Swimming exercise significantly reversed the aging-related decline in myocyte fractional shortening (7.60 vs 4.56, p<0.01) and improved structural abnormalities in senescent female rat hearts.
Does swimming exercise improve aging-related contractile and structural abnormalities in female rat hearts?
Swimming exercise improves contractile function and structural abnormalities in senescent female rat hearts by mitigating oxidative stress, without altering Ca2+ handling.
Absolute Event Rate: 7.6% vs 4.56%
p-value: p=<0.01
BACKGROUND: The objective of this study was to examine the effect of swimming exercise on aging-related Ca2+ handling alterations and structural abnormalities of female rat heart. METHODS: For this purpose, 4-month and 24-month old female rats were used and divided into three following groups: sedentary young (SY), sedentary old (SO), and exercised old (Ex-O). Swimming exercise was performed for 8 weeks (60 min/day, 5 days/week). Myocyte shortening, L-type Ca2+ currents and associated Ca2+ transients were measured from ventricular myocytes at 36 ± 1°C. NOX-4 levels, aconitase activity, glutathione measurements and ultrastructural examination by electron microscopy were conducted in heart tissue. RESULTS: Swimming exercise reversed the reduced shortening and slowed kinetics of aged cardiomyocytes. Although the current density was similar for all groups, Ca2+ transients were higher in SO and Ex-O myocytes with respect to the SY group. Caffeine-induced Ca2+ transients and the integrated NCX current were lower in cardiomyocytes of SY rats compared with other groups, suggesting an increased sarcoplasmic reticulum Ca2+ content in an aged heart. Aging led to upregulated cardiac NOX-4 along with declined aconitase activity. Although it did not reverse these oxidative parameters, swimming exercise achieved a significant increase in glutathione levels and improved structural alterations of old rats' hearts. CONCLUSIONS: We conclude that swimming exercise upregulates antioxidant defense capacity and improves structural abnormalities of senescent female rat heart, although it does not change Ca2+ handling alterations further. Thereby, it improves contractile function of aged myocardium by mitigating detrimental effects of oxidative stress.
Öztürk et al. (Mon,) conducted a other in Aging-related cardiac contractile abnormalities (n=60). Swimming exercise vs. Sedentary old (SO) and Sedentary young (SY) was evaluated on Myocyte fractional shortening (p=<0.01). Swimming exercise significantly reversed the aging-related decline in myocyte fractional shortening (7.60 vs 4.56, p<0.01) and improved structural abnormalities in senescent female rat hearts.