Running is a common form of activity worldwide, and participants range from"weekend warriors"to Olympians. Unfortunately, few studies have examined efficacy of various ergogenic aids in runners because the majority of the literature consists of cycling-based protocols, which do not relate to running performance. The majority of running studies conducted markedly vary in regards to specific distance completed, subject fitness level, and effectiveness of the ergogenic aid examined. The aim of this article was to systematically examine the literature concerning utility of several ergogenic aids on middle-distance running (400-5,000 m) and long-distance running (10,000 meters marathon = 42.2 km) performance. In addition, this article highlights the dearth of running-specific studies in the literature and addresses recommendations for future research to optimize running performance through nutritional intervention. Results revealed 23 studies examining effects of various ergogenic aids on running performance, with a mean Physiotherapy Evidence Database score equal to 7.85± 0.70. Of these studies, 71% (n = 15) demonstrated improved running performance with ergogenic aid ingestion when compared with a placebo trial. The most effective ergogenic aids for distances from 400 m to 40 km included sodium bicarbonate (4 studies; 1.5 ± 1.1% improvement), sodium citrate (6 studies; 0.3 ± 1.7% improvement), caffeine (CAFF) (7 studies; 1.1 ± 0.4% improvement), and carbohydrate (CHO) (6 studies; 4.1 ± 4.4% improvement). Therefore, runners may benefit from ingestion of sodium bicarbonate to enhance middle distance performance and caffeine and carbohydrate to enhance performance at multiple distances.

Theoretically, we humans should be better adapted physiologically to the diet our ancestors were exposed to during millions of years of hominid evolution than to the diet we have been eating since the agricultural revolution a mere 10,000 years ago, and since industrialization only 200 years ago. Among the many health problems resulting from this mismatch between our genetically determined nutritional requirements and our current diet, some might be a consequence in part of the deficiency of potassium alkali salts (K-base), which are amply present in the plant foods that our ancestors ate in abundance, and the exchange of those salts for sodium chloride (NaCl), which has been incorporated copiously into the contemporary diet, which at the same time is meager in K-base-rich plant foods. Deficiency of K-base in the diet increases the net systemic acid load imposed by the diet. We know that clinically-recognized chronic metabolic acidosis has deleterious effects on the body, including growth retardation in children, decreased muscle and bone mass in adults, and kidney stone formation, and that correction of acidosis can ameliorate those conditions. Is it possible that a lifetime of eating diets that deliver evolutionarily superphysiologic loads of acid to the body contribute to the decrease in bone and muscle mass, and growth hormone secretion, which occur normally with age? That is, are contemporary humans suffering from the consequences of chronic, diet-induced low-grade systemic metabolic acidosis? Our group has shown that contemporary net acid-producing diets do indeed characteristically produce a low-grade systemic metabolic acidosis in otherwise healthy adult subjects, and that the degree of acidosis increases with age, in relation to the normally occurring age-related decline in renal functional capacity. We also found that neutralization of the diet net acid load with dietary supplements of potassium bicarbonate (KHCO3) improved calcium and phosphorus balances, reduced bone resorption rates, improved nitrogen balance, and mitigated the normally occurring age-related decline in growth hormone secretion--all without restricting dietary NaCl. Moreover, we found that co-administration of an alkalinizing salt of potassium (potassium citrate) with NaCl prevented NaCl from increasing urinary calcium excretion and bone resorption, as occurred with NaCl administration alone. Earlier studies estimated dietary acid load from the amount of animal protein in the diet, inasmuch as protein metabolism yields sulfuric acid as an end-product. In cross-cultural epidemiologic studies, Abelow found that hip fracture incidence in older women correlated with animal protein intake, and they suggested a causal relation to the acid load from protein. Those studies did not consider the effect of potential sources of base in the diet. We considered that estimating the net acid load of the diet (i. e., acid minus base) would require considering also the intake of plant foods, many of which are rich sources of K-base, or more precisely base precursors, substances like organic anions that the body metabolizes to bicarbonate. In following up the findings of Abelow et al., we found that plant food intake tended to be protective against hip fracture, and that hip fracture incidence among countries correlated inversely with the ratio of plant-to-animal food intake. These findings were confirmed in a more homogeneous population of white elderly women residents of the U.S. These findings support affirmative answers to the questions we asked above. Can we provide dietary guidelines for controlling dietary net acid loads to minimize or eliminate diet-induced and age-amplified chronic low-grade metabolic acidosis and its pathophysiological sequelae. We discuss the use of algorithms to predict the diet net acid and provide nutritionists and clinicians with relatively simple and reliable methods for determining and controlling the net acid load of the diet. A more difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.

