Hormonal contraceptive use, menstrual cycle characteristics and training/nutrition related profiles of elite, sub-elite and amateur athletes and exercisers: one size is unlikely to fit all

The aim of the present study was to simultaneously audit hormonal contraceptive (HC) use, menstrual cycle characteristics and training/nutrition related profiles in pre-menopausal women from varying athletic and exercise backgrounds. Elite (n = 51), sub-elite (n = 118) and amateur (n = 392) female athletes and exercisers were examined via an anonymous quantitative/qualitative survey tool. All analyses for ratio data were conducted utilising one- and two-way ANOVA/ANCOVA and odds ratio models, with ordinal data analysed via Pearson's Chi-squared tests. HC use was similar across elite, sub-elite and amateurs (34–44%). Menstrual cycle length was not different (P = 0.08) between competitive levels (28 ± 13 days), but 66% of respondents reported cycle variability (10 ± 11 days). Training profiles were not different based on contraceptive status (P > 0.05) yet were across competitive groups (P 0.05), though elite and sub-elite groups reported a higher daily meal consumption compared to amateurs (P < 0.01). Forty percent of all respondents skipped meals, attributed to lack of time, schedule and alterations in appetite, with reported changes in taste preferences during pre-menses (14–35%) and menses (15–25%) towards sweet foods (60%), with cravings for chocolate and other confectionary (25%). Prevalence of dietary supplement use was not influenced by contraceptive status (P = 0.31), though elites (76%) reported higher use (P = 0.04) than amateurs (63%). Data demonstrates that in female athletes and exercisers, competitive level appears to affect simple markers of training and nutrition practice, yet contraceptive status does not

Graded reductions in pre-exercise glycogen concentration do not augment exercise-induced nuclear AMPK and PGC-1α protein content in human muscle.

NEW FINDINGS: What is the central question of this study? What is the absolute level of pre-exercise glycogen concentration required to augment the exercise-induced signalling response regulating mitochondrial biogenesis? What is the main finding and its importance? Commencing high-intensity endurance exercise with reduced pre-exercise muscle glycogen concentrations confers no additional benefit to the early signalling responses that regulate mitochondrial biogenesis. ABSTRACT: We examined the effects of graded muscle glycogen on the subcellular location of AMPK and PGC-1α protein content and mRNA expression of genes associated with the regulation of mitochondrial biogenesis and substrate utilisation in human skeletal muscle. In a repeated measures design, eight trained male cyclists completed acute high-intensity interval (HIT) cycling (8 × 5 min at 80% peak power output) with graded concentrations of pre-exercise muscle glycogen. Following initial glycogen depleting exercise, subjects ingested  2 g kg-1  (L-CHO), 6 g kg-1  (M-CHO) or 14 g kg-1  (H-CHO) of carbohydrate during a 36 h period, such that exercise was commenced with graded (P < 0.05) muscle glycogen concentrations (H-CHO; 531 ± 83, M-CHO; 332 ± 88, L-CHO; 208 ± 79 mmol·kg-1  dw). Exercise depleted muscle glycogen to < 300 mmol·kg-1 dw in all trials (H-CHO; 270 ± 88, M-CHO; 173 ± 74, L-CHO; 100 ± 42 mmol·kg-1 dw) and induced comparable increases in nuclear AMPK protein content (∼2 fold) and PGC-1α (∼5 fold), p53 (∼1.5 fold) and CPT-1 (∼2 fold) mRNA between trials (all P < 0.05). The magnitude of increase in PGC-1α mRNA was also positively correlated with post-exercise glycogen concentration (P < 0.05). In contrast, exercise nor carbohydrate availability affected the subcellular location of PGC-1α protein or PPAR, SCO2, SIRT1, DRP1, MFN2 or CD36 mRNA. Using a sleep-low, train-low model with a high-intensity endurance exercise stimulus, we conclude that pre-exercise muscle glycogen does not modulate skeletal muscle cell signalling. This article is protected by copyright. All rights reserved

¹³C-glucose-fructose labeling reveals comparable exogenous CHO oxidation during exercise when consuming 120 g/h in fluid, gel, jelly chew, or coingestion:CHO oxidation from fluid, semi-solid and solid

We examined the effects of carbohydrate (CHO) delivery form on exogenous CHO oxidation, gastrointestinal discomfort, and exercise capacity. In a randomized repeated-measures design [after 24 h of high CHO intake (8 g·kg ₋1) and preexercise meal (2 g·kg ₋1)], nine trained males ingested 120 g CHO·h ₋1 from fluid (DRINK), semisolid gel (GEL), solid jelly chew (CHEW), or a coingestion approach (MIX). Participants cycled for 180 min at 95% lactate threshold, followed by an exercise capacity test (150% lactate threshold). Peak rates of exogenous CHO oxidation (DRINK 1.56 ± 0.16, GEL 1.58 ± 0.13, CHEW 1.59 ± 0.08, MIX 1.66 ± 0.02 g·min ₋1) and oxidation efficiency (DRINK 72 ± 8%, GEL 72 ± 5%, CHEW 75 ± 5%, MIX, 75 ± 6%) were not different between trials (all P &gt; 0.05). Despite ingesting 120 g·h ₋1, participants reported minimal symptoms of gastrointestinal distress across all trials. Exercise capacity was also not significantly different (all P &gt; 0.05) between conditions (DRINK 446 ± 350, GEL 529 ± 396, CHEW 596 ± 416, MIX 469 ± 395 s). Data represent the first time that rates of exogenous CHO oxidation (via stable isotope methodology) have been simultaneously assessed with feeding strategies (i.e., preexercise CHO feeding and the different forms and combinations of CHO during exercise) commonly adopted by elite endurance athletes. We conclude that 120 g·h ₋1 CHO (in a 1:0.8 ratio of maltodextrin or glucose to fructose) is a practically tolerable strategy to promote high CHO availability and oxidation during exercise. NEW &amp; NOTEWORTHY We demonstrate comparable rates of exogenous CHO oxidation from fluid, semisolid, solid, or a combination of sources. Considering the sustained high rates of total and exogenous CHO oxidation and relative lack of gastrointestinal symptoms, consuming 120 g CHO·h ₋1 appears to be a well-tolerated strategy to promote high CHO availability during exercise. Additionally, this is the first time that rates of exogenous CHO oxidation have been assessed with feeding strategies (e.g., coingestion of multiple CHO forms) typically reported by endurance athletes. </p

