| Summary: | Low exercise capacity has been identified as a stronger predictor of morbidity and mortality relative to other commonly reported risk factors. Substrate metabolism, especially lipid storage, lipolysis and transportation in the skeletal muscles is strongly linked to aerobic capacity. The physical topographical properties of some myocellular particles and or organelles such mitochondria, lipid droplets (LDs) and perilipine-5 (Plin5) proteins in the skeletal muscle tissues have been implicated in the onset of most metabolic diseases and may also predict overall physical capacity. We tested the effect of innate high aerobic capacity (genetics) and acquired aerobic capacity (voluntary running) on the number, location and colocalization of the aforementioned particles in the gastrocnemius muscle cells, between the low and high capacity runner rats.
Muscle samples from the gastrocnemius muscle of the specially bred rat model with high aerobic capacity (HCR) (n=20) and low aerobic capacity (LCR) (n=20) were used in this study. The samples were obtained from 4 equal subgroups; high capacity runner control (HCR-C) (n=10), high capacity runner receiving exercise intervention (HCR-R) (n=10), low capacity runner control (LCR-C) (n=10) and low capacity runner receiving exercise intervention (LCR-R) (n=10). Immunocytochemistry, confocal microscopy and bioinformatics were used in data collections and analysis. A one-way between subject analysis of variance (ANOVA) show statistically significant difference in the content of mitochondria (F (3,24) = 4.24, p<.0.05) and PLIN5 particles (F (3,24) = 3.8, p<.005). There were no significant differences in the number of LD (F (3,24) = 0.43, p>0.05) or in the colocalization of the LD and PLIN5 particles (F (3,24) = 1.2, p>.005) and LD and COXIV particles (F (3,24) = 1, p>.005) across the groups.
The result suggests a strong interplay between genetic background and exercise stimulus. These factors may influence the skeletal muscle properties at the cellular level, effect of which may not only affect performance component but also health component of physical fitness. Physical activity may, however, enhance the cellular function or reverse genetic lags in cellular properties.
|
|---|