The Impact of a Short-Term Ketogenic Low-Carbohydrate High-Fat Diet on Biomarkers of Intestinal Epithelial Integrity and Gastrointestinal Symptoms.

Endurance exercise can disturb intestinal epithelial integrity, leading to increased systemic indicators of cell injury, hyperpermeability, and pathogenic translocation. However, the interaction between exercise, diet, and gastrointestinal disturbance still warrants exploration. This study examined whether a 6-day dietary intervention influenced perturbations to intestinal epithelial disruption in response to a 25-km race walk. Twenty-eight male race walkers adhered to a high carbohydrate (CHO)/energy diet (65% CHO, energy availability = 40 kcal·kg FFM-1·day-1) for 6 days prior to a Baseline 25-km race walk. Athletes were then split into three subgroups: high CHO/energy diet (n = 10); low-CHO, high-fat diet (LCHF: n = 8; <50 g/day CHO, energy availability = 40 kcal·kg FFM-1·day-1); and low energy availability (n = 10; 65% CHO, energy availability = 15 kcal·kg FFM-1·day-1) for a further 6-day dietary intervention period prior to a second 25-km race walk (Adaptation). During both trials, venous blood was collected pre-, post-, and 1 hr postexercise and analyzed for markers of intestinal epithelial disruption. Intestinal fatty acid-binding protein concentration was significantly higher (twofold increase) in response to exercise during Adaptation compared to Baseline in the LCHF group (p = .001). Similar findings were observed for soluble CD14 (p < .001) and lipopolysaccharide-binding protein (p = .003), where postexercise concentrations were higher (53% and 36%, respectively) during Adaptation than Baseline in LCHF. No differences in high CHO/energy diet or low energy availability were apparent for any blood markers assessed (p > .05). A short-term LCHF diet increased intestinal epithelial cell injury in response to a 25-km race walk. No effect of low energy availability on gastrointestinal injury or symptoms was observed.

Running at Increasing Intensities in the Heat Induces Transient Gut Perturbations.

PURPOSE: The risk of exercise-induced endotoxemia is increased in the heat and is primarily attributable to changes in gut permeability resulting in the translocation of lipopolysaccharides (LPS) into the circulation. The purpose of this study was to quantify the acute changes in gut permeability and LPS translocation during submaximal continuous and high-intensity interval exercise under heat stress. METHODS: A total of 12 well-trained male runners (age 37 [7] y, maximal oxygen uptake [VO2max] 61.0 [6.8] mL·min-1·kg-1) undertook 2 treadmill runs of 2 × 15-minutes at 60% and 75% VO2max and up to 8 × 1-minutes at 95% VO2max in HOT (34°C, 68% relative humidity) and COOL (18°C, 57% relative humidity) conditions. Venous blood samples were collected at the baseline, following each running intensity, and 1 hour postexercise. Blood samples were analyzed for markers of intestinal permeability (LPS, LPS binding protein, and intestinal fatty acid-binding protein). RESULTS: The increase in LPS binding protein following each exercise intensity in the HOT condition was 4% (5.3 µg·mL-1, 2.4-8.4; mean, 95% confidence interval, P < .001), 32% (4.6 µg·mL-1, 1.8-7.4; P = .002), and 30% (3.0 µg·mL-1, 0.03-5.9; P = .047) greater than in the COOL condition. LPS was 69% higher than baseline following running at 75% VO2max in the HOT condition (0.2 endotoxin units·mL-1, 0.1-0.4; P = .011). Intestinal fatty acid-binding protein increased 43% (2.1 ng·mL-1, 0.1-4.2; P = .04) 1 hour postexercise in HOT compared with the COOL condition. CONCLUSIONS: Small increases in LPS concentration during exercise in the heat and subsequent increases in intestinal fatty acid-binding protein and LPS binding protein indicate a capacity to tolerate acute, transient intestinal disturbance in well-trained endurance runners.

Adaptation to a low carbohydrate high fat diet is rapid but impairs endurance exercise metabolism and performance despite enhanced glycogen availability.

