Dietary sodium bicarbonate as a treatment for exertional rhabdomyolysis in a horse.

This research study investigates the use of dietary sodium bicarbonate as a treatment for exertional rhabdomyolysis in horses, showing significant improvement during exercise when the supplement was included in the horse’s diet.

Study Design and Methodology

• The subject of the study was a 3-year-old mare that exhibited signs of rhabdomyolysis, which is a breakdown of muscle tissues caused by strenuous exercise.
• The horse was observed over 7 alternating periods, during which its diet was supplemented with sodium bicarbonate, while the basal regime consisted of timothy hay and oats.
• Different measurements were taken at rest and after exercise, including physical signs, venous blood pH and gases, blood glucose, lactate levels, serum electrolytes, enzymes and creatinine, as well as urine pH.

Observations and Results

• Supplementation with dietary sodium bicarbonate slightly increased resting venous blood pH and bicarbonate levels and significantly increased urine pH.
• An exercise test involving 5 minutes of walking followed by 20 minutes of trotting was conducted. During the non-supplemented periods, the horse exhibited muscle stiffness, muscle fasciculations (muscle twitching), and muscle hardening. However, these symptoms were not observed during the periods when the horse’s diet was supplemented with sodium bicarbonate.
• The study found that myoglobin, a protein that carries oxygen in muscle cells, was present in significantly less urine samples following exercise during periods of bicarbonate supplementation.
• Supplementation also significantly reduced the blood lactic acid, serum creatine kinase and aspartate transaminase responses to exercise, markers that give an indication of muscle damage.

Conclusions and Implications

• This experiment demonstrated that dietary sodium bicarbonate can be an effective treatment for horses with exertional rhabdomyolysis. It improved the animal’s responses to exercise and effectively dampened the physical, chemical and enzymatic changes generally associated with the condition.
• This study indicates that the mechanism of action may involve enhancing the buffering capacity in muscle tissue fluids, helping to prevent the severe muscle damage that causes the clinical symptoms of the condition.
• These findings provide a basis for further research, potentially expanding treatment options for other animals and even humans suffering from similar muscle conditions.