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results of these studies suggested that heat stress is effective in prevention of disuse muscle atrophy. All reports described above-employed 7- or 8-week-old rats; however, effects of aging on the prevention of disuse muscle atrophy attributable to heat
eyes, cataracts, vitreous floaters, and age-related macular degeneration. Industrialised nations are ageing societies with a rapidly growing proportion of people over age 65, and in many countries, this is the fastest-growing segment of society
chronic illnesses, it showed ageing as a natural process. The definition and medicalization of old age have previously resulted in the second half of life being the age of various illnesses, and death was a medical failure factor. Elderly people were
ageing: mechanisms and interventions . Front Aging 2022 ; 3 : 866718 . https://doi.org/10.3389/fragi.2022.866718 . 35821824 6. Xu M , Pirtskhalava T , Farr JN , Weigand BM , Palmer AK , Weivoda MM , et al. Senolytics improve
markers and leg muscle size. Mech. Ageing Dev., 2013, 134 (11–12), 531–540. Bouzid, M. A., Hammouda, O., Matran, R., et al.: Low intensity aerobic exercise and oxidative stress markers in older adults. J. Aging Phys
life expectancy is greatly increased, the population pyramid is described with a rectangular shape [ 2 ]. The ageing causes many physiological changes in the skin. According to the WHO classification, old age from the age of 75, but also
Obesity of middle-aged mammals is followed at old age by anorexia and cachexia leading to sarcopenia. Complex age- and body composition-related alterations in the regulation of energy homeostasis may be assumed in the background. We aimed to test the possible contribution of age- and body composition-related changes of satiety responses to catabolic brain-gut-axis peptide cholecystokinin (CCK) to these alterations in energy balance during aging. Male Wistar rats (6–8 animals/group) aged 2 months (juvenile), 3 months (young adult), 6 or 12 months (early or late middle-aged), and 24 months (old) were injected intraperitoneally with 5 μg CCK-8 prior to re-feeding after 48-h food-deprivation. CCK suppressed re-feeding in young adult (26.8%), early middle-aged (35.5%), and old (31.4%) animals, but not in juvenile or late middle-aged rats (one-way ANOVA). CCK-resistance of 12 months old rats was prevented by life-long calorie-restriction: CCK suppressed their re-feeding by 46.8%. Conversely, in highfat diet-induced obese 6 months old rats CCK failed to suppress re-feeding. In conclusion, age-related changes in satiety responsiveness to CCK may contribute to the age-related obesity of middle-aged as well as to the anorexia of old animals. CCK-responsiveness is also influenced by body composition: calorie-restriction prevents the resistance to CCK, pre-existing obesity enhances it.
The purpose of our study was to investigate whether endothelium-derived relaxations induced by store depletion are altered in aging rat thoracic aorta. Vascular responses were measured in aortic segments isolated from young (2–4 month) and old (20–24 month) male Sprague-Dawley rats. In phenylephrine-contracted intact tissues, receptor-mediated and receptor-independent endothelium-derived relaxations were induced by acetylcholine (ACh) and sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) blocker cyclopiazonic acid (CPA), respectively. In addition, CPA-induced changes in intracellular calcium levels were monitored in fura-2-loaded endothelium-denuded tissues. Real-time quantitative reverse transcription polymerase chain reaction and western blot analysis were performed to determine the transient receptor potential canonical (TRPC) 4 mRNA and protein levels. Endothelial TRPC4 mRNA levels were apparently decreased in aging rats. Immunoblot analysis showed that TRPC4 protein levels significantly decreased in intact aorta from 20- to 24-month-old rats compared to that from 2- to 4-month-old rats. ACh- and CPA-induced endothelium-dependent relaxations decreased in old rat aorta without any change in direct vasodilation induced by sodium nitroprusside. Store-operated Ca2+ entry (SOCE) induced by CPA was significantly decreased, whereas sarcoplasmic reticulum Ca2+ release was unaffected in endothelium-denuded aging rat aorta. In conclusion, TRPC4 downregulation could be associated with decreased endothelium-dependent vasorelaxations. As endothelial nitric oxide synthase is activated by SOCE-induced caveolar internalization, tracking the expression levels of SERCA, ion channels, and/or associated proteins involved in SOCE would lead to the development of novel therapeutics for age-related vasospastic disorders with dysfunctional endothelium.
It is unknown whether age-related site-specific muscle loss is associated with areal bone mineral density (aBMD) in older adults. To examine the relationships between aBMD and whole-body muscle thickness distribution, 97 healthy adults (46 women and 51 men) aged 50–78 years volunteered. Total and appendicular lean soft tissue mass, aBMD of the lumbar spine (LS-aBMD) and femoral neck (FN-aBMD) were determined using dual-energy X-ray absorptiometry. Muscle thickness (MT) was measured by ultrasound at nine sites of the body (forearm, upper arm, trunk, upper leg, and lower leg). Relationships of each co-variate with aBMD were tested partialling out the effect of age. aBMD was not correlated with either MT of the trunk or anterior lower leg in either sex. In men, significant and relatively strong correlations were observed between anterior and posterior upper arms, posterior lower leg, and anterior upper leg MT and LS-aBMD or FN-aBMD. In women, significant correlations were observed between anterior and posterior upper legs, posterior lower leg, and anterior upper arm MT and FN-aBMD. LS-aBMD was only correlated with forearm and posterior upper leg MT in women. In conclusion, the site-specific association of MT and aBMD differs between sexes and may be associated with the participants’ daily physical activity profile.
For evaluating the age-related change in noradrenaline (NA)-induced contraction of isolated rat carotid artery (CA), the effect of α and β adrenoreceptor (AR) blockers and the role of nitric oxide (NO) were investigated. Methods: Concentration-response curves to NA (10−10–10−4 M) and α1 agonist phenylephrine (PE; 10−10–10−5 M) were constructed in isolated CA rings from young and middle-aged rats. The effects of nitric oxide synthase (NOS) inhibitor (L-NAME; 100 μM), α1-AR antagonist (prazosin; 0.1 μM), α2-AR antagonist (yohimbine; 0.1 μM) and β-AR antagonist (propranolol; 1 μM) on NA-induced contraction of isolated CA rings were examined. In CA rings preconstricted with NA, the responses to α2-AR agonist (clonidine; 10−7–10−5 M), β-AR agonist (isoprenaline; 10−8–10−5 M),), sodium nitroprusside (SNP; 10−9–10−5 M) were assessed. Results: The maximum contractile response of CA to NA and to PE was higher in younger than in middle-aged rats. Prazosin reduced the contractile response to NA in both groups, while propranolol, yohimbine and L-NAME did not affect NA-induced contraction in either of them. Clonidine, isoprenaline and SNP produced a dose-dependent vasorelaxation of CA rings, isoprenaline-induced vasodilatation was lower in middle-aged rats, while there was no difference in clonidine or SNP-induced relaxant effect between the two groups. Conclusions: NA-induced contraction of isolated rat CA rings is decreased in old rats, this is related to α1-AR. β-AR mediated dilatation was compromised in middle-aged rats (endothelium-dependent). α2-AR and SNP-mediated dilator effect seems to be unchanged.
