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: 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 expired¹³CO₂enrichment. 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⁻¹with 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.

Manferdelli, Giorgio, Benjamin J. Narang, Mathias Poussel, Damjan Osredkar, Grégoire P. Millet, and Tadej Debevec. Long-term effects of prematurity on resting ventilatory response to hypercapnia. High Alt Med Biol . 22:420–425, 2021. Background: This study investigated the resting ventilatory response to hypercapnia in prematurely born adults. Materials and Methods: Seventeen preterm and fourteen full-term adults were exposed to normoxic hypercapnia (two 5-minute periods at 3% and 6% carbon dioxide [CO ₂ ] interspersed by 5-minute in normoxia). Pulmonary ventilation ( ) and end-tidal partial pressure of CO ₂ (P etco ₂ ) were measured continuously. Results: No difference in lung function was observed between preterm and full-term adults. P etco ₂ was lower in preterm than in full-term adults ( p < 0.05) during normoxia. During exposure to 3% CO ₂ , both and P etco ₂ increased in a similar way in preterm and full-term adults. However, at the end of the 6% CO ₂ period, there was a significantly higher in preterm compared with full-term adults (30.2 ± 7.5 vs. 23.7 ± 4.5 L/min, p < 0.0001), whereas no difference was observed for P etco ₂ (46.9 ± 2.1 vs. 50.6 ± 2.1 L/min, p = 0.99). Breath frequency was higher in preterm than in full-term adults (17.9 ± 4.0 vs. 12.8 ± 3.5 b/min, p < 0.01) during 6% CO ₂ exposure. Conclusions: Although data suggest that prematurity results in resting hypocapnia, the exact underlying mechanisms remain to be elucidated. Moreover, preterm adults seem to have increased chemosensitivity to hypercapnia.

Pre-term birth is associated with numerous cardio-respiratory sequelae in children. Whether these impairments impact the responses to exercise in normoxia or hypoxia remains to be established. Fourteen prematurely-born (PREM) (Mean ± SD; gestational age 29 ± 2 weeks; age 9.5 ± 0.3 years), and 15 full-term children (CONT) (gestational age 39 ± 1 weeks; age 9.7 ± 0.9 years), underwent incremental exercise tests to exhaustion in normoxia (FiO₂ = 20.9%) and normobaric hypoxia (FiO₂ = 13.2%) on a cycle ergometer. Cardio-respiratory variables were measured throughout. Peak power output was higher in normoxia than hypoxia (103 ± 17 vs. 77 ± 18 W; p < 0.001), with no difference between CONT and PREM (94 ± 23 vs. 86 ± 19 W; p = 0.154). VO₂peak was higher in normoxia than hypoxia in CONT (50.8 ± 7.2 vs. 43.8 ± 9.9 mL·kg⁻¹·min⁻¹; p < 0.001) but not in PREM (48.1 ± 7.5 vs. 45.0 ± 6.8 mL·kg⁻¹·min⁻¹; p = 0.137; interaction p = 0.044). Higher peak heart rate (187 ± 11 vs. 180 ± 10 bpm; p = 0.005) and lower stroke volume (72 ± 13 vs. 77 ± 14 mL; p = 0.004) were observed in normoxia versus hypoxia in CONT, with no such differences in PREM (p = 0.218 and >0.999, respectively). In conclusion, premature birth does not appear to exacerbate the negative effect of hypoxia on exercise capacity in children. Further research is warranted to identify whether prematurity elicits a protective effect, and to clarify the potential underlying mechanisms.

Recent evidence suggests that different hypoxic modalities might accelerate the rehabilitation process in injured athletes. In this review, the application of hypoxia during rehabilitation from musculoskeletal injury is explored in relation to two principles: (1) facilitating the healing of damaged tissue, and (2) mitigating detraining and inducing training adaptations with a reduced training load. Key literature that explores the underlying mechanisms for these themes is presented, and considerations for practice and future research directions are outlined. For principle (1), passive intermittent hypoxic exposures might accelerate tissue healing through angiogenic and osteogenic mechanisms. Experimental evidence is largely derived from rodent research, so further work is warranted to establish whether clinically meaningful effects can be observed in humans, before optimal protocols are determined (duration, frequency, and hypoxic severity). Regarding principle (2), a hypoxia-related increase in the cardiometabolic stimulus imposed by low-load exercise is appealing for load-compromised athletes. As rehabilitation progresses, a variety of hypoxic modalities can be implemented to enhance adaptation to energy-systems and resistance-based training, and more efficiently return the athlete to competition readiness. While hypoxic modalities seem promising for accelerating musculoskeletal injury rehabilitation in humans, and are already being widely used in practice, a significant gap remains regarding their evidence-based application.