Lactic acid is the chemical name of 2- hydroxypropanoic acid and is a 3 carbon
carboxylic acid. When the proton has been removed from the carboxylytic
functional group, the molecule is called Lactate. The remaining
negative charge can be balanced by a cation, such as sodium or
potassium, which can form sodium or potassium lactate. For Lactic Acid,
50% of it metabolite is in the form of Lactic Acid, and 50% of its form
is Lactate, for example when pH is 3.67. This represents a very acidic
environment given the normal pH range of 6.1- 7.05. Therefore, the
proportion of unbound Lactate varies from 99.06- 99.38, therefore,
trace amount of Lactic Acid occur inside the body, and thus this terms
"Lactic Acid", and "Lactic Acidosis" should not be used. The reader is
referred the review by Robergs and Colleagues (2004) for a further in
depth discussion.
Understanding
this fundamental difference between Lactic Acid and Lactate are
essential to understanding of what the true markers of acidosis
actually are. Considering for more than 60 years, the idea/belief that
Lactic Acid causes acidosis and that Lactate is a negative aspect of
exercise physiology and high intensity exercise involving a high rate
of ATP turnover is just not true.
Lactate Production
Lactate
production is incredibly important during skeletal muscle contraction,
during intense contractions, and involving a high rate of ATP turnover.
In addition, it is a rapid and valuable resource for the muscle cytosol
to maintain NAD+ supply, as well as buffer the release of protons
during Glycolysis. It is produced by the LDH reaction:
Pyruvate + NADH + H+ < > Lactate + NAD+
*Pyruvate conversion to Lactate is termed the "mass action effect"
Essentially,
since pyruvate is in the acid salt form, means no H+ (hydrogen ion) is
released on the carboxylytic acid groups during lactate production,
therefore, the protons that are released from Glycolysis DO NOT come
from the production of metabolic acids. Therefore, Lactate is not
detrimental but instead of producing a proton, lactate production
CONSUMES a proton, and termed "metabolic proton buffering", thereby
retarding acidosis.
For
example, accumulation of muscle and blood lactate after exercise,
lactate can be oxidized back to pyruvate for gluconeogenic conversion
to glucose in the liver or converted to pyruvate in the muscle and
other tissues for further catabolism within the mitochondria for ATP
production.
During
intense exercise sessions, there is a substantial increase in the rate
of substrate flux through glycolysis simply because the stimulation of
glycogenolysis (i.e. increased Pi, increased AMP, increased CA++) and
glycolysis are so high. Depending on the distribution and/or proportion
of fast twitch and slow twitch muscle fibers and motor units, the
ability for converting pyruvate to acetyl CoA and in conjunction of the
glycerol-3- phosphate shuttle to run at similar rates, all depend on
the mitochondrial mass of working skeletal muscle. Highly trained
endurance individuals have a greater affinity of the contracting muscle
to use Mitochondrial Respiration to supply most of the ATP production
to regenerate most of NAD+. Nonetheless, there are many circumstances
(high intensity resistance training or interval training) where the
rate of ATP demand exceeds the ability of muscle fibers to maintain ATP
demand from mitochondrial respiration. Therefore, in these specific
situations, contracting muscle must depend on the LDH reaction to
regenerate NAD+. Hence, the increased Lactate production (not caused by
lack of 02 or being the cause of acidosis) represents the increased
reliance on the glycolytic and phosphagen energy systems to regenerate
ATP for muscle contraction. Thus, the production of lactate coincides
with the release of a proton (H+) and decrease in pH. It is the
decrease in cellular and blood pH with high rates of lactate production
that has a detrimental effect to enzymes of energy metabolism and
muscle contraction.
In
addition, because of the increased rate of these pathways, it also
involves the CrP (creatine phosphate reaction/shuttle). Since the CrP
reaction involves free protons, acidosis effects restoration of CrP
stores. Hence, the greater the acidosis, the longer the recovery
period. Muscle CrP recovery reveals a dual exponential curve having a
fast and slow component. This fast component is complete within 2
minutes and represents 80-90% of complete CrP recovery.
Interestingly,
if muscle did not produce or could not produce lactate, and as soon as
exercise intensity increased, there would be no means to rely on
addition ATP from glycolysis, and no reactions would take place in the
cytosol to regenerate NAD+ from NADH, and thus this "redox potential"
would decrease the rate of the glyeraldehyde-3-phosphate dehydrogenase
reaction and completely shut down the glycolytic energy pathway.
So, what
are the causes of metabolic acidosis in skeletal muscle? Acidosis
develops when the rate of H+ production exceeds the rate of H+
removal/buffering.
H+ Production
H+ Removal/buffering
Glycolytic
Flux
CrP Hydrolysis
ATP
Hydrolysis Mitochondria Transport
Fast Twitch motor
units
Protein/amino acids
HCO3
Inorganic Phosphate
Sarcolemmal Transport
Lactate Production (on the removal side) is beneficial for:
- Regenerating NAD+
- Consuming Protons
- Facilitating proton efflux from cells
Reference:
Robergs, R.A., Ghiasvand, F., &
Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis.
American Journal of Physiology: Regulatory, Integrative and Comparative
Physiology. 287: R502-R516.
