Muscle Acidosis and Maximal Exercise in Horses – A Nutritional Intervention

Date: 11 May, 2016

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Most trainers will be familiar with lactic acid, although misconceptions might exist as to whether its production is good, bad or indifferent. Lactic acid is produced in muscle as a consequence of anaerobic energy generation and whilst it can be metabolised or reprocessed within muscle, it can and does accumulate during acute periods of maximal exercise when peak power output and speed is required such as the closing stages of a race, or during the effort of repetitive jumping. Accumulated lactic acid dissociates or separates to form lactate and a source of hydrogen ions (H+). Accumulation of H+ in muscle during exercise leads to a drop in pH and muscle acidosis, which contributes ultimately to muscle fatigue limiting performance. Lactic acid can also be produced as consequence of fermentation in the digestive tract, particularly the hindgut but this is a very different scenario to that which occurs in muscle. Research in horses and humans has shown how dietary intervention can be used to help tackle muscle acidosis, a key element in the process of muscle fatigue.

 

Lactic acid in the hindgut can be deleterious

In the digestive tract, certain types of bacteria, residing predominantly in the hindgut, are capable of producing lactic acid. These ‘lactate producers’ rapidly ferment carbohydrates, particularly starch that reaches the hindgut having escaped digestion in the small intestine. High starch containing diets, typical of horses in hard work, will result in more lactic acid production in the hind-gut compared with a high fibre diet. Excess production of lactic acid within the hindgut is almost always undesirable, as it creates a build up of acid (H+) or ‘acidosis’, which alters the fine balance of essential bacteria present. This then leads to a change in the pattern of fermentation, the movement of water in and out of the gut and also ultimately the integrity of the gut mucosa, potentially allowing undesirable substances to be absorbed into the horse’s circulation. Loose droppings, colic, sub-clinical or clinical laminitis, colitis or inflammation of the colon as well as insulin resistance are all potential outcomes from an acute or chronic acidosis in the hindgut.

The level of lactic acid that is deleterious for the hindgut is very low, typically less than 2 mMol/litre. There are numerous feed practices and supplements that can help combat hindgut acidosis. Good quality digestible forage is higher in energy and so reduces the requirement for excessive amounts of high starch-containing concentrates. Fibre fermentation also sustains the level of desirable ‘lactate utilisers’, which are bacteria capable of feeding on lactic acid to reduce level in the hindgut. Small meals, fed little and often, using cooked cereals will also promote starch digestion in the small intestine leaving less for hindgut fermentation. Live yeast supplements may also help to maintain a healthy balance between lactic acid producing and lactic acid utilising bacteria within the gut. There are also now supplements that utilise an encapsulated form of bicarbonate that is capable of reaching the hindgut where it is able to buffer lactic acid and ameliorate a drop in pH.

The level of lactic acid produced in the gut, however, pales into insignificance when contrasted with that generated in the horse’s skeletal muscles during exercise.

 

Lactic acid in muscle is a biochemical necessity for intense exercise

The scope for lactic acid production in horse muscles is enormous with levels in excess of 200mmol/kg (dry muscle) being attainable during maximal high intensity exercise. All horses produce lactic acid, whether they are sprinters, stayers, hurdlers, or chasers, eventers, showjumpers or dressage horses. Lactic acid is produced as a biochemical consequence of the anaerobic metabolism of glucose and glycogen to produce energy (ATP) needed to fuel muscle contraction and it is both useful and necessary. A low level of lactic acid is produced in muscles continuously at rest and during low intensity exercise, but it is during high intensity exercise where its production increases significantly and it starts to accumulate within muscle, which is reflected in the plasma lactate concentration (table 1). Increased muscle lactic acid production is necessary to deliver the energy (ATP) at a faster rate and under conditions where oxygen delivery to the muscles is limited. All of this is essential to deliver the sustained speed and power required to win races, or execute repetitive jumping at speed. The accumulating lactic acid rapidly separates or disassociates to form an anion lactate and a cation or proton (H+). It is the accumulation of acidic H+ species in muscle that if allowed to go unchecked, results in muscle acidosis and a concomitant drop in pH.

 

Table 1 – Comparison of plasma lactate following treadmill exercise or racing

Speed (Meters/sec)Distance (Meters)Plasma Lactate (mMol/L)
67203.5
89607.9
10120013.6
12144023.8
~15.5140030.2
~15.0200033.1
~14.5280030.0
~11.0380037.6

Adapted from Harris et al 1991 and Sewell et al 1992

Significant muscle acidosis ultimately contributes to muscle fatigue. As muscle acidity increases (pH declines) it reaches a level where it can interfere with normal muscle contraction and muscle energy generation pathways. Practically speaking, horses will slow down when experiencing muscle fatigue, or where jumping is involved they may make crucial mistakes. We have all felt that ‘burn’ associated with muscle fatigue, even if it was only running for the train rather than around the track. Nature is, however, a clever architect and has given horses like humans various mechanisms to counteract the potential negative impact of muscle acidosis on muscle function.