Nutritional Modulation of Sleep Latency, Duration, and Efficiency: A Randomised, Repeated-Measures, Double-Blind Deception Study

Purpose To test the hypothesis that a novel nutritional blend comprised of tryptophan, glycine, magnesium, tart cherry powder and L-theanine, enhances subjective and objective measures of sleep during free living conditions. Methods In a randomised, repeated measures crossover and double blind deception design, participants (n = 9 male and 7 female; age: 24 ± 3 years; body mass: 69.8 ± 11.6 kg; stature: 170.8 ± 9.1 cm) completed a 3 day familiarisation period, followed by 3 day intervention and placebo trials. Subjective Pittsburgh Quality Sleep Index, Core Consensus Sleep Diary and Karolinska Sleepiness Scale survey tools, alongside objective actigraphy measures of sleep were assessed, with daily nutritional intake, activity and light exposure standardised between trials. Participants provided daily urine samples for assessment of targeted and untargeted metabolomes. Results The intervention trial reduced sleep onset latency (-24 ± 25 mins; p = 0.002), increased total sleep time (22 ± 32 mins; p = 0.01) and sleep efficiency (2.4 ± 3.9 %; p = 0.03), whilst also reducing morning sleepiness (p = 0.02). Throughout the study, 75 % of participants remained blinded to sleep assessment as a primary outcome measure, with 56 % subjectively indicating improved sleep during the intervention trial. Metabolomic analysis highlighted several significantly altered metabolomes related to sleep regulation between trials, inclusive of 6-sulfatoxymelatonin, D-serine and L-glutamic acid. Conclusions Data demonstrate that employing the proposed blend of novel nutritional ingredients during free living conditions reduced sleep onset latency, increased total sleep duration and increased sleep efficiency, leading to reduced perceptions of morning sleepiness. These effects may be mediated by the upregulation of key metabolites involved in the neurophysiological modulation of the sleep/wake cycle

13C-glucose-fructose labeling reveals comparable exogenous CHO oxidation during exercise when consuming 120 g/h in fluid, gel, jelly chew, or coingestion

We examined the effects of carbohydrate (CHO) delivery form on exogenous CHO oxidation, gastrointestinal discomfort, and exercise capacity. In a randomized repeated-measures design [after 24 h of high CHO intake (8 g·kg−1) and preexercise meal (2 g·kg−1)], nine trained males ingested 120 g CHO·h−1 from fluid (DRINK), semisolid gel (GEL), solid jelly chew (CHEW), or a coingestion approach (MIX). Participants cycled for 180 min at 95% lactate threshold, followed by an exercise capacity test (150% lactate threshold). Peak rates of exogenous CHO oxidation (DRINK 1.56 ± 0.16, GEL 1.58 ± 0.13, CHEW 1.59 ± 0.08, MIX 1.66 ± 0.02 g·min−1) and oxidation efficiency (DRINK 72 ± 8%, GEL 72 ± 5%, CHEW 75 ± 5%, MIX, 75 ± 6%) were not different between trials (all P > 0.05). Despite ingesting 120 g·h−1, participants reported minimal symptoms of gastrointestinal distress across all trials. Exercise capacity was also not significantly different (all P > 0.05) between conditions (DRINK 446 ± 350, GEL 529 ± 396, CHEW 596 ± 416, MIX 469 ± 395 s). Data represent the first time that rates of exogenous CHO oxidation (via stable isotope methodology) have been simultaneously assessed with feeding strategies (i.e., preexercise CHO feeding and the different forms and combinations of CHO during exercise) commonly adopted by elite endurance athletes. We conclude that 120 g·h−1 CHO (in a 1:0.8 ratio of maltodextrin or glucose to fructose) is a practically tolerable strategy to promote high CHO availability and oxidation during exercise. NEW & NOTEWORTHY We demonstrate comparable rates of exogenous CHO oxidation from fluid, semisolid, solid, or a combination of sources. Considering the sustained high rates of total and exogenous CHO oxidation and relative lack of gastrointestinal symptoms, consuming 120 g CHO·h−1 appears to be a well-tolerated strategy to promote high CHO availability during exercise. Additionally, this is the first time that rates of exogenous CHO oxidation have been assessed with feeding strategies (e.g., coingestion of multiple CHO forms) typically reported by endurance athletes