Rats Bred For Low Aerobic Capacity Become Rapidly Fatigued And Have Slow Metabolic Recovery After Stimulated Muscle Contractions

Abstract

Good aerobic capacity has a hypothesized role in increased health and longevity. Since impaired oxidative metabolism underlies several complex diseases, such as type 2 diabetes and cardiovascular disease, it is generally thought that the ability to increase oxygen transport and utilization capacity by exercise training stimulus helps prevent one from developing the aforementioned diseases. However, the magnitude of exercise capacity differs substantially between individuals. Primary assumption is that this heterogeneity is the consequence of variation distributed across a large number of genes for both the intrinsic (untrained) aerobic capacity and that accrued from exercise training. To address the intrinsic component, Koch and Britton (Physiol Genomics, 2001) developed two rat strains by artificial selection for low and high endurance treadmill running capacity in the untrained condition. These contrasting rat models, termed low capacity runner (LCR) and high capacity runner (HCR), are excellent biological models for evaluating the interplay of genetic and environmental factors as determinants of high health and aerobic capacity. PURPOSE: Our long-term aim is to evaluate the influence of life-long aerobic exercise training on aging and longevity using the LCR/HCR model system. Such studies require the application of non-invasive functional measures across time. Here we report on our first measurements of skeletal muscle energy metabolism in non-trained LCR and HCR rats. METHODS: Muscle function was studied in electrically stimulated contracting gastrocnemius muscle using 1H-magnetic resonance imaging (MRI) and 31P-MR spectroscopy. The simultaneous force output was measured with an ergometer connected to a foot pedal. RESULTS: Our results from mechanical measurement (force output) show a significant difference between LCR and HCR groups for the decrease in the isometric force during transcutaneous stimulation, the decrease being greater in LCR rats (P<0,001). 31P-MR spectroscopy results demonstrated that phosphocreatine resynthesis after stimulation was significantly slower in LCR group (P<0,02). CONCLUSIONS: Consistent with diminished treadmill running capacity, this study shows that skeletal muscle in LCR rats becomes fast fatigued during maximal muscle stimulation. 31P-MR spectroscopy seems to be a valid non-invasive method to investigate consecutive differentials in skeletal muscle energy metabolism between the LCR and HCR rats, making longitudinal studies feasible. Supported by the Ministry of Education and Culture (Finland) and the National Center for Research Resources (a component of the NIH).