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European Journal of Sport Science Jun 2023This study aimed to investigate the isolated effects of NaHCO on cycling time-trial performance. Furthermore, we investigated whether the ingestion time of NaHCO,... (Meta-Analysis)
Meta-Analysis
This study aimed to investigate the isolated effects of NaHCO on cycling time-trial performance. Furthermore, we investigated whether the ingestion time of NaHCO, standardized or individualized based on time to peak, could be effective in improving cycling time-trial performance. A systematic review was carried out on randomized placebo-controlled studies. A random-effects meta-analysis assessed the standardized mean difference (SMD) between NaHCO and placebo conditions. Eighteen studies were qualitatively (systematic review) and quantitatively (meta-analysis) analysed concerning mean power output (W) ( = 182) and time performance ( = 201). The reviewed studies showed a low risk of bias and homogenous results for W (I = 0%) and performance time (I= 0%). Overall, when compared to placebo, the NaHCO ingestion improved the W (SMD: 0.42; 95% CI: 0.21-0.63; = 0.001) and performance time (SMD: 0.22; 95% CI: 0.02-0.43; = 0.03). Similarly, the NaHCO ingestion using a time-to-peak strategy improved the W (SMD: 0.39; 95% CI: 0.03-0.75; = 0.04; I= 15%) and performance time (SMD: 0.34; 95% CI: 0.07-0.61, = 0.01, I= 0%). The present findings reveal that NaHCO ingestion has the potential to increase the overall performance time and W in cycling time trials.NaHCO is an effective strategy to increase cycling time-trial performance.The standardized protocol did not improve the cycling time-trial performance parameters.The individualized time-to-peak NaHCO ingestion has a positive effect on time and W during cycling time-trial performance.
Topics: Humans; Sodium Bicarbonate; Randomized Controlled Trials as Topic; Bicycling; Eating
PubMed: 35633035
DOI: 10.1080/17461391.2022.2071171 -
Case Reports in Medicine 2019Gitelman syndrome is one of the few inherited causes of metabolic alkalosis due to salt losing tubulopathy. It is caused by tubular defects at the level of distal...
Gitelman syndrome is one of the few inherited causes of metabolic alkalosis due to salt losing tubulopathy. It is caused by tubular defects at the level of distal convoluted tubules, mimicking a thiazide-like tumor. It usually presents in late childhood or in teenage as nonspecific weakness, fatigability, polyuria, and polydipsia but very rarely with seizures. It is classically associated with hypokalemia, hypomagnesemia, hypocalciuria, hyperreninemia, and hyperaldosteronism. However, less frequently, it can present with normal magnesium levels. It is even rarer to find normomagnesemic patients of GS who develop seizures as the main complication since hypomagnesemia is considered the principal etiology of abnormal foci of seizure-related brain activity in GS cases. Interestingly, patients with GS are oftentimes diagnosed during pregnancy when the classic electrolyte pattern consistent with GS is noticed. Our case presents GS with normal serum magnesium in a patient, with seizures being the main clinical presentation. We also did a comprehensive literature review of 122 reported cases to show the prevalence of normal magnesium in GS cases and an overview of clinical and biochemical variability in GS. We suggest that further studies and in-depth analysis are required to understand the pathophysiology of seizures in GS patients with both normal and low magnesium levels.
PubMed: 30867665
DOI: 10.1155/2019/4204907