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The aim of the current study was to investigate interindividual differences in muscle thickness of the rectus femoris (MTRF) following 12 wk of resistance training (RT) or high-intensity interval training (HIIT) to explore the genetic architecture underlying skeletal muscle hypertrophy and to construct predictive models. We conducted musculoskeletal ultrasound assessments of the MTRF response in 440 physically inactive adults after the 12-wk exercise period. A genome-wide association study was used to identify variants associated with the MTRF response, separately for RT and HIIT. Using the polygenic predictor score (PPS), we estimated the genetic contribution to exercise-induced hypertrophy. Predictive models for the MTRF response were constructed using random forest (RF), support vector mac (SVM), and generalized linear model (GLM) in 10 cross-validated approaches. MTRF increased significantly after both RT (8.8%, P < 0.05) and HIIT (5.3%, P < 0.05), but with considerable interindividual differences (RT: -13.5 to 38.4%, HIIT: -14.2 to 30.7%). Eleven lead single-nucleotide polymorphisms in RT and eight lead single-nucleotide polymorphisms in HIIT were identified at a significance level of P < 1 × 10-5. The PPS was associated with the MTRF response, explaining 47.2% of the variation in response to RT and 38.3% of the variation in response to HIIT. Notably, the GLM and SVM predictive models exhibited superior performance compared with RF models (P < 0.05), and the GLM demonstrated optimal performance with an area under curve of 0.809 (95% confidence interval: 0.669-0.949). Factors such as PPS, baseline MTRF, and exercise protocol exerted influence on the MTRF response to exercise, with PPS being the primary contributor. The GLM and SVM predictive model, incorporating both genetic and phenotypic factors, emerged as promising tools for predicting exercise-induced skeletal muscle hypertrophy.NEW & NOTEWORTHY The interindividual variability induced muscle hypertrophy by resistance training (RT) or high-intensity interval training (HIIT) and the associated genetic architecture remain uncertain. We identified genetic variants that underlie RT- or HIIT-induced muscle hypertrophy and established them as pivotal factors influencing the response regardless of the training type. The genetic-phenotype predictive model developed has the potential to identify nonresponders or individuals with low responsiveness before engaging in exercise training.

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PURPOSE: Enteric-coated sodium bicarbonate (NaHCO3) can attenuate gastrointestinal (GI) symptoms following acute bicarbonate loading, although the subsequent effects on exercise performance have not been investigated. The purpose of this study was to examine the effects of enteric-coated NaHCO3 supplementation on high-intensity exercise performance and GI symptoms. METHODS: Eleven trained male cyclists completed three 4 km time trials after consuming; a placebo or 0.3 g∙kg-1 body mass NaHCO3 in enteric-coated or gelatin capsules. Exercise trials were timed with individual peak blood bicarbonate ion concentration ([HCO3-]). Blood acid-base balance was measured pre-ingestion, pre-exercise, and post-exercise, whereas GI symptoms were recorded pre-ingestion and immediately pre-exercise. RESULTS: Pre-exercise blood [HCO3-] and potential hydrogen (pH) were greater for both NaHCO3 conditions (P < 0.0005) when compared to placebo. Performance time was faster with enteric-coated (- 8.5 ± 9.6 s, P = 0.044) and gelatin (- 9.6 ± 7.2 s, P = 0.004) NaHCO3 compared to placebo, with no significant difference between conditions (mean difference = 1.1 ± 5.3 s, P = 1.000). Physiological responses were similar between conditions, although blood lactate ion concentration was higher with gelatin NaHCO3 (2.4 ± 1.7 mmol∙L-1, P = 0.003) compared with placebo. Furthermore, fewer participants experienced GI symptoms with enteric-coated (n = 3) compared to gelatin (n = 7) NaHCO3. DISCUSSION: Acute enteric-coated NaHCO3 consumption mitigates GI symptoms at the onset of exercise and improves subsequent 4 km cycling TT performance. Athletes who experience GI side-effects after acute bicarbonate loading may, therefore, benefit from enteric-coated NaHCO3 supplementation prior to exercise performance.

