Blood Lactate Report

Blood lactate profile report

Trained -v- Untrained

The purpose of this test was to determine individuals, (trained and untrained) lactate threshold and subsequently interpret the results. This will allow for a comparison in how training affects the accumulation of blood lactate by using the results from the trained versus the untrained individual.

When the rate of lactate production exceeds the rate of uptake, lactic acid accumulates in the blood volume, and then we see the onset of blood lactate accumulation. This is what known as the traditional "Lactate Threshold" (LT)(1). This occurs when during exercise of an increasing intensity the lactate levels rise above that of resting levels.

When glucose is broken down it forms pyruvate. This pyruvate then gets converted to lactic acid via the enzyme lactate dehydrogenase. Lactate is formed from both aerobic and anaerobic glycolysis, however lactate does not so much accumulate in aerobic conditions as they body has the ability under these conditions to clear the lactate at the same time as it produces it. During anaerobic glycolysis, production rate is greater than clearance and lactic acid accumulates in the muscle tissue and can spill over into the bloodstream. This causes blood pH to increase and thus the blood acidity levels rise. Lactate is only harmful to exercise performance with the dissociation of the hydrogen ions from lactate causing the changes in pH levels. This shift in pH is thought to be a significant contributor to fatigue during exercise performance in many ways: (1) by inhibiting phosphofrucktokinase, and enzyme important for glycolysis; (2) by displacing calcium ions from troponin thus shutting down crossbridge cycling and decreasing the force of muscle contraction thus decreasing performance; (3) by stimulating local pain receptors; (4) by acting on the brain to cause pain and nausea; (5) and by interfering with hormone-sensitive lipase, an intra-cellular hormone that that is responsible for mobilizing free fatty acids(2).

Although costly and often impractical, finding an athlete's lactate threshold can be very beneficial. By measuring blood glucose levels during exercise one can predict endurance performance. It is thought that lactate measurements are more sensitive than VO2max and thus a better indicator. It also allows the measurement of training stress on the body and thus the monitoring of muscle adaptations. Levels of aerobic fitness can be taken and so an appropriate training intensity can be determined that is suitable to the athlete's specific needs and the demands of the sport (3).

Factors which are thought to lead to the accumulation of blood lactate include: (i) an imbalance between glycolysis and mitochondrial respiration (ii) lowered blood oxygen content (iii) increased NADH relative to NAD+ and (iv) lowered blood flow to the working skeletal muscles. This build up of lactate and the dissociation of hydrogen ions from it have been shown to contribute to exhaustion and fatigue and as a result decrease performance. This hydrogen ion accumulation is what causes muscle acidification and a resulting condition known as muscle acidosis. Muscle pH is usually around 7.1 but due to the bodies buffering capacity the H+ concentration stays relatively low and even at exhaustion will not let muscle pH fall below 6.4.

Many adaptations occur within the body as a result of training. When a body is trained aerobically the muscles gain the ability to store more fat and glycogen. Lipids are usually only used as an energy source when working at low intensities but with aerobic training one can work at a higher intensity using fats as a source of energy fro the working muscles. A rise in capillary levels increase the mobilisation of FFAs and thus their usage in order to spare glycogen. The body becomes more efficient at utilizing fat for energy when aerobically trained. This adaptation results in the sparing of muscle and liver glycogen usage for the production of ATP and a subsequent decrease in lactate production. There is also an increase in the number, function and size of mitochondria present in the muscles. As a result the mitochondria provide the muscle with a more efficient oxidative metabolism. An increase in myoglobin content sees more oxygen stored and ensures that it is released to the mitochondria when oxygen supply is limited during muscle action. Increased oxygen in the muscle facilitates the removal of waste products produced during respiration. Arterial venous difference is increased with trained individuals which allows a greater uptake of oxygen from the blood. There is also an increase in stroke volume resulting in an increased cardiac output. The increased cardiac output will result in a greater blood supply to the working muscles and will in turn facilitate increased lactate clearance. Holloszy and Coyle (4) argue that a major metabolic consequence of aerobic training is the slower use of muscle glycogen and a reduced production of lactate during exercise at a given intensity.

With anaerobic training the body has the ability to tolerate a higher level of acidity in the muscles as it accumulates. Buffers such as muscle phosphates and bicarbonate combine with hydrogen reducing muscle fibers acidity resulting in a delayed onset of fatigue. An increase of 12% to 50% in muscle buffering capacity with anaerobic training. With enhanced buffering capacity muscles can now generate energy for longer periods of time prior to the H+ concentration becoming so high that it inhibits the contractile process. Lactic acid becomes neutralized and higher levels of muscle and blood lactate levels are permitted.

Muscle fibre type affects the lactate threshold. Fast twitch type IIb fibres are more anaerobic and less fatigue resistant fibres and increase lactate production. Type I fibres are more aerobic, fatigue resistant fibres and are able to oxidise the lactate produced during exercise.

For reasons discussed above it is understood that trained individuals can work at higher intensities before reaching a fatigued state. For example untrained persons can only work at 50%-60% of their VO2max before beginning