Twelve weeks of treadmill exercise does not alter age–dependent chronic kidney disease in the Fisher 344 male rat

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Non–technical summary

In older people, the function of the kidney deteriorates, and one possible way to slow this process down is through exercise. Exercise increases the abundance of important enzymes that are needed for optimal vessel health and kidney function, for instance the nitric oxide synthase and superoxide dismutase (SOD) enzymes. It also reduces oxidative stress, a type of cellular injury caused by highly reactive molecules. When we compared young and old sedentary rats to young and old exercise–trained (12 weeks treadmill) rats, we found that exercise was not effective in reversing the age–related kidney changes. In old rats, renal function declined as did the abundance of the protective SOD enzymes, and oxidative stress increased; interestingly, exercise did not influence these changes. Our results suggest that the cardiovascular benefits of exercise do not necessarily extend to the kidney.

The ageing kidney exhibits slowly developing chronic kidney disease (CKD) and is associated with nitric oxide (NO) deficiency and increased oxidative stress. The impact of exercise on the ageing kidney is not well understood. Here, we determined whether 12 weeks of treadmill exercise can influence age–dependent CKD in old (22–24 months) Fisher 344 (F344) male rats by comparing sedentary (SED) and exercise (EX) trained rats; young (3 months) rats were also studied. In addition to renal structure and function, we assessed protein levels of various isoforms of the NO synthases (NOS) and superoxide dismutase (SOD) enzymes as well as markers of oxidative stress, in kidney cortex and medulla. Renal function as determined by plasma creatinine, proteinuria, and glomerular structural injury worsened with age and was unaffected by exercise. Ageing also increased the protein abundance of neuronal NOSβ and p22phox while decreasing extracellular (EC) and copper/zinc (CuZn) SOD, in kidney cortex and medulla. H2O2 content and nitrotyrosine abundance also increased in the kidney with age. None of these age–related changes were altered with exercise. However, exercise did increase renal cortical endothelial (e)NOS and EC SOD in young rats. Data indicate that exercise–induced increases in eNOS and EC SOD seen in young rats are lost with age. We conclude that chronic exercise is ineffective in reversing age–dependent CKD in the male F344 rat.

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