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The present study aimed to show whether long-term moderate magnesium (Mg)-deficient (150 mg/kg) and Mg-supplemented (3200 mg/kg) diets (versus control diet: 800 mg/kg), modified the occurrence of cardiovascular risk induced by aging in the rat.Cardiovascular and arterial functions were determined by a systemic hemodynamic study and by ex vivo measurements of vasoconstriction and endothelium dependent-vasorelaxation. Arterial wall structure was determined using pressure myograph chamber and histomorphometric methods.The main changes observed in old rats (96 weeks old) fed a control diet, in comparison to adult rats (16 weeks old) were increased pulse pressure, a loss of aortic endothelium-dependent relaxation, increased aortic wall thickness and a decrease of the aortic wall elastin/collagen ratio. Long-term moderate Mg deficiency progressively increased systolic blood pressure. Intra-arterial pulse pressure was higher in Mg-deficient old rats than in age-matched control rats. Histological examination showed that Mg deficiency increased the age-induced deleterious effects on composition and structure of aorta (media thickness, increased collagen content and reduction in the elastin/collagen ratio), which lead to large artery rigidity. Hypertension and increased pulse pressure may have contributed to the increase in the mortality rate observed in the hypertensive Mg-deficient group. Although the long-term Mg-supplemented diet lowered blood pressure and decreased the mortality rate, it had no significant effect on aortic wall thickening and stiffening.It is suggested that a long-term and moderate Mg-deficient diet increases age-induced arterial thickness and stiffness in rats, and thus increases the cardiovascular risks incurred by aging.

The antiatherogenic role of exercise is poorly understood. We examined the swimming exercise-induced vascular mechanisms which enhance the endothelial vasodilator function in apoE(-/-) mice. Male apoE(-/-) mice treated for 9 weeks with a lipid-rich diet were divided into two groups: the exercise group (apoE(-/-) X), which underwent a 9-week swimming protocol (50 min/day; 5days/week) and the sedentary group (apoE(-/-) S). C57BL/6 mice were used as the control group. Atherosclerotic lesions in the aortic roots were significantly reduced in apoE(-/-) X compared to apoE(-/-) S. Relaxation to acetylcholine was improved in apoE(-/-) X as compared to apoE(-/-) S and control mice with E(max) and pD(2) values significantly higher. pD(2) values in response to papaverine were higher in apoE(-/-) X than in the other groups. Relaxation in response to A23187 and DEA-NONOate were similar. These findings suggest that swimming training may increase the sensitivity of relaxation to acetylcholine, which in turn activates acetylcholine-mediated signaling pathways leading to increased NO bioactivity. Swimming may also prolong the signaling actions of NO by stimulating the sensitivity of vascular smooth muscle cells to cyclic nucleotides. These appear to be the key mechanisms underlying the improvement of the NO-cGMP pathway in exercised apoE(-/-) mice.

International audience; Epidemiological and experimental studies have indicated a relationship among aging, dietary Mg, inflammatory stress, and cardiovascular disease. Our aim in the present study was to investigate possible links between dietary Mg, oxidant stress parameters, and inflammatory status with aging in rats. We designed a long-term study in which rats were fed for 22 months with moderately deficient (150 mg/kg), standard (800 mg/kg), or supplemented (3200 mg/kg) Mg diets. Comparisons were made with young rats fed with the same diets for 1 month. Compared to the standard and supplemented diets, the Mg-deficient diet significantly increased blood pressure, plasma interleukin-6, fibrinogen, and erythrocyte lysophosphatidylcholine, particularly in aging rats, it decreased plasma albumin. The impairment of redox status was indicated by increases in plasma thiobarbituric acid reactive substances and oxysterols and an increased blood susceptibility to in vitro free-radical-induced hemolysis. We concluded that Mg deficiency induced a chronic impairment of redox status associated with inflammation which could significantly contribute to increased oxidized lipids and promote hypertension and vascular disorders with aging. Extrapolating to the human situation and given that Mg deficiency has been reported to be surprisingly common, particularly in the elderly, Mg supplementation might be useful as an adjuvant therapy in preventing cardiovascular disease.

Soybean proteins, a rich source of isoflavones, taken immediately after an ovariectomy prevent bone loss in rats. Exercise-induced stimuli are essential for bone growth. Few studies exist about the combined effects of swim training and soybean protein supplementation on bone metabolism. So, the purpose of this study was to investigate, in 48 female Sprague-Dawley rats (12 weeks old) the effects of an 8-week swim-training regimen (1 h/day, 5 days/week) and dietary soybean proteins (200 g/kg diet) on bone metabolism. Rats were randomly assigned to four groups: (1) ovariectomized fed with a semisynthetic control diet; (2) ovariectomized fed with a soybean protein-enriched semisynthetic diet; (3) ovariectomized trained to exercise and fed with control diet; (4) ovariectomized trained to exercise and fed with a soybean protein diet. Following the treatment period, body weight gain was identical in the four groups. Soybean protein supplementation increased bone calcium content, and reduced plasma osteocalcin values, without significant modification of calcium balance and net calcium absorption. Swim training enhanced plasma and bone calcium content and calcium balance and net calcium absorption. It did not modify either plasma osteocalcin values or urinary deoxypyridinoline excretion. Both exercise and soybean protein intake increased plasma on bone calcium without modifying net calcium absorption or bone markers. In conclusion, we demonstrated, in ovariectomized rats, that swimming exercise and dietary supplementation with soy proteins do not have synergistic effects on calcium metabolism and bone markers.

