Lactate Buffering Resource
This resource shows a few of the results that show why acid-buffering is becoming such a “sexy” area in
sports science. These strategies allow athletes to stand up to the “acid test”!
Muscle Carnosine Correlates to performance
Suzuki, Y., O. Ito, et al. (2002). "High level of skeletal muscle carnosine contributes to the latter half of
exercise performance during 30-s maximal cycle ergometer sprinting." Jpn J Physiol 52(2): 199-205.
The histidine-containing dipeptide carnosine (beta-alanyl-L-histidine) has been shown to significantly
contribute to the physicochemical buffering in skeletal muscles, which maintains acid-base balance when a
large quantity of H(+) is produced in association with lactic acid accumulation during high-intensity exercise.
The purpose of the present study was to examine the relations among the skeletal muscle carnosine
concentration, fiber-type distribution, and high-intensity exercise performance. The subjects were 11 healthy
men. Muscle biopsy samples were taken from the vastus lateralis at rest. The carnosine concentration was
determined by the use of an amino acid autoanalyzer. The fiber-type distribution was determined by the
staining intensity of myosin adenosinetriphosphatase. The high-intensity exercise performance was assessed
by the use of 30-s maximal cycle ergometer sprinting. A significant correlation was demonstrated between the
carnosine concentration and the type IIX fiber composition (r=0.646, p<0.05). The carnosine concentration was
significantly correlated with the mean power per body mass (r=0.785, p<0.01) during the 30-s sprinting. When
dividing the sprinting into 6 phases (0-5, 6-10, 11-15, 16-20, 21-25, 26-30 s), significant correlations were
observed between the carnosine concentration and the mean power per body mass of the final 2 phases (2125 s: r=0.694, p<0.05; 26-30 s: r=0.660, p<0.05). These results indicated that the carnosine concentration could
be an important factor in determining the high-intensity exercise performance.
Tallon, M. J., R. C. Harris, et al. (2007). "Carnosine, taurine and enzyme activities of human skeletal muscle
fibres from elderly subjects with osteoarthritis and young moderately active subjects." Biogerontology. 8(2):
129-137.
Ageing is associated with a reduction in muscle carnosine (beta-alanyl-L-histidine), but there are no
data on the changes specifically in type I and type II muscle fibres. Given the higher carnosine content of type II
fibers, changes observed in whole muscle may be secondary to a shift in fibre composition. Carnosine, betaalanine, histidine, taurine, and citrate synthase (CS) and glycogen phosphorylase (Phos), were measured in
pools of single muscle fibres from freeze-dried muscle biopsies of vastus lateralis of nine elderly sedentary
subjects (65-80 years) with osteoarthritis of the knee and undergoing total knee replacement, and nine young
moderately active healthy subjects (20-35 years). Fibres were characterised as type I or II by myosin ATPase
activity. Carnosine was 53.2% lower in type II fibres of older subjects resulting in an estimated 7% (and most
probably still higher) decline in intracellular physico-chemical buffering capacity. Younger subjects showed
higher CS activities in type I and higher Phos activities in type II fibres. These differences were less apparent in
elderly subjects. Possible causes for the change in the carnosine content are reduced physical activity, reduced
meat intake, or the result of progressive denervation
Muscle Carnosine Levels and Supplementation
Artioli, G. G., B. Gualano, et al. (2010). "Role of beta-alanine supplementation on muscle carnosine and
exercise performance." Med Sci Sports Exerc 42(6): 1162-1173.
In this narrative review, we present and discuss the current knowledge available on carnosine and
beta-alanine metabolism as well as the effects of beta-alanine supplementation on exercise performance.
Intramuscular acidosis has been attributed to be one of the main causes of fatigue during intense exercise.
Carnosine has been shown to play a significant role in muscle pH regulation. Carnosine is synthesized in
skeletal muscle from the amino acids l-histidine and beta-alanine. The rate-limiting factor of carnosine
synthesis is beta-alanine availability. Supplementation with beta-alanine has been shown to increase muscle
carnosine content and therefore total muscle buffer capacity, with the potential to elicit improvements in
physical performance during high-intensity exercise. Studies on beta-alanine supplementation and exercise
performance have demonstrated improvements in performance during multiple bouts of high-intensity
exercise and in single bouts of exercise lasting more than 60 s. Similarly, beta-alanine supplementation has
been shown to delay the onset of neuromuscular fatigue. Although beta-alanine does not improve maximal
strength or VO2max, some aspects of endurance performance, such as anaerobic threshold and time to
exhaustion, can be enhanced. Symptoms of paresthesia may be observed if a single dose higher than 800 mg is
ingested. The symptoms, however, are transient and related to the increase in plasma concentration. They can
be prevented by using controlled release capsules and smaller dosing strategies. No important side effect was
related to the use of this amino acid so far. In conclusion, beta-alanine supplementation seems to be a safe
nutritional strategy capable of improving high-intensity anaerobic performance.