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Enteric-formulated capsules can mitigate gastrointestinal (GI) side effects following sodium bicarbonate (NaHCO3) ingestion; however, it remains unclear how encapsulation alters postingestion symptoms and acid-base balance. The current study aimed to identify the optimal ingestion form to mitigate GI distress following NaHCO3 ingestion. Trained males (n = 14) ingested 300 mg/kg body mass of NaHCO3 in gelatin (GEL), delayed-release (DEL), and enteric-coated (ENT) capsules or a placebo in a randomized cross-over design. Blood bicarbonate anion concentration, potential hydrogen, and GI symptoms were measured pre- and postingestion for 3 hr. Fewer GI symptoms were reported with ENT NaHCO3 than with GEL (p = .012), but not with DEL (p = .106) in the postingestion phase. Symptom severity decreased with DEL (4.6 ± 2.8 arbitrary units) compared with GEL (7.0 ± 2.6 arbitrary units; p = .001) and was lower with ENT (2.8 ± 1.9 arbitrary units) compared with both GEL (p < .0005) and DEL (p = .044) NaHCO3. Blood bicarbonate anion concentration increased in all NaHCO3 conditions compared with the placebo (p < .0005), although this was lower with ENT than with GEL (p = .001) and DEL (p < .0005) NaHCO3. Changes in blood potential hydrogen were reduced with ENT compared with GEL (p = .047) and DEL (p = .047) NaHCO3, with no other differences between the conditions. Ingestion of ENT NaHCO3 attenuates GI disturbances for up to 3 hr postingestion. Therefore, ENT ingestion forms may be favorable for those who report GI disturbances with NaHCO3 supplementation or for those who have previously been deterred from its use altogether.

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BACKGROUND: Sodium bicarbonate (NaHCO3) is a well-established nutritional ergogenic aid, though gastrointestinal (GI) distress is a common side-effect. Delayed-release NaHCO3 may alleviate GI symptoms and enhance bicarbonate bioavailability following oral ingestion, although this has yet to be confirmed. METHODS: In a randomised crossover design, pharmacokinetic responses and acid-base status were compared following two forms of NaHCO3, as were GI symptoms. Twelve trained healthy males (mean ± SD age 25.8 ± 4.5 years, maximal oxygen uptake ([Formula: see text]) 58.9 ± 10.9 mL kg min-1, height 1.8 ± 0.1 m, body mass 82.3 ± 11.1 kg, fat-free mass 72.3 ± 10.0 kg) underwent a control (CON) condition and two experimental conditions: 300 mg kg-1 body mass NaHCO3 ingested as an aqueous solution (SOL) and encased in delayed-release capsules (CAP). Blood bicarbonate concentration, pH and base excess (BE) were measured in all conditions over 180 min, as were subjective GI symptom scores. RESULTS: Incidences of GI symptoms and overall severity were significantly lower (mean difference = 45.1%, P < 0.0005 and 47.5%, P < 0.0005 for incidences and severity, respectively) with the CAP than with the SOL. Symptoms displayed increases at 40 to 80 min post-ingestion with the SOL that were negated with CAP (P < 0.05). Time to reach peak bicarbonate concentration, pH and BE were significantly longer with CAP than with the SOL. CONCLUSIONS: In summary, CAP can mitigate GI symptoms induced with SOL and should be ingested earlier to induce similar acid-base changes. Furthermore, CAP may be more ergogenic in those who experience severe GI distress with SOL, although this warrants further investigation.

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BACKGROUND: Individual time to peak blood bicarbonate (HCO3-) has demonstrated good to excellent reproducibility following ingestion of both 0.2 g kg-1 body mass (BM) and 0.3 g kg-1 BM sodium bicarbonate (NaHCO3), but the consistency of the time trial (TT) performance response using such an individualised NaHCO3 ingestion strategy remains unknown. This study therefore evaluated the reproducibility of 4-km TT performance following NaHCO3 ingestion individualised to time to peak blood bicarbonate. METHODS: Eleven trained male cyclists completed five randomised treatments with prior ingestion of 0.2 g kg-1 (SBC2) or 0.3 g kg-1 BM (SBC3) NaHCO3, on two separate occasions each, or a control trial entailing no supplementation. Participants completed a 4-km cycling TT on a Velotron ergometer where time to complete, power and speed were measured, whilst acid-base blood parameters were also recorded (pH and blood bicarbonate concentration HCO3-) and lactate [La-]. RESULTS: Alkalosis was achieved prior to exercise in both SBC2 and SBC3, as pH and HCO3- were greater compared to baseline (p < 0.001), with no differences between treatments (p > 0.05). The reproducibility of the mean absolute change from baseline to peak in HCO3- was good in SBC2 (r = 0.68) and excellent in SBC3 (r = 0.78). The performance responses following both SBC2 and SBC3 displayed excellent reproducibility (r range = 0.97 to 0.99). CONCLUSIONS: Results demonstrate excellent reproducibility of exercise performance following individualised NaHCO3 ingestion, which is due to the high reproducibility of blood acid-base variables with repeat administration of NaHCO3. Using a time to peak HCO3- strategy seems to cause no dose-dependent effects on performance for exercise of this duration and intensity; therefore, athletes may consider smaller doses of NaHCO3 to mitigate gastrointestinal (GI) discomfort.