 

Efficient buffering is crucial to intense exercise

Blood Buffering

Once significant amounts of H+ has been formed in muscle, a proportion will be transported out into the blood, where it can be buffered or rendered harmless by the bicarbonate buffering system. Bicarbonate is able to accept or buffer H+ , eliminating its acidity. This then allows more H+ to pass from muscle into the blood helping to control muscle acidosis and attenuate the fall in muscle pH.

 

‘Milkshaking’ involves the invasive administration of large quantities of bicarbonate via nasogastric tube on race day giving an acute but transient increase in the buffering capacity of blood. Whilst milkshaking has been shown to be effective biochemically in horses, it is strictly against the rules of racing all over the world. The tell tale increase in the concentration of carbon dioxide in blood provides a highly effective testing procedure for regulators to help eliminate its use. Whilst unlikely in isolation to trigger a post race positive in PCO2, small additions of bicarbonate to the diet on a daily basis will not improve bicarbonate buffering appreciably and larger amounts may result in scouring.

 

Tackling the source – Muscle buffering

As well as being buffered in blood, the H+ arising from accumulating lactic acid and other metabolic pathways can be buffered at source in the muscle. There are a number of processes or elements that contribute to reducing the free H+ in muscle including:

  • Conversion of phosphocreatine to creatine
  • Production of Ammonium
  • ATP breakdown
  • Presence of intramuscular buffers including bicarbonate, hydrogen phosphate, histidine and carnosine.

One of the most interesting aspects to muscle buffering due to the significant research carried out in horses is the presence of carnosine. Carnosine not to be confused with L- carnitine is an important peptide or ‘small protein’ like compound found in muscle at a high level in horses, Man and other athletic animals. Due to its chemical structure, carnosine is able to accept or buffer hydrogen ions (H+) to help stabilise muscle pH.

Fig 1 – Increase in H+ buffering with increasing muscle carnosine content.

 

Variation in muscle carnosine

Carnosine concentration is highest in fast twitch muscle fibres (IIb and IIa) and lowest in slow twitch type 1 fibres. Considerable variation in muscle carnosine concentration exists between horses, which helps explain some of the variation in innate talent of individual horses. Muscle carnosine increases with age in horses until maturity and then slowly declines. This is interesting given the increased use of older horses in certain equestrian disciplines such as eventing and showjumping. Research in humans indicates that muscle carnosine is also lower in females than males. A small adaptive increase in muscle carnosine content is seen with anaerobic training in horses.

 

Building blocks for carnosine

Carnosine is made from two key amino acids namely histidine and b-alanine, both of which are found in the horse’s diet naturally. It is the histidine component within carnosine that is able to accept a H+ and so gives carnosine its buffering capacity. The second amino acid, is needed to prevent the incorporation of the histidine molecule into protein, where its buffering ability would be reduced significantly.

Dr’s Mark Dunnett and Roger Harris uncovered the muscle carnosine story in horses whilst at the world famous Animal Health Trust, in Newmarket and they went on to show how the synthesis of muscle carnosine can be optimised through diet. Interestingly, in this area of research, horses led and humans followed. This equine research initiated an explosion of studies in humans showing the beneficial effect of increasing muscle carnosine in human sports and it is widely reported in the scientific literature.

Studies in horses show that muscle carnosine is increased significantly following supplementation with a bioavailable source of histidine and b-alanine (ProCarnosine®). The the use of this important amino acid to improve buffering in horses, man and other animals is covered by a suite of global patents. ProCarnosine® is an important and exclusively available active component in the equine sports supplement STORM®.

ProCarnosine® has been shown to be absorbed from the digestive tract and is taken up into muscle where it is then available for carnosine synthesis. However, synthesis is slow with 4-8 weeks of supplementation being required to affect the level of carnosine in muscle. To optimise carnosine production an elevated and steady level in blood needs to be achieved through appropriate supplementation and feeding.

Although a number of other ingredients are available to potentially modify lactic acid production or H+ buffering such as creatine, citrate or DMG (dimethylglycine), no credible evidence has been published to support beneficial effects in horses.

In summary, whilst lactic acid may be viewed as a metabolic pariah, its formation in muscle represents an essential biochemical step to facilitate high intensity exercise performance. This should not be confused, however, with the undesirable excess production of lactic acid within the hindgut. In both cases, however there are useful nutritional strategies that can be used to ameliorate the negative impact of acidosis.

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