A Comparison of Critical Speed and Critical Power in Runners Using Stryd Running Power.

PURPOSE: Although running traditionally relies on critical speed (CS) as an indicator of critical intensity, portable inertial measurement units offer a potential solution for estimating running mechanical power to assess critical power (CP) in runners. The purpose of this study was to determine whether CS and CP differ when assessed using the Stryd device, a portable inertial measurement unit, and if 2 running bouts are sufficient to determine CS and CP. METHODS: On an outdoor running track, 10 trained runners (V˙O2max, 59.0 [4.2] mL·kg-1·min-1) performed 3 running time trials (TT) between 1200 and 4400 m on separate days. CS and CP were derived from 2-parameter hyperbolic speed-time and power-time models, respectively, using 2 (CS2TT and CP2TT) and 3 (CS3TT and CP3TT) TTs. Subsequently, runners performed constant-intensity running for 800 m at their calculated CS3TT and CP3TT. RESULTS: Running at the calculated CS3TT speed (3.88 [0.44] m·s-1) elicited an average Stryd running power (271 [28] W) not different from the calculated CP3TT (270 [28]; P = .940; d = 0.02), with excellent agreement between the 2 values (intraclass correlation coefficient = .980). The CS2TT (3.97 [0.42] m·s-1) was not higher than CS3TT (3.89 [0.44] m·s-1; P = .178; d = 0.46); however, CP2TT (278 [29] W) was greater than CP3TT (P = .041; d = 0.75). CONCLUSION: The running intensities at CS and CP were similar, supporting the use of running power (Stryd) as a metric of aerobic fitness and exercise prescription, and 2 trials provided a reasonable, albeit higher, estimate of CS and CP.

Is Running Power a Useful Metric? Quantifying Training Intensity and Aerobic Fitness Using Stryd Running Power Near the Maximal Lactate Steady State.

We sought to determine the utility of Stryd, a commercially available inertial measurement unit, to quantify running intensity and aerobic fitness. Fifteen (eight male, seven female) runners (age = 30.2 [4.3] years; V·O2max = 54.5 [6.5] ml·kg-1·min-1) performed moderate- and heavy-intensity step transitions, an incremental exercise test, and constant-speed running trials to establish the maximal lactate steady state (MLSS). Stryd running power stability, sensitivity, and reliability were evaluated near the MLSS. Stryd running power was also compared to running speed, V·O2, and metabolic power measures to estimate running mechanical efficiency (EFF) and to determine the efficacy of using Stryd to delineate exercise intensities, quantify aerobic fitness, and estimate running economy (RE). Stryd running power was strongly associated with V·O2 (R2 = 0.84; p < 0.001) and running speed at the MLSS (R2 = 0.91; p < 0.001). Stryd running power measures were strongly correlated with RE at the MLSS when combined with metabolic data (R2 = 0.79; p < 0.001) but not in isolation from the metabolic data (R2 = 0.08; p = 0.313). Measures of running EFF near the MLSS were not different across intensities (~21%; p > 0.05). In conclusion, although Stryd could not quantify RE in isolation, it provided a stable, sensitive, and reliable metric that can estimate aerobic fitness, delineate exercise intensities, and approximate the metabolic requirements of running near the MLSS.

Select human milk oligosaccharide supplementation in post-weanling rats affects metabolism and gut microbiota into adulthood.

OBJECTIVE: Feeding infants with human milk versus formula can produce long-lasting benefits, including reduced risk of inflammatory diseases. Most infant formulas do not contain human milk oligosaccharides (HMOs), which are important carbohydrates in human breast milk displaying prebiotic properties. The study's aim was to examine the effect of select HMOs in the post-weaning period. METHODS: Metabolic and microbial outcomes were measured in female and male rats whose post-weaning diet was supplemented with 3'sialyllactose and 2'-O-fucosyllactose (low dose, 0.75% of each, or high dose, 2% of each). It was determined whether exposure to the HMOs would attenuate metabolic dysfunction associated with a high fat/sucrose (HFS) diet. RESULTS: HMO supplementation resulted in dose-dependent and sex-dependent effects, with the high HMO female group displaying reduced food intake and percentage body fat and an increase in Blautia abundance. Early life HMO supplementation did not prevent the effects of an HFS diet on metabolic outcomes; however, rats that received high dose HMOs followed by the HFS diet were the only HFS group that maintained a measurable abundance of Blautia. CONCLUSIONS: This study highlights the potential for HMOs in follow-up infant formulas. Further investigation should include variable HMO mixtures and doses to optimize infant nutrition at this critical stage.

