Induced Metabolic Acidosis by Ammonium Chloride: Action Mechanisms, Dose and Effects on Athletic Performance

Correia-Oliveira, Carlos Rafaell; Kiss, Maria Augusta P. D.

doi:10.4025/jphyseduc.v28i1.2860

Cited by 3 publications

(2 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3). Blood lactate concentrations are also decreased in acidosis, likely due to the attenuation of glycolytic activity [23]. This may negatively impact training adaptations as lactate signaling can influence mitochondrial biogenesis [24] and the chronic adaptive response to training [25].…”

Section: Buffering Agentsmentioning

confidence: 99%

Effects of Dietary Supplements on Adaptations to Endurance Training

Rothschild

Bishop

2019

Sports Med

View full text Add to dashboard Cite

Endurance training leads to a variety of adaptations at the cellular and systemic levels that serve to minimise disruptions in whole-body homeostasis caused by exercise. These adaptations are differentially affected by training volume, training intensity, and training status, as well as by nutritional choices that can enhance or impair the response to training. A variety of supplements have been studied in the context of acute performance enhancement, but the effects of continued supplementation concurrent to endurance training programs are less well characterised. For example, supplements such as sodium bicarbonate and beta-alanine can improve endurance performance and possibly training adaptations during endurance training by affecting buffering capacity and/or allowing an increased training intensity, while antioxidants such as vitamin C and vitamin E may impair training adaptations by blunting cellular signaling but appear to have little effect on performance outcomes. Additionally, limited data suggest the potential for dietary nitrate (in the form of beetroot juice), creatine, and possibly caffeine, to further enhance endurance training adaptation. Therefore, the objective of this review is to examine the impact of dietary supplements on metabolic and physiological adaptations to endurance training. Abstract word count: 185 Word count: 6,498 Number of tables: 5 Number of figures: 4 Key Points  Many supplements have been studied in the context of acute performance enhancement, but the effects of continued supplementation concurrent to endurance training programs are less well characterised.  Supplements including sodium bicarbonate, beta-alanine, dietary nitrates, antioxidants, caffeine, and creatine have the potential to modify the adaptive response to endurance training (either positively or negatively) by affecting acidbase balance, redox status, oxidant signaling, or cumulative training load, thereby affecting the cellular signaling responses to training.

show abstract

Section: Buffering Agentsmentioning

confidence: 99%

Effects of Dietary Supplements on Adaptations to Endurance Training

Rothschild

Bishop

2019

Sports Med

View full text Add to dashboard Cite

show abstract

“…[NH 3 ] on the other hand being a weak base with a dissociation constant (kb) of 1.80 × 10 −5 will only partially ionize to produce ammonium cations and hydroxide anions. Therefore, a decrease in pH and the HCO 3 - concentrations is expected after the NH 4 Cl administration [ 22 ]. The blood pressure measurements of the conscious rats by a tail-cuff showed an increase in the mean arterial pressure starting at week 5, and it was sustained through week 8 in the acidotic rats as compared to that of the control group.…”

Section: Discussionmentioning

confidence: 99%

Chronic Metabolic Acidosis Elicits Hypertension via Upregulation of Intrarenal Angiotensin II and Induction of Oxidative Stress

et al. 2020

View full text Add to dashboard Cite

Chronic metabolic acidosis (CMA) can be a consequence of persistent hypertension but could potentially play a role in invoking hypertension. Currently, there is a scarcity of studies examining the outcome of induced chronic acidosis on blood pressure regulation. This study investigates CMA as a cause of hypertension. Chronic acidosis was induced in Sprague Dawley rats (100–150 g) by providing a weak acid solution of 0.28 M ammonium chloride (NH4Cl) in tap water for 8 weeks. To determine whether the rats were acidotic, blood pH was measured, while blood pressure (BP) was monitored by tail-cuff plethysmography weekly. Rats were divided into five groups: control, CMA, CMA ± spironolactone, captopril, and tempol. Serum sodium and potassium; renal interstitial fluid (for Angiotensin II concentration); and kidney proximal tubules (for Na+/K+ ATPase- α1 concentration) were analyzed. Reactive oxygen species (ROS) were detected in renal cortical homogenates using electron paramagnetic resonance (EPR). In the CMA rats, a sustained elevation in mean arterial pressure (MAP) associated with a significant decrease in blood pH was observed compared to that of control over the 8 weeks. A significant decrease in MAP was observed in acidotic rats treated with captopril/tempol, whereas spironolactone treatment caused no decrease in MAP as compared to that of the CMA group. The interstitial angiotensin II was increased in the CMA group but decreased in the CMA with captopril and tempol groups. In addition, the urinary sodium was decreased, and the serum sodium levels increased significantly in the CMA groups as compared to that of control. However, the acidotic groups with captopril and tempol showed reduced levels of serum sodium and an elevation in urinary sodium as compared to that of the CMA group. In addition, there was a significant increase in plasma renin and no change in plasma aldosterone in the CMA group with no significant differences in plasma renin or aldosterone observed during spironolactone, captopril, or tempol treatments. The increased expression of Na+/K+ ATPase-α1 in the CMA group suggests that active transport of Na+ to the blood could be causative of the observed hypertension. Furthermore, the EPR analysis confirmed an elevation in superoxide (O2-) radical levels in the CMA group, but the tempol/captopril treated acidotic groups showed less (O2-) compared to that of either the CMA group or control. Taken together, our data suggest that induction of CMA could potentially be causative of hypertension, while the mechanisms underlying the increased BP could be through the activation of intrarenal Ang II and induction of oxidative stress.

show abstract

Caffeine Combined With Sodium Bicarbonate Improves Pacing and Overall Performance During a High-Intensity Time Trial

Correia-Oliveira

Franchini

2022

Research Quarterly for Exercise and Sport

View full text Add to dashboard Cite

Induced Metabolic Acidosis by Ammonium Chloride: Action Mechanisms, Dose and Effects on Athletic Performance

Cited by 3 publications

References 25 publications

Effects of Dietary Supplements on Adaptations to Endurance Training

Effects of Dietary Supplements on Adaptations to Endurance Training

Chronic Metabolic Acidosis Elicits Hypertension via Upregulation of Intrarenal Angiotensin II and Induction of Oxidative Stress

Caffeine Combined With Sodium Bicarbonate Improves Pacing and Overall Performance During a High-Intensity Time Trial

Contact Info

Product

Resources

About