Harris, R. C., M. J. Tallon, et al. (2006). "The absorption of orally supplied β-alanine and its effect on muscle
carnosine synthesis in human vastus lateralis." Amino Acids 30(3): 279-289.
Summary.&nbsp;&nbsp;β-Alanine in blood-plasma when administered as A) histidine dipeptides
(equivalent to 40 mg • kg−1 bwt of β-alanine) in chicken broth, or B) 10, C) 20 and D) 40 mg • kg−1 bwt βalanine (CarnoSyn™, NAI, USA), peaked at 428 ± SE 66, 47 ± 13, 374 ± 68 and 833 ± 43 µM. Concentrations
regained baseline at 2 h. Carnosine was not detected in plasma with A) although traces of this and anserine
were found in urine. Loss of β-alanine in urine with B) to D) was &lt;5%. Plasma taurine was increased by βalanine ingestion but this did not result in any increased loss via urine. Pharmacodynamics were further
investigated with 3 × B) per day given for 15 d. Dietary supplementation with I) 3.2 and II) 6.4 g • d−1 β-alanine
(as multiple doses of 400 or 800 mg) or III) L-carnosine (isomolar to II) for 4 w resulted in significant increases
in muscle carnosine estimated at 42.1, 64.2 and 65.8%.
Chronic Beta Alanine Loading and Performance
STOUT, J. R., J. T. CRAMER, et al. (2006). "Effects of Twenty-Eight Days of Beta-Alanine and Creatine
Monohydrate Supplementation on the Physical Working Capacity At Neuromuscular Fatigue Threshold." The
Journal of Strength & Conditioning Research 20(4): 928-931.
The purpose of this study was to examine the effects of 28 days of beta-alanine (b-Ala) and creatine
monohydrate (CrM) supplementation on the onset of neuromuscular fatigue by using the physical working
capacity at neuromuscular fatigue threshold (PWCFT) test in untrained men. Fifty-one men (mean age +/- SD =
24.5 +/- 5.3 years) volunteered to participate in this 28-day, double-blind, placebo-controlled study and were
randomly assigned to 1 of 4 groups: placebo (PLA; 34 g dextrose; n = 13), CrM (5.25 g CrM plus 34 g dextrose; n
= 12), b-Ala (1.6 g b-Ala plus 34 g of dextrose; n = 12), or b-Ala plus CrM (CrBA; 5.25 g CrM plus 1.6 g b-Ala plus
34 g dextrose; n = 14). The supplement was ingested 4 times per day for 6 consecutive days, then twice per
day for 22 days before posttesting. Before and after the supplementation, subjects performed a continuous
incremental cycle ergometry test while a surface electromyographic signal was recorded from the vastus
lateralis muscle to determine PWCFT. The adjusted mean posttest PWCFT values (covaried for pretest PWCFT
values) for the b-Ala and CrBA groups were greater than those for the PLA group (p <= 0.05). However, there
were no differences between the CrM vs. PLA, CrBA vs. b-Ala, CrM vs. b-Ala, or CrM vs. CrBA groups (p > 0.05).
These findings suggested that b-Ala supplementation may delay the onset of neuromuscular fatigue.
Furthermore, there appeared to be no additive or unique effects of CrM vs. b-Ala alone on PWCFT. (C) 2006
National Strength and Conditioning Association
Zoeller, R. F., J. R. Stout, et al. (2007). "Effects of 28 days of beta-alanine and creatine monohydrate
supplementation on aerobic power, ventilatory and lactate thresholds, and time to exhaustion." Amino
Acids 33(3): 505-510.
Summary.&nbsp;&nbsp;The effect of beta-alanine (β-Ala) alone or in combination with creatine
monohydrate (Cr) on aerobic exercise performance is unknown. The purpose of this study was to examine the
effects of 4 weeks of β-Ala and Cr supplementation on indices of endurance performance. Fifty-five men (24.5
± 5.3 yrs) participated in a double-blind, placebo-controlled study and randomly assigned to one of 4 groups;
placebo (PL, n = 13), creatine (Cr, n = 12), beta-alanine (β-Ala, n = 14), or beta-alanine plus creatine (CrBA, n =
16). Prior to and following supplementation, participants performed a graded exercise test on a cycle
ergometer to determine VO2peak, time to exhaustion (TTE), and power output, VO2, and percent VO2peak
associated with VT and LT. No significant group effects were found. However, within groups, a significant time
effect was observed for CrBa on 5 of the 8 parameters measured. These data suggest that CrBA may
potentially enhance endurance performance.
