Estimated energy expenditures and energy intakes of international female rugby sevens players in five days of a training camp and competition preparation

To understand the energy balance of international female rugby sevens (R7s) players in applied environments, this study estimated the energy intakes (EI) and total daily estimated energy expenditures (TDEE) during a five-day training camp (TRAIN) and phase of competition preparation (COMP) of equal duration. Tri-axial accelerometer devices were worn throughout both scenarios to estimate TDEE, whereas EI was estimated via self-reported food diaries. Energy deficits of −47% (TDEETRAIN: 14.6 ± 1.6 MJ·day−1, EITRAIN: 7.7 ± 0.9 MJ·day−1, p ≤ 0.001, d = 5.1) and −50% (TDEECOMP: 15.5 ± 1.6 MJ·day−1, EICOMP: 7.7 ± 1.0 MJ·day−1, p ≤ 0.001, d = 5.7) were observed throughout TRAIN (n = 11; age: 25 ± 4 years, height: 170 ± 6 cm, weight: 71 ± 7 kg) and COMP (n = 8; age: 25 ± 3 years, height: 172 ± 5 cm, weight: 72 ± 6 kg), respectively. Carbohydrate intakes were below the lower range of sports nutrition recommendations in both TRAIN (−62%; 2.3 ± 0.3 g·kg−1 BM, p ≤ 0.001) and COMP (−60%; 2.4 ± 0.5 g·kg−1 BM, p ≤ 0.001). For protein (TRAIN: 1.7 ± 0.4 g·kg−1 BM, COMP: 1.5 ± 0.1 g·kg−1 BM), intakes met the lower range of recommendations. Fat intake exceeded recommendations of the percentage of total EI (COMP: 39 ± 5%). Accordingly, the dietary strategies of international female R7s players may warrant optimization, as carbohydrate and fat intakes were less than optimal when compared to current performance-based sports nutrition guidelines

Liver and muscle glycogen oxidation and performance with dose variation of glucose-fructose ingestion during prolonged (3 h) exercise

Purpose This study investigated the effect of small manipulations in carbohydrate (CHO) dose on exogenous and endogenous (liver and muscle) fuel selection during exercise. Method Eleven trained males cycled in a double-blind randomised order on 4 occasions at 60% V˙O2max for 3 h, followed by a 30-min time-trial whilst ingesting either 80 g h−1 or 90 g h−1 or 100 g h−1 13C-glucose-13C-fructose [2:1] or placebo. CHO doses met, were marginally lower, or above previously reported intestinal saturation for glucose–fructose (90 g h−1). Indirect calorimetry and stable mass isotope [13C] techniques were utilised to determine fuel use. Result Time-trial performance was 86.5 to 93%, ‘likely, probable’ improved with 90 g h−1 compared 80 and 100 g h−1. Exogenous CHO oxidation in the final hour was 9.8–10.0% higher with 100 g h−1 compared with 80 and 90 g h−1 (ES = 0.64–0.70, 95% CI 9.6, 1.4 to 17.7 and 8.2, 2.1 to 18.6). However, increasing CHO dose (100 g h−1) increased muscle glycogen use (101.6 ± 16.6 g, ES = 0.60, 16.1, 0.9 to 31.4) and its relative contribution to energy expenditure (5.6 ± 8.4%, ES = 0.72, 5.6, 1.5 to 9.8 g) compared with 90 g h−1. Absolute and relative muscle glycogen oxidation between 80 and 90 g h−1 were similar (ES = 0.23 and 0.38) though a small absolute (85.4 ± 29.3 g, 6.2, − 23.5 to 11.1) and relative (34.9 ± 9.1 g, − 3.5, − 9.6 to 2.6) reduction was seen in 90 g h−1 compared with 100 g h−1. Liver glycogen oxidation was not significantly different between conditions (ES < 0.42). Total fat oxidation during the 3-h ride was similar in CHO conditions (ES < 0.28) but suppressed compared with placebo (ES = 1.05–1.51). Conclusion ‘Overdosing’ intestinal transport for glucose–fructose appears to increase muscle glycogen reliance and negatively impact subsequent TT performance

Fuel Use during Exercise at Altitude in Women with Glucose–Fructose Ingestion

Purpose: This study compared the co-ingestion of glucose and fructose on exogenous and endogenous substrate oxidation during prolonged exercise at terrestrial high altitude (HA) versus sea level, in women. Method: Five women completed two bouts of cycling at the same relative workload (55% Wmax) for 120 minutes on acute exposure to HA (3375m) and at sea level (~113m). In each trial, participants ingested 1.2 g.min-1 of glucose (enriched with 13C glucose) and 0.6 g.min-1 of fructose (enriched with 13C fructose) before and every 15 minutes during exercise. Indirect calorimetry and isotope ratio mass spectrometry were used to calculate fat oxidation, total and exogenous carbohydrate oxidation, plasma glucose oxidation and endogenous glucose oxidation derived from liver and muscle glycogen. Results: The rates and absolute contribution of exogenous carbohydrate oxidation was significantly lower at HA compared with sea level (ES>0.99, P<0.024), with the relative exogenous carbohydrate contribution approaching significance (32.6±6.1 vs. 36.0±6.1%, ES=0.56, P=0.059) during the second hour of exercise. In comparison, no significant differences were observed between HA and sea level for the relative and absolute contributions of liver glucose (3.2±1.2 vs. 3.1±0.8%, ES=0.09, P=0.635 and 5.1±1.8 vs. 5.4±1.7 grams, ES=0.19, P=0.217), and muscle glycogen (14.4±12.2% vs. 15.8±9.3%, ES=0.11, P=0.934 and 23.1±19.0 vs. 28.7±17.8 grams, ES=0.30, P=0.367). Furthermore, there was no significant difference in total fat oxidation between HA and sea level (66.3±21.4 vs. 59.6±7.7 grams, ES=0.32, P=0.557). Conclusion: In women, acute exposure to HA reduces the reliance on exogenous carbohydrate oxidation during cycling at the same relative exercise intensity

Markers of physiological stress during exercise under conditions of normoxia, normobaric hypoxia, hypobaric hypoxia and genuine high altitude.

Purpose To investigate whether there is a differential response at rest and following exercise to conditions of genuine high altitude (GHA), normobaric hypoxia (NH), hypobaric hypoxia (HH) and normobaric normoxia (NN). Method Markers of sympathoadrenal and adrenocortical function (plasma normetanephrine [PNORMET], metanephrine [PMET], cortisol), myocardial injury (highly sensitive cardiac troponin T [hscTnT]) and function (N-terminal brain natriuretic peptide [NT-proBNP]) were evaluated at rest and with exercise under NN, at 3375 m in the Alps (GHA) and at equivalent simulated altitude under NH and HH. Participants cycled for 2 hours {15 minute warm-up, 105 minutes at 55% Wmax (maximal workload)} with venous blood samples taken prior (T0), immediately following (T120) and 2 hours post-exercise (T240). Results Exercise in the three hypoxic environments produced a similar pattern of response with the only difference between environments being in relation to PNORMET. Exercise in NN only induced a rise in PNORMET and PMET. Conclusion Biochemical markers that reflect sympathoadrenal, adrenocortical and myocardial responses to physiological stress demonstrate significant differences in the response to exercise under conditions of normoxia versus hypoxia while NH and HH appear to induce broadly similar responses to GHA and may therefore be reasonable surrogates