AMPK agonist AICAR delays the initial decline in lifetime-apex VO2 peak, while voluntary wheel running fails to delay its initial decline in female rats

We examined the ability of physical activity or 5 wk of 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) administration to delay the initial aging-induced decline in lifetime-apex Vo2 peak and potential underlying molecular mechanisms. Experiment 1 consisted of female rats with (RUN) and without (NO RUN) running wheels, while experiment 2 consisted of female nonrunning rats getting the AMPK agonist AICAR (0.5 mg/g/day) subcutaneously for 5 wk beginning at 17 wk of age. All rats underwent frequent, weekly or biweekly Vo2 peak tests beginning at 10 wk of age. In experiment 1, lifetime-apex Vo2 peak occurred at 19 wk of age in both RUN and NO RUN and decreased thereafter. Vo2 peak measured across experiment 1 was ~25% higher in RUN than in NO RUN. In experiment 2, AICAR delayed the chronological age observed in experiment 1 by 1 wk, from 19 wk to 20 wk of age. RUN and NO RUN showed different skeletal muscle transcriptomic profiles both pre- and postapex. Additionally, growth and development pathways are differentially regulated between RUN and NO RUN. Angiomotin mRNA was downregulated postapex in RUN and NO RUN. Furthermore, strong significant correlations to Vo2 peak and trends for decreased protein concentration supports angiomotin's potential importance in our model. Contrary to our primary hypothesis, wheel running was not sufficient to delay the chronological age of lifetime-apex Vo2 peak decline, whereas AICAR delayed it 1 wk.
Source: Physiological Genomics - Category: Genetics & Stem Cells Authors: Tags: Systems Biology of Exercise Source Type: research