A "Step-Ramp-Step" Protocol to Identify Running Speed and Power Associated with the Maximal Metabolic Steady State.

PURPOSE: A previously established Step-Ramp-Step (SRS) exercise protocol was able to accurately predict the work rate associated with the maximal metabolic steady state (MMSS) in cyclists. The purpose of this study was to determine whether a modified SRS protocol could predict the running speed and power associated with the MMSS. METHODS: Fifteen (8 male; 7 female) runners (V̇O 2max 54.5 [6.5] mL·kg -1 ·min -1 ) were recruited for this investigation composed of four to five visits. In the first visit, runners performed a moderate intensity step (MOD), an incremental exercise test, and a heavy intensity step (HVY), on a motorized treadmill. This SRS protocol was used to predict the running speed and power associated with the MMSS (i.e., the SRS-MMSS), where running power was assessed by a wearable device (Stryd) attached to each runner's shoe. Subsequent visits were used to confirm the maximal lactate steady state (MLSS) as a proxy measure of the MMSS (i.e., the MLSS-MMSS) and to validate the SRS-MMSS speed and power estimates. RESULTS: The estimated SRS-MMSS running speed (7.2 [0.6] mph) was significantly lower than confirmed running speed at MLSS-MMSS (7.5 [0.8] mph; bias = 3.6%, P = 0.005); however, the estimated SRS-MMSS running power (241 [35] W) was not different than the MLSS-MMSS confirmed running power (240 [37] W; bias = -0.6%; P = 0.435). V̇O 2 at SRS-MMSS (3.22 [0.49] L·min -1 ) was not different than respiratory compensation point (3.26 [0.58] L·min -1 ; P = 0.430). Similarly, V̇O 2 at MLSS-MMSS (3.30 [0.54] L·min -1 ) was not different than respiratory compensation point ( P = 0.438). CONCLUSIONS: The SRS protocol allows MMSS, as measured by MLSS, to be accurately determined using running power (Stryd), but not speed, in a single laboratory visit.

Unlocking a novel determinant of athletic performance: The role of the gut microbiota, short-chain fatty acids, and "biotics" in exercise.

The gut microbiota refers to the collection of trillions of intestinal microorganisms that modulate central aspects of health and disease through influential effects on host physiology. Recently, a connection has been made between the gut microbiota and exercise. Initial investigations demonstrated the beneficial effects of exercise on the gut microbiota, with cross-sectional studies revealing positive correlations between exercise-associated states, and healthy gut microbiota and exercise interventions showed post-intervention increases in the abundance of beneficial bacterial taxa. More recent investigations have focused on exploring the reverse relationship: the influence of the gut microbiota on exercise performance. Murine investigations have revealed that certain bacterial taxa may enhance endurance exercise performance by augmenting various aspects of lactate metabolism. Further, short-chain fatty acids-which modulate metabolism at various organ sites, including within skeletal muscle-have been shown to enhance endurance exercise capacity in mice. This review highlights what is currently known about the connection between the gut microbiota and exercise, with a particular focus on the ergogenic potential of the gut microbiota and how it may be leveraged to enhance endurance exercise performance.

Exercise and Prebiotic Fiber Provide Gut Microbiota-Driven Benefit in a Survivor to Germ-Free Mouse Translational Model of Breast Cancer.

The gut microbiota plays a role in shaping overall host health and response to several cancer treatments. Factors, such as diet, exercise, and chemotherapy, can alter the gut microbiota. In the present study, the Alberta Cancer Exercise (ACE) program was investigated as a strategy to favorably modify the gut microbiota of breast cancer survivors who had received chemotherapy. Subsequently, the ability of post-exercise gut microbiota, alone or with prebiotic fiber supplementation, to influence breast cancer outcomes was interrogated using fecal microbiota transplant (FMT) in germ-free mice. While cancer survivors experienced little gut microbial change following ACE, in the mice, tumor volume trended consistently lower over time in mice colonized with post-exercise compared to pre-exercise microbiota with significant differences on days 16 and 22. Beta diversity analysis revealed that EO771 breast tumor cell injection and Paclitaxel chemotherapy altered the gut microbial communities in mice. Enrichment of potentially protective microbes was found in post-exercise microbiota groups. Tumors of mice colonized with post-exercise microbiota exhibited more favorable cytokine profiles, including decreased vascular endothelial growth factor (VEGF) levels. Beneficial microbial and molecular outcomes were augmented with prebiotic supplementation. Exercise and prebiotic fiber demonstrated adjuvant action, potentially via an enhanced anti-tumor immune response modulated by advantageous gut microbial shifts.