Acute Bicarb Loading and Performance
Edge, J., D. Bishop, et al. (2006). "Effects of chronic NaHCO3 ingestion during interval training on changes to
muscle buffer capacity, metabolism, and short-term endurance performance." J Appl Physiol 101(3): 918925.
This study determined the effects of altering the H+ concentration during interval training, by
ingesting NaHCO3 (Alk-T) or a placebo (Pla-T), on changes in muscle buffer capacity ([beta]m), endurance
performance, and muscle metabolites. Pre- and posttraining peak O2 uptake ([IMG]f1.gif" ALT="V"
BORDER="0">O2 peak), lactate threshold (LT), and time to fatigue at 100% pretraining [IMG]f1.gif" ALT="V"
BORDER="0">O2 peak intensity were assessed in 16 recreationally active women. Subjects were matched on
the LT, were randomly placed into the Alk-T (n = 8) or Pla-T (n = 8) groups, and performed 8 wk (3 days/wk) of
six to twelve 2-min cycle intervals at 140-170% of their LT, ingesting NaHCO3 or a placebo before each training
session (work matched between groups). Both groups had improvements in [beta]m (19 vs. 9%; P < 0.05) and
[IMG]f1.gif" ALT="V" BORDER="0">O2 peak (22 vs. 17%; P < 0.05) after the training period, with no differences
between groups. There was a significant correlation between pretraining [beta]m and percent change in
[beta]m (r = -0.70, P < 0.05). There were greater improvements in both the LT (26 vs. 15%; P = 0.05) and time
to fatigue (164 vs. 123%; P = 0.05) after Alk-T, compared with Pla-T. There were no changes to pre- or
postexercise ATP, phosphocreatine, creatine, and intracellular lactate concentrations, or pHi after training. Our
findings suggest that training intensity, rather than the accumulation of H+ during training, may be more
important to improvements in [beta]m. The group ingesting NaHCO3 before each training session had larger
improvements in the LT and endurance performance, possibly because of a reduced metabolic acidosis during
training and a greater improvement in muscle oxidative capacity.
Forbes, S. C., G. H. Raymer, et al. (2005). "NaHCO3-induced alkalosis reduces the phosphocreatine slow
component during heavy-intensity forearm exercise." J Appl Physiol 99(5): 1668-1675.
During heavy-intensity exercise, the mechanisms responsible for the continued slow decline in
phosphocreatine concentration ([PCr]) (PCr slow component) have not been established. In this study, we
tested the hypothesis that a reduced intracellular acidosis would result in a greater oxidative flux and,
consequently, a reduced magnitude of the PCr slow component. Subjects (n = 10) performed isotonic wrist
flexion in a control trial and in an induced alkalosis (Alk) trial (0.3g/kg oral dose of NaHCO3, 90 min before
testing). Wrist flexion, at a contraction rate of 0.5 Hz, was performed for 9 min at moderate- (75% of onset of
acidosis; intracellular pH threshold) and heavy-intensity (125% intracellular pH threshold) exercise. 31P-
magnetic resonance spectroscopy was used to measure intracellular [H+], [PCr], [Pi], and [ATP]. The initial
recovery data were used to estimate the rate of ATP synthesis and oxidative flux at the end of heavy-intensity
exercise. In repeated trials, venous blood sampling was used to measure plasma [H+], [HCO3-], and [Lac-].
Throughout rest and exercise, plasma [H+] was lower (P < 0.05) and [HCO3-] was elevated (P < 0.05) in Alk
compared with control. During the final 3 min of heavy-intensity exercise, Alk caused a lower (P < 0.05)
intracellular [H+] [246 (SD 117) vs. 291 nmol/l (SD 129)], a greater (P < 0.05) [PCr] [12.7 (SD 7.0) vs. 9.9 mmol/l
(SD 6.0)], and a reduced accumulation of [ADP] [0.065 (SD 0.031) vs. 0.098 mmol/l (SD 0.059)]. Oxidative flux
was similar (P > 0.05) in the conditions at the end of heavy-intensity exercise. In conclusion, our results are
consistent with a reduced intracellular acidosis, causing a decrease in the magnitude of the PCr slow
component. The decreased PCr slow component in Alk did not appear to be due to an elevated oxidative flux.
Raymer, G. H., G. D. Marsh, et al. (2004). "Metabolic effects of induced alkalosis during progressive forearm
exercise to fatigue." J Appl Physiol 96(6): 2050-2056.
