Resumen de The effects of omtermittent hypobaric hypoxia and exercise on the recovery of induces skeletal muscle damage in trained laboratory rats: performance evaluation, plasma markers and m. Soleus differential gene expression
Juan Gabriel Ríos Kristjánsson
One of the key players in the regenerating injured skeletal muscle fibers are their surrounding satellite cells (specific stem cells), arranged between the basal lamina and the sarcolemma, in relatively few numbers per fiber. The satellite cells, which are myogenic precursor cells are activated during injury to fuse and mature into the injured fiber. Some studies have demonstrated that exercise and hypoxia facilitate the activation and migration into the blood circulation, moving more stem cells to an injured or activated area which in turn aids the repairing of the injury. The aim of this thesis was to study the regeneration profile over fourteen days after an eccentric-exercise induction of skeletal muscle damage in treadmill-trained laboratory rat, submitting them to series of daily (4 h) intermittent hypobaric hypoxia (with the simulated altitude of 4000 m) with or without the combination of light exercise as part of their rehabilitation. The rats could potentially react differently to the exercise training prior and post the induction of muscle damage, and furthermore, be differently susceptible to the injury-induction protocol, influenced by their training. This premise led to the formation of the rat AEY performance score, throughout the study, as a complementary tool for the data acquired during the injury regeneration. The regeneration was profiled four times over the recovery fourteen days from the injury induction via the concentration of myoglobin and creatine kinase (CK-MM) plasma markers and differential gene expression analysis in m. soleus, which is generally considered to be one of the most susceptible muscle to eccentric-exercise injury when running downhill. The plasma marker results indicate that the effect of the injury-induction protocol was very short lived, as after the significantly different peak concentrations for the control (passive recovery) and they hypoxia groups (sessions of intermittent hypoxia during recovery) 1 day post injury, had dropped down to basal level again 3 days post injury. However, the hypoxia+exercise group (sessions of intermittent hypoxia followed by light exercise during recovery) had a distinct profile with its slowly rising peak 3 days post injury and then dropping down again. Still, this profile was only significant for the CK-MM measurements, whilst myoglobin did not show any significant change following injury. It is clear that the hypoxia-exercise conditions cause different physiological reactions to the injury. However, the level of the injury would need to be greater in order to obtain a more significant pattern and to be able to interpret if the pattern is reflecting potentially beneficial effects or not. The differential gene expression analysis also indicates that the injury induction needed to have been greater to achieve differential expression. The hypoxia and hypoxia+exercise profiles are not parallel to each other, still the data also suggest that the hypoxia sessions could have been more effective. Therefore, it is difficult to give a general conclusion to which hypoxia or hypoxia+exercise facilitate the injury regeneration to a higher degree. The certain fact is that there are ethical and humane factors that need to be respected, but limit the margin of how the injury-induction can be carried out in the way it was done in this study.