KEY POINTS: Brief (5-6 days) adaptation to a low carbohydrate high fat diet in elite athletes increased exercise fat oxidation to rates previously observed with medium (3-4 weeks) or chronic (>12 months) adherence to this diet, with metabolic changes being washed out in a similar time frame. Increased fat utilisation during exercise was associated with a 5-8% increase in oxygen cost at speeds related to Olympic Programme races. Acute restoration of endogenous carbohydrate (CHO) availability (24 h high CHO diet, pre-race CHO) only partially restored substrate utilisation during a race warm-up. Fat oxidation continued to be elevated above baseline values although it was lower than achieved by 5-6 days' keto adaptation; CHO oxidation only reached 61% and 78% of values previously seen at exercise intensities related to race events. Acute restoration of CHO availability failed to overturn the impairment of high-intensity endurance performance previously associated with low carbohydrate high fat adaptation, potentially due to the blunted capacity for CHO oxidation. ABSTRACT: We investigated substrate utilisation during exercise after brief (5-6 days) adaptation to a ketogenic low-carbohydrate (CHO), high-fat (LCHF) diet and similar washout period. Thirteen world-class male race walkers completed economy testing, 25 km training and a 10,000 m race (Baseline), with high CHO availability (HCHO), repeating this (Adaptation) after 5-6 days' LCHF (n = 7; CHO: <50 g day-1 , protein: 2.2 g kg-1 day-1 ; 80% fat) or HCHO (n = 6; CHO: 9.7 g kg-1 day-1 ; protein: 2.2 g kg-1 day-1 ) diet. An Adaptation race was undertaken after 24 h HCHO and pre-race CHO (2 g kg-1 ) diet, identical to the Baseline race. Substantial (>200%) increases in exercise fat oxidation occurred in the LCHF Adaptation economy and 25 km tests, reaching mean rates of ∼1.43 g min-1 . However, relative V̇O2 (ml min-1  kg-1 ) was higher (P < 0.0001), by ∼8% and 5% at speeds related to 50 km and 20 km events. During Adaptation race warm-up in the LCHF group, rates of fat and CHO oxidation at these speeds were decreased and increased, respectively (P < 0.001), compared with the previous day, but were not restored to Baseline values. Performance changes differed between groups (P = 0.009), with all HCHO athletes improving in the Adaptation race (5.7 (5.6)%), while 6/7 LCHF athletes were slower (2.2 (3.4)%). Substrate utilisation returned to Baseline values after 5-6 days of HCHO diet. In summary, robust changes in exercise substrate use occurred in 5-6 days of extreme changes in CHO intake. However, adaptation to a LCHF diet plus acute restoration of endogenous CHO availability failed to restore high-intensity endurance performance, with CHO oxidation rates remaining blunted.

The effects of intensified training on resting metabolic rate (RMR), body composition and performance in trained cyclists.

BACKGROUND: Recent research has demonstrated decreases in resting metabolic rate (RMR), body composition and performance following a period of intensified training in elite athletes, however the underlying mechanisms of change remain unclear. Therefore, the aim of the present study was to investigate how an intensified training period, designed to elicit overreaching, affects RMR, body composition, and performance in trained endurance athletes, and to elucidate underlying mechanisms. METHOD: Thirteen (n = 13) trained male cyclists completed a six-week training program consisting of a "Baseline" week (100% of regular training load), a "Build" week (~120% of Baseline load), two "Loading" weeks (~140, 150% of Baseline load, respectively) and two "Recovery" weeks (~80% of Baseline load). Training comprised of a combination of laboratory based interval sessions and on-road cycling. RMR, body composition, energy intake, appetite, heart rate variability (HRV), cycling performance, biochemical markers and mood responses were assessed at multiple time points throughout the six-week period. Data were analysed using a linear mixed modeling approach. RESULTS: The intensified training period elicited significant decreases in RMR (F(5,123.36) = 12.0947, p = <0.001), body mass (F(2,19.242) = 4.3362, p = 0.03), fat mass (F(2,20.35) = 56.2494, p = <0.001) and HRV (F(2,22.608) = 6.5212, p = 0.005); all of which improved following a period of recovery. A state of overreaching was induced, as identified by a reduction in anaerobic performance (F(5,121.87) = 8.2622, p = <0.001), aerobic performance (F(5,118.26) = 2.766, p = 0.02) and increase in total mood disturbance (F(5, 110.61) = 8.1159, p = <0.001). CONCLUSION: Intensified training periods elicit greater energy demands in trained cyclists, which, if not sufficiently compensated with increased dietary intake, appears to provoke a cascade of metabolic, hormonal and neural responses in an attempt to restore homeostasis and conserve energy. The proactive monitoring of energy intake, power output, mood state, body mass and HRV during intensified training periods may alleviate fatigue and attenuate the observed decrease in RMR, providing more optimal conditions for a positive training adaptation.

Effect of Intensified Endurance Training on Pacing and Performance in 4000-m Cycling Time Trials.

Studies examining pacing strategies during 4000-m cycling time trials (TTs) typically ensure that participants are not prefatigued; however, competitive cyclists often undertake TTs when already fatigued. This study aimed to determine how TT pacing strategies and sprint characteristics of cyclists change during an intensified training period (mesocycle). Thirteen cyclists regularly competing in A- and B-grade cycling races and consistently training (>10 h/wk for 4 [1] y) completed a 6-wk training mesocycle. Participants undertook individually prescribed training, using training stress scores (TrainingPeaks, Boulder, CO), partitioned into a baseline week, a build week, 2 loading weeks (designed to elicit an overreached state), and 2 recovery weeks. Laboratory-based tests (15-s sprint and TT) and Recovery-Stress Questionnaire (RESTQ-52) responses were repeatedly undertaken over the mesocycle. TT power output increased during recovery compared with baseline and loading weeks (P = .001) with >6-W increases in mean power output (MPO) detected for 400-m sections (10% bins) from 1200 to 4000 m in recovery weeks. Decreases in peak heart rate (P < .001) during loading weeks and postexercise blood lactate (P = .005) during loading week 2 and recovery week 1 were detected. Compared with baseline, 15-s sprint MPO declined during loading and recovery weeks (P < .001). An interaction was observed between RESTQ-52 total stress score with a 15-s sprint (P = .003) and with a TT MPO (P = .04), indicating that participants who experienced greater stress during loading weeks exhibited reduced performance. To conclude, intensified endurance training diminished sprint performance but improved 4000-m TT performance, with a subtle change in MPO evident over the last 70% of TTs.