Hypoxia-inducible factor-1 (HIF-1) is a heterodimer transcription factor whose elevated activity in many cancers helps them to survive under hypoxic conditions and enhances their capacity to grow invasively, establish metastases, and survive chemo- or radiotherapy. Optimal intracellular levels of ascorbate suppress the level and transcriptional activity of HIF-1under normoxic or mildly hypoxic conditions by supporting the activity of proly and asparagyl hydroxylases that target HIF-1alpha. High intracellular ascorbate can also work in various ways to down-regulate activation of NF-kappaB which, like HIF-1 is constitutively active in many cancers and promotes aggressive behavior - in part by promoting transcription of HIF-1alpha. Yet recent evidence suggests that, even in the context of adequate ascorbate nutrition, the intracellular ascorbate content of many aggressive cancers may be supoptimal for effective HIF-1 control. This likely reflects low expression or activity of the SVCT2 ascorbate transporter. The expression of SVCT2 in cancers has so far received little study; but the extracellular acidity characteristic of many tumors would be expected to reduce the activity of this transporter, which has a mildly alkaline pH optimum. Unfortunately, since SVCT2 has a high affinity for ascorbate, and its activity is nearly saturated at normal healthy serum levels of this vitamin, increased oral administration of ascorbate would be unlikely to have much impact on the intracellular ascorbate content of tumors. However, cancers in which HIF-1 is active express high levels of glucose transporters such as GLUT-1, and these transporters can promote influx of dehydroascorbic acid (DHA) via facilitated diffusion; once inside the cell, DHA is rapidly reduced to ascorbate, which effectively is"trapped"within the cell. Hence, episodic intravenous infusions of modest doses of DHA may have potential for optimizing the intracellular ascorbate content of cancers, potentially rendering them less aggressive. Indeed, several published studies have concluded that parenteral DHA--sometimes in quite modest doses--can retard the growth of transplanted tumors in rodents. As an alternative or adjunctive strategy, oral administration of sodium bicarbonate, by normalizing the extracellular pH of tumors, has the potential to boost the activity of SCTV2 in tumor cells, thereby promoting increased ascorbate uptake. Indeed, the utility of oral sodium bicarbonate for suppressing metastasis formation in nude mice xenografted with a human breast cancer has been reported. Hence, oral sodium bicarbonate and intravenous DHA may have the potential to blunt the aggressiveness of certain cancers in which suboptimal intracellular ascorbate levels contribute to elevated HIF-1 activity.

This study evaluated the ingestion of sodium bicarbonate (NaHCO3) on post-exercise acid-base balance recovery kinetics and subsequent high-intensity cycling time to exhaustion. In a counterbalanced, crossover design, nine healthy and active males (age: 23±2 years, height: 179±5 cm, body mass: 74±9 kg, peak mean minute power (WPEAK) 256±45 W, peak oxygen uptake (V̇O2PEAK) 46±8 ml.kg(-1).min(-1)) performed a graded incremental exercise test, two familiarisation and two experimental trials. Experimental trials consisted of cycling to volitional exhaustion (TLIM1) at 100% WPEAK on two occasions (TLIM1 and TLIM2) interspersed by a 90 min passive recovery period. Using a double blind approach, 30 min into a 90 min recovery period participants ingested either 0.3 g.kg(-1) body mass sodium bicarbonate (NaHCO3) or a placebo (PLA) containing 0.1 g.kg(-1) body mass sodium chloride (NaCl) mixed with 4 ml.kg(-1) tap water and 1 ml.kg(-1) orange squash. The mean differences between TLIM2 and TLIM1 was larger for PLA compared to NaHCO3 (-53±53 vs. -20±48 s; P=0.008, d=0.7, CI=-0.3, 1.6), indicating superior subsequent exercise time to exhaustion following NaHCO3. Blood lactate [BLa(-)] was similar between treatments post TLIM1, but greater for NaHCO3 post TLIM2 and 5 min post TLIM2. Ingestion of NaHCO3 induced marked increases (P<0.01) in both blood pH (+0.07±0.02, d=2.6, CI=1.2, 3.7) and bicarbonate ion concentration [HCO3(-)] (+6.8±1.6 mmo.l(-1), d=3.4, CI=1.8, 4.7) compared to the PLA treatment, prior to TLIM2. It is likely both the acceleration of recovery, and the marked increases of acid-base after TLIM1 contributed to greater TLIM2 performancecompared to the PLA condition.