International audience; The purpose of this study was to investigate the effects of a 8-week of swim training on total plasma homocysteine and cysteine levels in 16 male Sprague-Dawley rats aged 17 weeks. We also evaluated the activity of hepatic cystathionine beta-synthase (CBS), an enzyme involved in the metabolism of Hcy, the concentration of plasma glutathione, taurine, and a fraction of vitamin B6: the pyridoxal 5-phosphate (PLP). After one week of acclimatization, rats were randomly divided into two groups: 8 non-trained (NTR) and 8 trained rats (TR). Following the training period, body weight gain was lower in TR than in NTR. Plasma homocysteine did not differ among groups while significantly lower plasma cysteine and taurine levels were found in TR (157.83 +/- 8.6 micromol/L; 133.01 +/- 9.32 micromol/L; P < 0.05) compared with data of NTR (176.19 +/- 4.9 micromol/L; 162.57 +/- 8.16 micromol/L; P < 0.05). No significant changes in hepatic CBS activity were observed in TR compared with NTR. Moreover, values for plasma glutathione and PLP concentrations were not affected by training.These results indicate that training reduces plasma cysteine and taurine levels whereas it does not modify other studied parameters. Thus, physical training may regulate cysteine metabolism.

Aims: The aim of this study was to evaluate whether endurance exercise in middle-aged men induces changes in plasma total homocysteine (tHcy) and total cysteine (tCys), and whether these changes depend on the diet especially on vitamin B6, folic acid and vitamin B12 intakes. Methods: Twelve trained subjects (52.33 ± 2.4 years) and twelve untrained subjects (56.23 ± 0.9 years) volunteered for the present study. tHcy and tCys were measured with high-pressure liquid chromatography at rest in both groups and during an incremental exercise performed on a cycle ergometer until exhaustion in the trained subjects. Results: At baseline homocysteinemia and cysteinemia were lower in trained subjects (7.48 ± 0.4 and 183.45 ± 13.6 µmol/l) compared with untrained subjects (9.79 ± 0.4 µmol/l, p < 0.001; 229.01 ±14.7 µmol/l, p < 0.05, respectively). Incremental exercise also induced a decrease in tHcy and tCys concentrations. Moreover, tHcy concentration was negatively related to the folic acid and B12 intakes in untrained (r = –0.589, p < 0.05; r = –0.580, p < 0.05, respectively) as well as in trained groups (r = –0.709, p < 0.01; r = –0.731, p < 0.01, respectively) whereas no correlation between tCys and vitamin in the diet was observed. Conclusion: This study demonstrates that the combined effects of a chronic physical exercise and a high folate and vitamin B12 intake could be responsible for the reduction of plasma tHcy and tCys concentrations that might be a key for the prevention of many diseases.

Resume Introduction Le but de ce travail a ete d'evaluer, in vivo, les effets d'un entrainement isometrique sur la fonction endotheliale de rates Sprague–Dawley ovariectomisees. Synthese Les animaux ont ete randomises en quatre groupes : 1) temoin ; 2) ovariectomise sedentaire ; 3) ovariectomise sedentaire recevant une injection quotidienne de 17β-estradiol ; 4) ovariectomise entraine. La reactivite vasculaire a ete mesuree, sur des anneaux aortiques precontractes a la noradrenaline, par des doses croissantes d'acetylcholine. La relaxation induite par l'acetylcholine est significativement augmentee dans le groupe de rates entrainees. Conclusions Ces resultats indiquent que l'entrainement isometrique ameliore la fonction endotheliale de la rate ovariectomisee.

Using female 4-week-old Sprague–Dawley rats, we investigated the effects of 14 weeks of progressive strength isometric training on endothelium dysfunction after estrogen deficiency. We also proposed possible mechanism(s) by which such training acted on endothelium-dependent vasodilation in thoracic aortic rings. Rats were randomly divided into 4 groups of 8 rats: a sham operated group, an ovariectomized sedentary group receiving 17β-estradiol vehicle s.c. daily, an ovariectomized sedentary group receiving a daily injection of 20 µg·kg–1 17β-estradiol s.c., and an ovariectomized exercised group receiving daily s.c. vehicle. Vascular reactivity of aortic rings have been evaluated by a cumulative dose of acetylcholine (ACh), in the presence or absence of l-NAME (N-nitro-l-arginine methyl ester), indomethacin, thapsigargin, iberiotoxin, apamin, and tetraethylammonium. Ovariectomy markedly decreased the relaxation caused by ACh, whereas 17β-estradiol treatment induced a significant increase in the relaxation elicited by ACh. Isometric exercise enhanced relaxation due to ACh. This enhancement was attenuated in the presence of l-NAME, indomethacin, thapsigargin, iberiotoxin, and apamin. Our data indicated, for the first time, that the endothelium-dependent relaxant response to ACh was markedly improved in trained ovariectomized rats. This increased vasodilation is mediated by nitric oxide, cyclooxygenase, sarco-endoplasmic reticulum Ca2+-ATPase pathways, and endothelium-derived hyperpolarizing factor. Finally, this study suggested that resistance training may provide benefits in addressing vascular dysfunction consequent to a decline in estrogen levels after menopause. However, any benefits for age-related vascular dysfunction remain to be demonstrated.