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Phosphate is integral to numerous metabolic processes, several of which strongly predict exercise performance (i.e., cardiac function, oxygen transport, and oxidative metabolism). Evidence regarding phosphate loading is limited and equivocal, at least partly because studies have examined sodium phosphate supplements of varied molar mass (e.g., mono/di/tribasic, dodecahydrate), thus delivering highly variable absolute quantities of phosphate. Within a randomized cross-over design and in a single-blind manner, 16 well-trained cyclists (age 38 ± 16 years, mass 74.3 ± 10.8 kg, training 340 ± 171 min/week; mean ± SD) ingested either 3.5 g/day of dibasic sodium phosphate (Na₂HPO₄: 24.7 mmol/day phosphate; 49.4 mmol/day sodium) or a sodium chloride placebo (NaCl: 49.4 mmol/day sodium and chloride) for 4 days prior to each of two 30-km time trials, separated by a washout interval of 14 days. There was no evidence of any ergogenic benefit associated with phosphate loading. Time to complete the 30-km time trial did not differ following ingestion of sodium phosphate and sodium chloride (3,059 ± 531 s vs. 2,995 ± 467 s). Accordingly, neither absolute mean power output (221 ± 48 W vs. 226 ± 48 W) nor relative mean power output (3.02 ± 0.78 W/kg vs. 3.08 ± 0.71 W/kg) differed meaningfully between the respective intervention and placebo conditions. Measures of cardiovascular strain and ratings of perceived exertion were very closely matched between treatments (i.e., average heart rate 161 ± 11 beats per minute vs. 159 ± 12 beats per minute; Δ2 beats per minute; and ratings of perceived exertion 18 [14–20] units vs. 17 [14–20] units). In conclusion, supplementing with relatively high absolute doses of phosphate (i.e., >10 mmol daily for 4 days) exerted no ergogenic effects on trained cyclists completing 30-km time trials.

The aim of this study was to examine the effect of delayed evening mealtime on sleep quality in young athletes. Twelve rugby players (age 15.8 ± 0.7 years) participated in a crossover within-participant design. Adolescents spent five consecutive days in each of two conditions, separated by a 2-week washout period: routine dinner (3.5 hr before bedtime) and late dinner (LD, 1.5 hr before bedtime). Other mealtimes as well as bedtime and wake-up time were usual and remained the same in both conditions. Their schedules, dietary intakes, and physical activity were controlled and kept constant throughout the study. Sleep was assessed using polysomnography on the first and the last nights in the individual rooms of the boarding school. An increase in total sleep time by 24 min (p = .001, d = 1.24) and sleep efficiency by 4.8% was obtained during LD (p = .001, d = 1.24). Improvement in sleep efficiency was mainly due to a lower wake after sleep onset (−25 min, p = .014, d = −3.20), a decrease of microarousals (−25%, p = .049, d = −0.64), and awakenings ≥90 s (−30%, p < .01, d = −0.97) in LD compared to routine dinner. There were no significant differences in sleep architecture except for a shorter slow-wave sleep (N3) latency (−6.9 min, p = .03, d = −0.778) obtained during LD. In this study, evening dinner 1.5 hr before bedtime leads to better quality and less fragmented sleep compared to evening dinner 3.5 hr before bedtime in young athletes.

The relationship between inflammatory markers and bone turnover in adults is well known, and a negative association between cardiorespiratory fitness (CRF) and inflammatory markers has also been described. Hence, we tested whether the association between CRF and bone turnover markers is mediated by inflammatory markers in adults with metabolic syndrome. A total of 81 adults (58.5 ± 5.0 years, 62.7% women) were included in the analysis. CRF was measured by the 6-min walking test. Serum interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor alpha, high-sensitivity c-reactive protein (hsCRP) and vascular endothelial growth factor, collagen type I cross-linked C-telopeptide, procollagen type I N-terminal propeptide (P1NP), and total osteocalcin were assessed using a sensitive ELISA kit. Body composition was assessed by dual-energy X-ray absorptiometry. Partial correlation was used to test the relationship between CRF, inflammatory markers, and bone turnover markers, controlling for sex, lean mass, and fat mass. Boot-strapped mediation procedures were performed, and indirect effects with confidence intervals not including zero were interpreted as statistically significant. CRF was positively correlated with P1NP levels (r = .228, p = .044) and osteocalcin levels (r = .296, p = .009). Furthermore, CRF was positively correlated with IL-1β levels (r = .340, p = .002) and negatively correlated with hsCRP levels (r = −.335, p = .003), whereas IL-1β levels were positively correlated with P1NP levels (r = .245, p = .030), and hsCRP levels were negatively correlated with P1NP levels (r = −.319, p = .004). Finally, the association between CRF and P1NP levels was totally mediated by hsCRP (percentage of mediation = 39.9). Therefore, CRF benefits on bone formation could be dependent on hsCRP concentrations in this population.

Dual-energy X-ray absorptiometry (DXA) is a popular technique used to quantify physique in athletic populations. Due to biological variation, DXA precision error (PE) may be higher than desired. Adherence to standardized presentation for testing has shown improvement in consecutive-day PE. However, the impact of short-term diet and physical activity standardization prior to testing has not been explored. This warrants investigation, given the process may reduce variance in total body water and muscle solute, both of which can have high daily flux amongst athletes. Twenty (n = 10 males, n = 10 females) recreationally active individuals (age: 30.7 ± 7.5 years; stature: 176.4 ± 9.1 cm; mass: 74.6 ± 14.3 kg) underwent three DXA scans; two consecutive scans on 1 day, and a third either the day before or after. In addition to adhering to standardized presentation for testing, subjects recorded all food/fluid intake plus activity undertaken in the 24 hr prior to the first DXA scan and replicated this the following 24 hr. International Society of Clinical Densitometry recommended techniques were used to calculate same- and consecutive-day PE. There was no significant difference in PE of whole-body fat mass (479 g vs. 626 g) and lean mass (634 g vs. 734 g) between same- and consecutive-day assessments. Same- and consecutive-day PE of whole-body fat mass and lean mass were less than the smallest effect size of interest. Inclusion of 24-hr standardization of diet and physical activity has the potential to reduce biological error further, but this needs to be verified with follow-up investigation.

The aim of this systematic review was to examine the effects of physical exercise training on cerebral blood flow (CBF), which is a physiological marker of cerebrovascular function. Relationships between training-induced effects on CBF with changes in cognitive performance were also discussed. A systematic search was performed up to July 2022. Forty-five intervention studies with experimental, quasi-experimental, or pre–post designs were included. Sixteen studies (median duration: 14 weeks) investigated effects of physical exercise training on CBF markers using magnetic resonance imaging, 20 studies (median duration: 14 weeks) used transcranial Doppler ultrasound, and eight studies (median duration: 8 weeks) used near-infrared spectroscopy. Studies using magnetic resonance imaging observed consistent increases in CBF in the anterior cingulate cortex and hippocampus, but not in whole-brain CBF. Effects on resting CBF—measured with transcranial Doppler ultrasound and near-infrared spectroscopy—were variable, while middle cerebral artery blood flow velocity increased in some studies following exercise or hypercapnic stimuli. Interestingly, concomitant changes in physical fitness and regional CBF were observed, while a relation between training-induced effects on CBF and cognitive performance was evident. In conclusion, exercise training improved cerebrovascular function because regional CBF was changed. Studies are however still needed to establish whether exercise-induced improvements in CBF are sustained over longer periods of time and underlie the observed beneficial effects on cognitive performance.