The results of an exploratory, multicenter clinical study confirmed the hypothesis that a novel, natural, and safe oral care product (OCP) reduced the rate of plaque formation on teeth of dogs consuming the OCP (antimicrobial plant-derived enzymes, organic matcha green tea, cultured dextrose, sodium bicarbonate, and ascorbic acid) compared to controls. Healthy dogs without periodontitis, of varying breeds, sex, and age, were recruited and enrolled, using nonrandomized stratification methods, into a control and treatment groups. Treatment group dogs drank only water into which OCP was suspended, for 28 days. Control group dogs drank their normal household water. On day 0 all teeth were cleaned by a veterinarian and gingivitis was assessed. On days 14, 21, and 28 plaque index, plaque thickness, gingivitis, freshness of breath, and general health were assessed. Over the 28 days of study, dogs on the OCP had significant reduction in plaque index and plaque thickness compared to controls. By day 14 OCP reduced plaque formation by 37%; the 28-day reduction in plaque index and coverage averaged 22% with no measurable gingivitis or calculus. Conclusion. Using the OCP attenuated dental plaque formation when consumed as normal drinking water and in the absence of other modes of oral care.

We tested the hypothesis that ingestion of sodium bicarbonate (NaHCO3) prior to an acute session of high-intensity interval training (HIIT) would augment signalling cascades and gene expression linked to mitochondrial biogenesis in human skeletal muscle. On two occasions separated by ~1 wk, nine men (22±2 y; 78±13 kg, VO2peak = 48±8 mL kg(-1) min(-1); mean ± SD) performed 10x60-s cycling efforts at an intensity eliciting ~90% of maximal heart rate (263±40 W), interspersed with 60 s of recovery. In a double-blind, crossover manner, subjects ingested a total of 0.4 g kg b.w.(-1) NaHCO3 prior toexercise (BICARB) or an equimolar amount of the placebo, sodium chloride (PLAC). Venous blood bicarbonate and pH were elevated at all time points post-ingestion (p<0.05) in BICARB vs. PLAC. During exercise, muscle glycogen utilization (126±47 vs. 53±38 mmol kg d.w.(-1); p<0.05) and blood lactate accumulation (12.8±2.6 vs. 10.5±2.8 mmol L(-1); p<0.05) were greater in BICARB vs. PLAC. The acute exercise-induced increase in the phosphorylation of acetyl-CoA carboxylase, a downstream marker of AMP-activated protein kinase activity, and p38 mitogen-activated protein kinase were similar between treatments (p>0.05). However, the increase in PGC-1α mRNA expression after 3 h of recovery was higher in BICARB vs. PLAC (~7- vs. 5-fold compared to rest, p<0.05). We conclude that NaHCO3 prior to HIIT alters the mRNA expression of this key regulatory protein associated with mitochondrial biogenesis. The elevated PGC-1α mRNA response provides a putative mechanism to explain the enhanced mitochondrial adaptation seen after chronic NaHCO3-supplemented HIIT in rats.

BACKGROUND:Sodium bicarbonate intake has been shown to improve exercise tolerance, but the effects on high-intensity intermittent exercise are less clear. Thus, the aim of the present study was to determine the effect of sodium bicarbonate intake on Yo-Yo intermittent recovery test level 2 performance in trained young men.

METHOD:Thirteen men aged 23 ± 1 year (height: 180 ± 2 cm, weight: 78 ± 3 kg; VO2max: 61.3 ± 3.3 mlO2 · kg(-1) · min(-1); means ± SEM) performed the Yo-Yo intermittent recovery test level 2 (Yo-Yo IR2) on two separate occasions in randomized order with (SBC) and without (CON) prior intake ofsodium bicarbonate (0.4 g · kg(-1) body weight). Heart rate and rating of perceived exertion (RPE) were measured during the test and venous blood samples were taken frequently.

