Purpose Maximizing carbohydrate availability is important for many endurance events. Combining pectin and sodium alginate with ingested maltodextrin–fructose (MAL + FRU + PEC + ALG) has been suggested to enhance carbohydrate delivery via hydrogel formation, but the influence on exogenous carbohydrate oxidation remains unknown. The primary aim of this study was to assess the effects of MAL + FRU + PEC + ALG on exogenous carbohydrate oxidation during exercise compared with a maltodextrin–fructose mixture (MAL + FRU). MAL + FRU has been well established to increase exogenous carbohydrate oxidation during cycling compared with glucose-based carbohydrates (MAL + GLU). However, much evidence focuses on cycling, and direct evidence in running is lacking. Therefore, a secondary aim was to compare exogenous carbohydrate oxidation rates with MAL + FRU versus MAL + GLU during running. Methods Nine trained runners completed two trials (MAL + FRU and MAL + FRU + PEC + ALG) in a double-blind, randomized crossover design. A subset (n = 7) also completed a MAL + GLU trial to address the secondary aim, and a water trial to establish background expired 13CO2 enrichment. Participants ran at 60% V˙O2peak for 120 min while ingesting either water only or carbohydrate solutions at a rate of 1.5 g carbohydrate per minute. Results At the end of 120 min of exercise, exogenous carbohydrate oxidation rates were 0.9 (SD 0.5) g·min−1 with MAL + GLU ingestion. MAL + FRU ingestion increased exogenous carbohydrate oxidation rates to 1.1 (SD 0.3) g·min−1 (P = 0.038), with no further increase with MAL + FRU + PEC + ALG ingestion (1.1 (SD 0.3) g·min−1; P = 1.0). No time–treatment interaction effects were observed for plasma glucose, lactate, insulin, or nonesterified fatty acids, or for ratings of perceived exertion or gastrointestinal symptoms (all, P > 0.05). Conclusion To maximize exogenous carbohydrate oxidation during moderate-intensity running, athletes may benefit from consuming glucose(polymer)–fructose mixtures over glucose-based carbohydrates alone, but the addition of pectin and sodium alginate offers no further benefit.

The analysis of time series data is common in nutrition and metabolism research for quantifying the physiological responses to various stimuli. The reduction of many data from a time series into a summary statistic(s) can help quantify and communicate the overall response in a more straightforward way and in line with a specific hypothesis. Nevertheless, many summary statistics have been selected by various researchers, and some approaches are still complex. The time-intensive nature of such calculations can be a burden for especially large data sets and may, therefore, introduce computational errors, which are difficult to recognize and correct. In this short commentary, the authors introduce a newly developed tool that automates many of the processes commonly used by researchers for discrete time series analysis, with particular emphasis on how the tool may be implemented within nutrition and exercise science research.

Purpose: Premature birth induces long-term sequelae on the cardiopulmonary system, leading to reduced exercise capacity. However, the mechanisms of this functional impairment during incremental exercise remain unclear. Also, a blunted hypoxic ventilatory response was found in preterm adults, suggesting an increased risk for adverse effects of hypoxia in this population. This study aimed to investigate the oxygen cascade during incremental exercise to exhaustion in both normoxia and hypobaric hypoxia in prematurely born adults with normal lung function and their term born counterparts. Methods: Noninvasive measures of gas exchange, cardiac hemodynamics, and both muscle and cerebral oxygenation were continuously performed using metabolic cart, transthoracic impedance, and near-infrared spectroscopy, respectively, during an incremental exercise test to exhaustion performed at sea level and after 3 d of high-altitude exposure in healthy preterm (n = 17; gestational age, 29 ± 1 wk; normal lung function) and term born (n = 17) adults. Results: At peak, power output, oxygen uptake, stroke volume indexed for body surface area, and cardiac output were lower in preterm compared with term born in normoxia (P = 0.042, P = 0.027, P = 0.030, and P = 0.018, respectively) but not in hypoxia, whereas pulmonary ventilation, peripheral oxygen saturation, and muscle and cerebral oxygenation were similar between groups. These later parameters were modified by hypoxia (P < 0.001). Hypoxia increased muscle oxygen extraction at submaximal and maximal intensity in term born (P < 0.05) but not in preterm participants. Hypoxia decreased cerebral oxygen saturation in term born but not in preterm adults at rest and during exercise (P < 0.05). Convective oxygen delivery was decreased by hypoxia in term born (P < 0.001) but not preterm adults, whereas diffusive oxygen transport decreased similarly in both groups (P < 0.001 and P < 0.001, respectively). Conclusions: These results suggest that exercise capacity in preterm is primarily reduced by impaired convective, rather than diffusive, oxygen transport. Moreover, healthy preterm adults may experience blunted hypoxia-induced impairments during maximal exercise compared with their term counterparts.

This study investigated whether carbohydrate-energy replacement immediately after prolonged endurance exercise attenuates insulin sensitivity the following morning, and whether exercise improves insulin sensitivity the following morning independent of an exercise-induced carbohydrate deficit. Oral glucose tolerance and whole-body insulin sensitivity were compared the morning after three evening conditions, involving: (1) treadmill exercise followed by carbohydrate replacement drink (200 or 150 g maltodextrin for males and females, respectively; CHO-replace); (2) treadmill exercise followed by a non-caloric, taste-matched placebo (CHO-deficit); or (3) seated rest with no drink provided (Rest). Treadmill exercise involved 90 minutes at ~80% age-predicted maximum heart rate. Seven males and two females (aged 23 ± 1 years; body mass index 24.0 ± 2.7 kg·m-2) completed all conditions in a randomized order. Matsuda index improved by 22% (2.2 [0.3, 4.0] au, p = .03) and HOMA2-IR improved by 10% (-0.04 [-0.08, 0.00] au, p = .04) in CHO-deficit versus CHO-replace, without corresponding changes in postprandial glycemia. Outcomes were similar between Rest and other conditions. These data suggest that improvements to insulin sensitivity in healthy populations following acute moderate/vigorous intensity endurance exercise may be dependent on the presence of a carbohydrate-energy deficit. NOVELTY • Restoration of carbohydrate balance following acute endurance exercise attenuated whole-body insulin sensitivity • Exercise per se failed to enhance whole-body insulin sensitivity • Maximizing or prolonging the post-exercise carbohydrate deficit may enhance acute benefits to insulin sensitivity