovascular function and strength, there is a reduced focus on physical function. The aim of this review was to determine whether exercise programs improve objective measures of physical function indicative of activities of daily living for patients with end-stage kidney disease on dialysis. A systematic search of Medline, Embase, the Cochrane Central Register of Controlled Trials, and Cumulative Index to Nursing and Allied Health Literature identified 27 randomized control trials. Only randomized control trials using an exercise intervention or significant muscular activation in the intervention, a usual care, nonexercising control group, and at least one objective measure of physical function were included. Participants were ≥18 yr of age, with end-stage kidney disease, undergoing hemo- or peritoneal dialysis. Systematic review of the literature and quality assessment of the included studies used the Cochrane Collaboration’s tool for assessing risk bias. A meta-analysis was completed for the 6-min walk test. Data from 27 studies with 1,156 participants showed that exercise, regardless of modality, generally increased 6-min walk test distance, sit-to-stand time or repetitions, and grip strength as well as step and stair climb times or repetitions, dynamic mobility, and short physical performance battery scores. From the evidence available, exercise, regardless of modality, improved objective measures of physical function for end-stage kidney disease patients undergoing dialysis. It is acknowledged that further well-designed randomized control trials are required.

Six men were studied during four 30-s “all-out” exercise bouts on an air-braked cycle ergometer. The first three exercise bouts were separated by 4 min of passive recovery; after the third bout, subjects rested for 4 min, exercised for 30 min at 30–35% peak O₂ consumption, and rested for a further 60 min before completing the fourth exercise bout. Peak power and total work were reduced ( P < 0.05) during bout 3 [765 ± 60 (SE) W; 15.8 ± 1.0 kJ] compared with bout 1 (1,168 ± 55 W, 23.8 ± 1.2 kJ), but no difference in exercise performance was observed between bouts 1 and 4 (1,094 ± 64 W, 23.2 ± 1.4 kJ). Before bout 3, muscle ATP, creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR) Ca²⁺ uptake were reduced, while muscle lactate and inosine 5′-monophosphate were increased. Muscle ATP and glycogen before bout 4 remained lower than values before bout 1( P < 0.05), but there were no differences in muscle inosine 5′-monophosphate, lactate, pH, and SR Ca²⁺ uptake. Muscle CP levels before bout 4 had increased above resting levels. Consistent with the decline in muscle ATP were increases in hypoxanthine and inosine before bouts 3 and 4. The decline in exercise performance does not appear to be related to a reduction in muscle glycogen. Instead, it may be caused by reduced CP availability, increased H⁺ concentration, impairment in SR function, or some other fatigue-inducing agent.