The aim of this study was to investigate the possible beneficial effects of exercise training (ET) with omega-3/Calanus oil supplementation on cardiorespiratory and adiposity parameters in elderly women. Fifty-five women (BMI: 19-37 kg/m2, 62-80 years old) were recruited and randomly assigned to the 4 month intervention with ET and omega-3 supplementation (Calanus oil, ET-Calanus) or ET and the placebo (sunflower oil; ET-Placebo). The body composition was determined by dual-energy X-ray absorptiometry (DXA), and cardiorespiratory parameters were measured using spiroergometry and PhysioFlow hemodynamic testing. Both interventions resulted in an increased lean mass whereas the fat mass was reduced in the leg and trunk as well as the android and gynoid regions. The content of trunk fat (in percent of the total fat) was lower and the content of the leg fat was higher in the ET-Calanus group compared with the ET-Placebo. Although both interventions resulted in similar improvements in cardiorespiratory fitness (VO2max), it was explained by an increased peripheral oxygen extraction (a-vO2diff) alone in the ET-Placebo group whereas increased values of both a-vO2diff and maximal cardiac output (COmax) were observed in the ET-Calanus group. Changes in COmax were associated with changes in systemic vascular resistance, circulating free fatty acids, and the omega-3 index. In conclusion, Calanus oil supplementation during a 4 month ET intervention in elderly women improved the cardiorespiratory function, which was due to combined central and peripheral cardiodynamic mechanisms.

• Keywords
• aging, body composition, cardiac output, cardiorespiratory fitness, omega-3 fatty acids,
• MeSH
• Vascular Resistance MeSH
• Exercise physiology   MeSH
• Cardiorespiratory Fitness physiology   MeSH
• Middle Aged MeSH
• Humans MeSH
• Cardiac Output MeSH
• Fatty Acids, Omega-3 administration & dosage   MeSH
• Plankton chemistry   MeSH
• Dietary Supplements * MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Body Composition MeSH
• Aging physiology   MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Fatty Acids, Omega-3 MeSH

The aging population faces two conditions that threaten healthy aging: high fat mass (obesity) and low muscle mass and function (sarcopenia). The combination of both-referred to as sarcopenic obesity-synergistically increases the risk of adverse health outcomes. The two conditions often co-occur because they reinforce each other and share common etiologies, including poor nutrition and inactivity. All aging people are at risk of gaining weight and losing muscle mass and could benefit from improvements in physical activity, exercise and dietary intake. one specific window of opportunity is during the transient time of retirement, as older adults already need to restructure their daily activities. It is key to change lifestyle behavior in a sustainable manner, providing scientifically proven, personalized, and acceptable principles that can be integrated in daily life. Health technologies (e.g., applications) can provide promising tools to deliver personalized and appealing lifestyle interventions to a large group of people while keeping health care costs low. Several studies show that health technologies have a strong positive effect on physical activity, exercise and dietary intake. Specifically, health technology is increasingly applied to older people, although strong evidence for long term effects in changing lifestyle behavior is generally lacking. Concluding, technology could play an important role in the highly warranted prevention of sarcopenic obesity in older adults. Although health technology seems to be a promising tool to stimulate changes in physical activity, exercise and dietary intake, studies on long lasting effects and specifically targeted on older people around the time of retirement are warranted.

• Keywords
• blended care, eHealth, elderly, nutrition, physical activity, sarcopenic obesity,
• Publication type
• Journal Article MeSH

Alzheimer's disease (AD) is a neurodegenerative disease associated with human aging. Ten percent of individuals over 65 years have AD and its prevalence continues to rise with increasing age. There are currently no effective disease modifying treatments for AD, resulting in increasingly large socioeconomic and personal costs. Increasing age is associated with an increase in low-grade chronic inflammation (inflammaging) that may contribute to the neurodegenerative process in AD. Although the exact mechanisms remain unclear, aberrant elevation of reactive oxygen and nitrogen species (RONS) levels from several endogenous and exogenous processes in the brain may not only affect cell signaling, but also trigger cellular senescence, inflammation, and pyroptosis. Moreover, a compromised immune privilege of the brain that allows the infiltration of peripheral immune cells and infectious agents may play a role. Additionally, meta-inflammation as well as gut microbiota dysbiosis may drive the neuroinflammatory process. Considering that inflammatory/immune pathways are dysregulated in parallel with cognitive dysfunction in AD, elucidating the relationship between the central nervous system and the immune system may facilitate the development of a safe and effective therapy for AD. We discuss some current ideas on processes in inflammaging that appear to drive the neurodegenerative process in AD and summarize details on a few immunomodulatory strategies being developed to selectively target the detrimental aspects of neuroinflammation without affecting defense mechanisms against pathogens and tissue damage.

• Keywords
• Alzheimer’s disease, DAMPs, SASP, astrocytes, immunosenescence, inflammasome, microglia, mitochondria, neuroinflammation,
• Publication type
• Journal Article MeSH
• Review MeSH

Muscle regeneration is regulated through interaction between muscle and immune cells. Studies showed that treatment with supra-physiological doses of Non-Steroidal Anti-Inflammatory Drug (NSAID) abolished inflammatory signaling and impaired muscle recovery. The present study examines the effects of pharmacologically-relevant NSAID treatment on muscle regeneration. C57BL/6 mice were injected in the tibialis anterior (TA) with either PBS or cardiotoxin (CTX). CTX-injected mice received ibuprofen (CTX-IBU) or were untreated (CTX-PLAC). After 2 days, Il-1beta and Il-6 expression was upregulated in the TA of CTX-IBU and CTX-PL vs. PBS. However, Cox-2 expression and macrophage infiltration were higher in CTX-PL vs. PBS, but not in CTX-IBU. At the same time, anabolic markers were higher in CTX-IBU vs. PBS, but not in CTX-PL. Nevertheless, ibuprofen did not affect muscle mass or muscle fiber regeneration. In conclusion, mild ibuprofen doses did not worsen muscle regeneration. There were even signs of a transient improvement in anabolic signaling and attenuation of inflammatory signaling.

• MeSH
• Anti-Inflammatory Agents, Non-Steroidal pharmacology   MeSH
• Wound Healing drug effects   physiology   MeSH
• Ibuprofen pharmacology   MeSH
• Cardiotoxins toxicity   MeSH
• Muscle, Skeletal drug effects   injuries   pathology   physiology   MeSH
• Disease Models, Animal MeSH
• Mice, Inbred C57BL MeSH
• Mice MeSH
• Regeneration drug effects   MeSH
• Signal Transduction drug effects   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Anti-Inflammatory Agents, Non-Steroidal MeSH
• Ibuprofen MeSH
• Cardiotoxins MeSH