International journal of sport nutrition and exercise metabolism最新文献

Deuterium oxide (D2O) appearance in blood is a marker of fluid bioavailability. However, whether biomarker robustness (e.g., relative fluid delivery speed) is consistent across analytical methods (e.g., cavity ring-down spectroscopy) remains unclear. Fourteen men ingested fluid (6 ml/kg body mass) containing 0.15 g/kg D2O followed by 45 min blood sampling. Plasma (D2O) was detected (n = 8) by the following: isotope-ratio mass spectrometry after vapor equilibration (IRMS-equilibrated water) or distillation (IRMS-plasma) and cavity ring-down spectroscopy. Two models calculated D2O halftime to peak (t1/2max): sigmoid curve fit versus asymmetric triangle (TRI). Background (D2O) differed (p < .001, η2 = .98) among IRMS-equilibrated water, IRMS-plasma, and cavity ring-down spectroscopy (152.2 ± 0.8, 147.2 ± 1.5, and 137.7 ± 2.2 ppm), but did not influence (p > .05) D2O appearance (Δppm), time to peak, or t1/2max. Stratifying participants based on mean t1/2max (12 min) into "slow" versus "fast" subgroups resulted in a 5.8 min difference (p < .001, η2 = .73). Significant t1/2max model (p = .01, η2 = .44) and Model × Speed Subgroup interaction (p = .005, η2 = .50) effects were observed. Bias between TRI and sigmoid curve fit increased with t1/2max speed: no difference (p = .75) for fast (9.0 min vs. 9.2 min, respectively) but greater t1/2max (p = .001) with TRI for the slow subgroup (16.1 min vs. 13.7 min). Fluid bioavailability markers are less influenced by which laboratory method is used to measure D2O as compared with the individual variability effects that influence models for calculating t1/2max. Thus, TRI model may not be appropriate for individuals with slow fluid delivery speeds.

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.

Carnosine (β-alanyl-L-histidine) and its methylated analogues anserine and balenine are highly concentrated endogenous dipeptides in mammalian skeletal muscle that are implicated in exercise performance. Balenine has a much better bioavailability and stability in human circulation upon acute ingestion, compared to carnosine and anserine. Therefore, ergogenic effects observed with acute carnosine and anserine supplementation may be even more pronounced with balenine. This study investigated whether acute balenine supplementation improves physical performance in four maximal and submaximal exercise modalities. A total of 20 healthy, active volunteers (14 males; six females) performed cycling sprints, maximal isometric contractions, a 4-km TT and 20-km TT following either preexercise placebo or 10 mg/kg of balenine ingestion. Physical, as well as mental performance, along with acid-base balance and glucose concentration were assessed. Balenine was unable to augment peak power (p = .3553), peak torque (p = .3169), time to complete the 4 km (p = .8566), nor 20 km time trial (p = .2660). None of the performances were correlated with plasma balenine or CN1 enzyme activity. In addition, no effect on pH, bicarbonate, and lactate was observed. Also, the supplement did not affect mental performance. In contrast, glucose remained higher during and after the 20 km time trial following balenine ingestion. In conclusion, these results overall indicate that the functionality of balenine does not fully resemble that of carnosine and anserine, since it was unable to elicit performance improvements with similar and even higher plasma concentrations.

