Effects of ageing and exercise training on endothelium‐dependent vasodilatation and structure of rat skeletal muscle arterioles

Abstract

Ageingreducesendothelium-dependentvasodilatationinhumansandanimals,andinhumans, exercise training reverses the ageing-associated reduction in endothelium-dependent vasodilatation. The purpose of this study was to determine the mechanism(s) by which 10-12 weeks of treadmill exercise enhances endothelium-dependent vasodilatation in muscles of differing fibre composition from young and old rats. Three-and 22-month-old male Fischer 344 rats were assigned to young sedentary, young exercise-trained, old sedentary, or old exercisetrained groups. Arterioles were isolated from the soleus and gastrocnemius muscles; luminal diameter changes were determined in response to the endothelium-dependent vasodilator acetylcholine (ACh, 10 −9 -10 −4 mol l −1 ) alone and in the presence of the nitric oxide synthase (NOS) inhibitor L-NAME (10 −5 mol l −1 ) or the combination of L-NAME and the cyclooxygenase inhibitor indomethacin (10 −5 mol l −1 ). Training ameliorated the ageing-induced reduction in endothelium-dependent vasodilatation in soleus muscle arterioles. Treatment with L-NAME alone and in combination with indomethacin abolished differences in ACh vasodilatation occurring with ageing and training. Expression of endothelial NOS (eNOS) mRNA in soleus arterioles was unaltered by ageing, whereas eNOS protein was increased with age; training elevated both eNOS mRNA and protein. In gastrocnemius muscle arterioles, ageing did not alter maximal vasodilatation, but ageing and training increased maximal arteriolar diameter. These results demonstrate that ageing-induced reductions and training-induced enhancement of endothelial vasodilatation both occur through the nitric oxide signalling mechanism in highly oxidative skeletal muscle, but ageing and training do not appear to act on the same portion of the signalling cascade.

Passive leg movement enhances interstitial VEGF protein, endothelial cell proliferation, and eNOS mRNA content in human skeletal muscle

“…Studies on the regulation of capillarization in response to exercise and training have shown that acute exercise enhances the protein and mRNA levels of several angiogenic factors such as vascular endothelial growth factor (VEGF) (21,31), matrix metalloproteinase-2 (MMP-2) (6,15), and endothelial nitric oxide synthase (eNOS) (11,34). In addition, acute exercise has been shown to cause an increase in the muscle interstitial concentration of VEGF (18,21), which, at least in part, appears to reflect a release of VEGF from skeletal muscle cells as demonstrated in cultured muscle cells (22).…”

The effect of scheduled forced wheel activity on body weight in male F344 rats undergoing chronic circadian desynchronization

“…13 On the other hand, the forced wheel activity might alter the metabolic system by which the weight-gaining effect of chronic mismatches of circadian rhythms was counteracted. Previous studies have established that, with the activity intensity above certain levels, exercises -either voluntarily 20,21,30 or involuntarily [31][32][33] -increase food intake but reduce body weight gain when compared with sedentary controls, that is, exercises reduce feed efficiency. Furthermore, the serum cholesterol 34 and triglyceride 21,30,34 levels were lower and the organ weight of the lungs, hearts 33 and adrenal glands 21,33 was higher in rats that were exercised.…”

Interleukin-6 and hepcidin expression changes in cardiac tissue of long-term trained and untrained rats after exhaustive exercise*

“…Exercise-trained rats (T) ran on the treadmill for 30 min, 5 days a week for 12 weeks (10). Each session included warm-up and cool-down periods (running 7 m/min, 0° incline).…”