Training induced adaptation in horse skeletal muscle

Abstract

It appears that the physiological and biochemical adaptation of skeletal muscle to training in equine species shows a lot of similarities with human and rodent physiological adaptation. On the other hand it is becoming increasingly clear that intra-cellular mechanisms of adaptation (substrate transport, enzyme activity, etc) differ considerably between species. The major drawbacks in equine training physiological research are the lack of an appropriate training model and the lack of control of sensitivity and specificity of parameters used in human and rodent research. Furthermore, scientists become aware of the fact that the coupling of biochemical properties of skeletal muscle and other physiological systems play a role in the whole body adaptation during training adaptation. The present thesis focuses on development of a scientific based controlled equine training model, based on equine training practice, and the adaptation in equine skeletal muscle physiological, biochemical, and neuromuscular pathways. During rest and exercise, glucose and triglycerides provide the most energy needed. Both substrates are stored in skeletal muscle, glucose as glycogen and triglycerides as lipid droplets. Transport of these substrates into skeletal muscle is primarily regulated by glucose transporter 4 (GLUT-4) and fatty acid translocase (FAT/CD36). In this thesis we show that the immunohistochemical distribution of these proteins is similar to human expression patterns. Accumulation of lactic acid during exercise is a major determinant of fatigue. Lactic acid is removed from the cell by specific membrane transport proteins, monocarboxylate transporters (MCT). These MCT proteins promote transport of lactate anions and protons from production sites (anaerobic metabolism, mainly in fast glycolytic muscle fibres) to oxidation sites (heart, brain and oxidative muscle fibres). This thesis identifies the expression of MCT1, 2 and 4 in Standardbred skeletal muscle. The training protocol used in this study resulted in changes in quantitative electromygraphic (EMG) values associated with training. Biochemical analysis of skeletal muscle biopsies resulted in less pronounced training adaptation than quantitative EMG. Quantitative EMG and biochemical analysis both showed no signs of mal-adaptation after intensified training compared to controls. There was however a stronger training associated adaptation observed upon intensified training. Finally, we applied these techniques to horses suffering from lower motor neuron disease (LMND), among others a model for denervation. This disease is characterized by increased whole body glucose metabolism and muscular atrophy and weight loss, due to degeneration of motor neurons in the spinal cord. Using these techniques we show that increased whole body glucose uptake is not accompanied by increased GLUT-4 expression. Furthermore we conclude that metabolic changes are secondary to denervation and reinnervation processes in this disease. The main conclusion from our results is that the intensified training protocol used in this study does not increases stress levels above the maximal threshold for skeletal muscle (mal)adaptation. Sarcolemmal substrate transport proteins for fatty acids (FAT/CD36), glucose (GLUT-4) and monocarboxylates (MCT), as identified in this thesis, may have an important function in (mal)adaptation of skeletal muscle metabolism to training and intensified training. Due to technical problems, we were unfortunately not able to perform these analysis.