Metabolic alkalosis induced by sodium bicarbonate (NaHCO3) ingestion has been shown to enhance
performance during brief high-intensity exercise. The mechanisms associated with this increase in
performance may include increased muscle phosphocreatine (PCr) breakdown, muscle glycogen utilization,
and plasma lactate (Lac-pl) accumulation. Together, these changes would imply a shift toward a greater
contribution of anaerobic energy production, but this statement has been subject to debate. In the present
study, subjects (n = 6) performed a progressive wrist flexion exercise to volitional fatigue (0.5 Hz, 14-21 min) in
a control condition (Con) and after an oral dose of NaHCO3 (Alk: 0.3 g/kg; 1.5 h before testing) to evaluate
muscle metabolism over a complete range of exercise intensities. Phosphorus-31 magnetic resonance
spectroscopy was used to continuously monitor intracellular pH, [PCr], [Pi], and [ATP] (brackets denote
concentration). Blood samples drawn from a deep arm vein were analyzed with a blood gas-electrolyte
analyzer to measure plasma pH, PCO2, and [Lac-]pl, and plasma [IMG]f1.gif" BORDER="0"> was calculated
from pH and PCO2. NaHCO3 ingestion resulted in an increased (P < 0.05) plasma pH and [IMG]f1.gif"
BORDER="0"> throughout rest and exercise. Time to fatigue and peak power output were increased (P < 0.05)
by [~]12% in Alk. During exercise, a delayed (P < 0.05) onset of intracellular acidosis (1.17 {+/-} 0.26 vs. 1.28
{+/-} 0.22 W, Con vs. Alk) and a delayed (P < 0.05) onset of rapid increases in the [Pi]-to-[PCr] ratio (1.21 {+/-}
0.30 vs. 1.30 {+/-} 0.30 W) were observed in Alk. No differences in total [H+], [Pi], or [Lac-]pl accumulation
were detected. In conclusion, NaHCO3 ingestion was shown to increase plasma pH at rest, which resulted in a
delayed onset of intracellular acidification during incremental exercise. Conversely, NaHCO3 was not
associated with increased [Lac-]pl accumulation or PCr breakdown.
Goldfinch, J., L. Mc Naughton, et al. (1988). "Induced metabolic alkalosis and its effects on 400-m racing
time." Eur J Appl Physiol Occup Physiol 57(1): 45-48.
Six trained male athletes who competed regularly in 400 metre races, were studied under control,
alkalotic (NaHCO3) and placebo (CaCO3) conditions to study the effect of induced metabolic alkalosis on 400 m
racing time. Pre and post exercise blood samples in the three conditions were analysed for pH, bicarbonate
and base excess. Following ingestion of NaHCO3, pre-exercise pH, bicarbonate and base excess levels were
significantly higher than either control or placebo conditions. In the alkalotic condition the subjects ran
significantly (p less than 0.005) faster (1.52 s) than either the control of placebo conditions. The post-exercise
pH, bicarbonate and base excess levels were all lower in the alkalotic condition than in the others. The results
suggest that NaH-CO3 can be used as an effective ergogenic aid and support the speculation that the increased
extracellular buffering afforded by NaHCO3 ingestion facilitated efflux of H+ from the working tissues, thus
decreasing intracellular pH and hence offsetting fatigue.
WILKES, D., N. GLEDHILL, et al. (1983). "Effect of acute induced metabolic alkalosis on 800-m racing time."
Medicine & Science in Sports & Exercise 15(4): 277-280.
WILKES, D., N. GLEDHILL, and R. SMYTH. Effect of acute induced metabolic alkalosis on 800-m racing
time. Med. Set. Sports Exerc., Vol. 15, No. 4, pp. 277-280, 1983. Six trained middle-distance runners were
studied under alkalotic (NaHCOa ingestion), placebo (CaCO3 ingestion), and control conditions to determine
the effect of an acute induced metabolic alkalosis on time to run an 800-m race. Pre-exercise, following
NaHCO3 ingestion, pH and standard [HCO3-] were significantly higher. In the alkalotic condition, subjects ran
faster (2.9 s) and the corresponding post-exercise values for blood [lactate] and extracellular H+ were higher
than in the control and placebo conditions, suggesting an increased anaerobic energy contribution. These
results support the speculation that the increase in extracellular buffering following NaHCO3 ingestion
facilitated H+ efflux from the cells of working muscle, thereby delaying the decrease in intracellular pH and
postponing fatigue. It is concluded that the ingestion of NaHCO3 by trained middle-distance runners prior to
an 800-m race has an ergogenic benefit. (C)1983The American College of Sports Medicine