Dietary fiber combinations to mitigate the metabolic, microbial, and cognitive imbalances resulting from diet-induced obesity in rats.

Dietary fiber promotes a healthy gut microbiome and shows promise in attenuating the unfavorable microbial changes resulting from a high-fat/sucrose (HFS) diet. High-fiber diets consisting of oligofructose alone (HFS/O) or in combination with ß-glucan (HFS/OB), resistant starch (HFS/OR), or ß-glucan and resistant starch (HFS/OBR) were fed to diet-induced obese rats for 8 weeks to determine if these fibers could attenuate the obese phenotype. Only the HFS/O group displayed a decrease in body weight and body fat, but all fiber interventions improved insulin sensitivity and cognitive function. The HFS/O diet was the least effective at improving cognitive function and only the HFS/OB group showed improvements in glucose tolerance, thus highlighting the differential effects of fiber types. Hippocampal cytokines (IL-6, IL-10) were more pronounced in the HFS/OB group which coincided with the most time spend in the open arms of the elevated plus maze. All fiber groups showed an increase in beneficial Bifidobacterium and Lactobacillus abundance while the HFS group showed higher abundance of Clostridium. Fecal microbiota transplant from fiber-treated rats into germ-free mice did not alter body composition in the mice but did result in a higher abundance of Bacteroides in the HFS/O and HFS/OB groups compared to HFS. The HFS/OB recipient mice also had higher insulin sensitivity compared to the other groups. This study highlights the influence of dietary fiber type on metabolic and cognitive outcomes suggesting that the type of supplementation (single or combined fibers) could be tailored to specific targeted outcomes.

Effect of supplementation with select human milk oligosaccharides on artificially reared newborn rats.

Early life nutrition fundamentally influences neonatal development and health. Human milk oligosaccharides (HMO) are key components of breast milk but not standard infant formula that support the establishment of the newborn gut microbiota. Using an artificial rearing system, our objective was to test the effect of two HMO on the whole body and organ growth, adiposity, glucose tolerance and faecal microbiota in young rat pups. From postnatal days 4 to 21, Sprague-Dawley rats were randomised to receive one of: (1) CTR (rat milk substitute); (2) 2'FL (CTR + 1·2 g/l 2'-fucosyllactose); (3) 3'SL (CTR + 1·2 g/l 3'-sialyllactose) and (4) 2'FL + 3'SL (CTR + 0·6 g/l 2'-FL + 0·6 g/l 3'-SL). Body weight (BW), bowel movements and food intake were monitored daily, faecal samples collected each week and oral glucose tolerance, body composition and organ weight measured at weaning. No significant differences were observed between groups in growth performance, body composition, organ weight and abundance of dominant faecal microbes. A decreased relative abundance of genus Proteus in week 1 faecal samples and Terrisporobacter in week 3 faecal samples (P < 0·05) was suggestive of a potential pathogen inhibitory effect of 3'SL. Longitudinal changes in the faecal microbiota of artificially reared suckling rats were primarily governed by age (P = 0·001) and not affected by the presence of 2'-FL and/or 3'-SL in rat milk substitutes (P = 0·479). Considering the known protective effects of HMO, further investigation of supplementation with these and other HMO in models of premature birth, extremely low BW or malnutrition may show more pronounced outcomes.

C-section birth increases offspring obesity risk dependent on maternal diet and obesity status in rats.

OBJECTIVE: The gut microbiota is a complex ecosystem that shapes host metabolism, especially in early life. Maternal vaginal and gut microbiota is vertically transmitted to offspring during natural birth. Offspring born by cesarean section (CS) do not receive these bacteria and exhibit higher obesity risk later in life. The objective of this study was to examine differences in obesity risk between offspring born naturally (NB) or by CS to lean/obese dams. METHODS: Lean and obese rat dams gave birth to offspring naturally or by CS. Offspring obesity risk was analyzed via body weight/composition, food intake, sucrose preference, gut microbiota, and gene expression in gut and brain tissues. RESULTS: Obese (O)+CS offspring showed greater weight gain and caloric intake but a reduction in hypothalamic agouti related neuropeptide, neuropeptide Y, and interleukin 1ß expression compared with O+NB offspring. Lean (L)+CS offspring had higher serum corticosterone concentration and reduced liver peroxisome proliferator-activated receptor γ expression compared with L+NB. O+CS offspring had long-term alterations to gut microbiota, including increased relative abundance of Faecalibaculum and reduced Muribaculaceae. CONCLUSIONS: Overall, CS alters obesity risk differentially based on maternal obesity status. Further studies looking at the risks of obesity associated with CS are needed, with special attention paid to maternal obesity status and gut microbiota.