It doesn't take a trip to the gym to know that we are not all equal in our capacity to exercise. Whether it results from our genes, our environment or both is a source of much debate. The age old question of nature vs nurture is certainly central to exercise physiology, notably because of the plasticity of exercise capacity (e.g. training) and the variation of innate traits associated with that capacity.
Sarah Lessard, Donato Rivas and colleagues from Royal Melbourne Institute of Technology University in Australia addressed this question by using rats artificially selected for high or low running capacities. After 22 generations of differential selection, the high-capacity runners exhibit a 5-fold higher running capacity than the low capacity animals. Furthermore, low capacity runners present several metabolic dysfunctions coupled with an impaired health profile that could explain their reduced athleticism. The team's primary hypothesis was that exercise training would reverse some of the metabolic dysfunctions exhibited by the rats selected for low running capacity.
The team trained the two different phenotypes with exercise for 6 weeks and compared the metabolic responses between these two groups and their sedentary matched controls. First, they measured whole body metabolic parameters. Training ‘couch-potato’ rats lowered their body mass, fat content and serum non-esterified fatty acid levels, suggesting an improvement of their metabolic function. In contrast, the trained ‘athletic’ rats did not show any significant changes in whole body metabolism, suggesting a status quo in metabolic function, at least under the training conditions of the study.
To get a better understanding of the metabolic changes involved with these improvements in low capacity rats, Lessard and her team investigated glucose and lipid metabolism in isolated skeletal muscle taken from both phenotypes. In agreement with their in vivo measurements, muscles of trained low capacity rats showed improvements in both fuel metabolisms compared with their sedentary counterparts. However, exercise training did not affect high capacity runners for any metabolic pathway examined.
Finally, the team looked at the protein levels of metabolic regulators and some of their targets. In sedentary animals, the β-adrenergic receptor and the nuclear receptor Nur77 were both upregulated in the high capacity rats compared with their low capacity counterparts. However, exercise training reduced these differences between the groups by triggering an increase in protein content in low capacity rats but not in high capacity animals. Further, several targets of Nur77 involved in lipid and carbohydrate metabolism (glucose transporter 4, fatty acid translocase CD36 and uncoupling protein 3) all followed a similar pattern. Indeed, these proteins were more abundant in the skeletal muscle of sedentary good runners compared with low capacity rats, but again these differences between the two groups faded following exercise training.
Overall, these results consistently point to an amelioration of the metabolic capacity of ‘couch-potato’ rats after short-term, low to moderate intensity exercise training. Interestingly, the effects of training were only evident in low capacity animals, with very little impact on the metabolic function of ‘good runners’. This probably means that I should really stop blaming my genes and hit the gym!