RESULTS:Yo-Yo IR2 performance was 14 % higher (P = 0.04) in SBC than in CON (735 ± 61 vs 646 ± 46 m, respectively). Blood pH and bicarbonate were similar between trials at baseline, but higher (P = 0.003) immediately prior to the Yo-Yo IR2 test in SBC than in CON (7.44 ± 0.01 vs 7.32 ± 0.01 and 33.7 ± 3.2 vs 27.3 ± 0.6 mmol · l(-1), respectively). Blood lactate was 0.9 ± 0.1 and 0.8 ± 0.1 mmol · l(-1) at baseline and increased to 11.3 ± 1.4 and 9.4 ± 0.8 mmol · l(-1) at exhaustion in SBC and CON, respectively, being higher (P = 0.03) in SBC. Additionally, peak bloodlactate was higher (P = 0.02) in SBC than in CON (11.7 ± 1.2 vs 10.2 ± 0.7 mmol · l(-1)). Blood glucose, plasma K(+) and Na(+) were not different between trials. Peak heart rate reached at exhaustion was 197 ± 3 and 195 ± 3 bpm in SBC and CON, respectively, with no difference between conditions. RPE was 7% lower (P = 0.003) in SBC than in CON after 440 m, but similar at exhaustion (19.3 ± 0.2 and 19.5 ± 0.2).

CONCLUSION:In conclusion, high-intensity intermittent exercise performance is improved by prior intake of sodium bicarbonate in trained young men, with concomitant elevations in blood alkalosis and peak blood lactate levels, as well as lowered rating of perceived exertion.

BACKGROUND:Sodium bicarbonate and ascorbic acid have been proposed to prevent contrast-induced nephropathy (CIN). The present study evaluated the effect of their combined use on CIN incidence.Methods and Results:We prospectively enrolled 429 patients with chronic kidney disease (CKD: baseline estimated glomerular filtration rate<60 mL/min/1.73 m(2)) prior to elective coronary catheterization. CIN was defined as absolute (≥0.5 mg/dL) or relative (≥25%) increase in serum creatinine within 72 h. In the saline hydration (n=218) and combined sodium bicarbonate+ascorbic acid (n=211) groups, a total of 1,500-2,500 mL 0.9% saline was given before and after the procedure. In addition, the combination group received 20 mEq sodium bicarbonate and 3 g ascorbic acid i.v. before the procedure, followed by 2 g ascorbic acid after the procedure and a further 2 g after 12 h. There were no significant differences between the basic characteristics and contrast volume in the 2 groups. CIN occurred in 19 patients (8.7%) in thesaline group, and in 6 patients (2.8%) in the combined treatment group (P=0.008).

CONCLUSIONS:Combined sodium bicarbonate and ascorbic acid could prevent CIN following catheterization in CKD patients.

Heat stress is exacerbated by global warming and affects human and animal health, leading to heart damage caused by imbalances in reactive oxygen species (ROS) and the antioxidant system, acid-base chemistry, electrolytes and respiratory alkalosis. Vitamin C scavenges excess ROS, and sodium bicarbonate maintains acid-base and electrolyte balance, and alleviates respiratory alkalosis. Herein, we explored the ability of vitamin C alone and in combination with equimolar sodium bicarbonate (Vitamin C-Na) to stimulate endogenous antioxidants and heat shock proteins (HSPs) to relieve heat stress in H9C2 cells. Control, vitamin C (20 μg/ml vitamin C for 16 h) and vitamin C-Na (20 μg/ml vitamin C-Na for 16 h) groups were heat-stressed for 1, 3 or 5 h. Granular and vacuolar degeneration, karyopyknosis and damage to nuclei and mitochondria were clearly reduced in treatment groups, as were apoptosis, lactate dehydrogenase activity and ROS and malondialdehyde levels, while superoxide dismutase activity was increased. Additionally, CRYAB, Hsp27, Hsp60 and Hsp70 mRNA levels were upregulated at 3 h (p < 0.01), and protein levels were increased for CRYAB at 0 h (p < 0.05) and 1 h (p < 0.01), and for Hsp70 at 3 and 5 h (p < 0.01). Thus, pre-treatment with vitamin C or vitamin C-Na might protect H9C2 cells against heat damage by enhancing the antioxidant ability and upregulating CRYAB and Hsp70.