Endurance training in fasted conditions (FAST) induces favorable skeletal muscle metabolic adaptations compared with carbohydrate feeding (CHO), manifesting in improved exercise performance over time. Sprint interval training (SIT) is a potent metabolic stimulus, however nutritional strategies to optimize adaptations to SIT are poorly characterized. Here we investigated the efficacy of FAST versus CHO SIT (4-6 × 30-s Wingate sprints interspersed with 4-min rest) on muscle metabolic, serum metabolome and exercise performance adaptations in a double-blind parallel group design in recreationally active males. Following acute SIT, we observed exercise-induced increases in pan-acetylation and several genes associated with mitochondrial biogenesis, fatty acid oxidation, and NAD+-biosynthesis, along with favorable regulation of PDK4 (p = .004), NAMPT (p = .0013), and NNMT (p = .001) in FAST. Following 3 weeks of SIT, NRF2 (p = .029) was favorably regulated in FAST, with augmented pan-acetylation in CHO but not FAST (p = .033). SIT induced increases in maximal citrate synthase activity were evident with no effect of nutrition, while 3-hydroxyacyl-CoA dehydrogenase activity did not change. Despite no difference in the overall serum metabolome, training-induced changes in C3:1 (p = .013) and C4:1 (p = .010) which increased in FAST, and C16:1 (p = .046) and glutamine (p = .021) which increased in CHO, were different between groups. Training-induced increases in anaerobic (p = .898) and aerobic power (p = .249) were not influenced by nutrition. These findings suggest some beneficial muscle metabolic adaptations are evident in FAST versus CHO SIT following acute exercise and 3 weeks of SIT. However, this stimulus did not manifest in differential exercise performance adaptations.

Whether caffeine (CAF) increases fat metabolism remains debatable. Using systematic review coupled with meta-analysis, our aim was to determine effects of CAF on fat metabolism and the relevant factors moderating this effect. Electronic databases PubMed, SPORTDiscus, and Web of Science were searched using the following string: CAF AND (fat OR lipid) AND (metabolism OR oxidation). A meta-analytic approach aggregated data from 94 studies examining CAF's effect on fat metabolism assessed by different biomarkers. The overall effect size (ES) was 0.39 (95% confidence interval [CI] [0.30, 0.47], p < .001), indicating a small effect of CAF to increase fat metabolism; however, ES was significantly higher (p < .001) based on blood biomarkers (e.g., free fatty acids, glycerol) (ES = 0.55, 95% CI [0.43, 0.67]) versus expired gas analysis (respiratory exchange ratio, calculated fat oxidation) (ES = 0.26, 95% CI [0.16, 0.37]), although both were greater than zero. Fat metabolism increased to a greater extent (p = .02) during rest (ES = 0.51, 95% CI [0.41, 0.62]) versus exercise (ES = 0.35, 95% CI [0.26, 0.44]) across all studies, although ES was not different for studies reporting both conditions (ES = 0.49 and 0.44, respectively). There were no subgroup differences based on participants' fitness level, sex, or CAF dosage. CAF ingestion increases fat metabolism but is more consistent with blood biomarkers versus whole-body gas exchange measures. CAF has a small effect during rest across all studies, although similar to exercise when compared within the same study. CAF dosage did not moderate this effect.

This review discusses the potential value of tracking interstitial glucose with continuous glucose monitors (CGMs) in athletes, highlighting possible applications and important considerations in the collection and interpretation of interstitial glucose data. CGMs are sensors that provide real time, longitudinal tracking of interstitial glucose with a range of commercial monitors currently available. Recent advancements in CGM technology have led to the development of athlete-specific devices targeting glucose monitoring in sport. Although largely untested, the capacity of CGMs to capture the duration, magnitude, and frequency of interstitial glucose fluctuations every 1-15 min may present a unique opportunity to monitor fueling adequacy around competitive events and training sessions, with applications for applied research and sports nutrition practice. Indeed, manufacturers of athlete-specific devices market these products as a "fueling gauge," enabling athletes to "push their limits longer and get bigger gains." However, as glucose homeostasis is a complex phenomenon, extensive research is required to ascertain whether systemic glucose availability (estimated by CGM-derived interstitial glucose) has any meaning in relation to the intended purposes in sport. Whether CGMs will provide reliable and accurate information and enhance sports nutrition knowledge and practice is currently untested. Caveats around the use of CGMs include technical issues (dislodging of sensors during periods of surveillance, loss of data due to synchronization issues), practical issues (potential bans on their use in some sporting scenarios, expense), and challenges to the underpinning principles of data interpretation, which highlight the role of sports nutrition professionals to provide context and interpretation.

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 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.

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.