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Background: Sarcopenia, delayed blood pressure (BP) recovery following standing, and orthostatic hypotension (OH) pose significant clinical challenges associated with ageing. While prior studies have established a link between sarcopenia and impaired BP recovery and OH, the underlying haemodynamic mechanisms remain unclear. Methods: We enrolled 107 participants aged 50 and above from a falls and syncope clinic, conducting an active stand test with continuous non-invasive haemodynamic measurements. Hand grip strength and five-chair stand time were evaluated, and muscle mass was estimated using bioelectrical impedance analysis. Participants were categorised as non-sarcopenic or sarcopenic. Employing mixed-effects linear regression, we modelled the effect of sarcopenia on mean arterial pressure and heart rate after standing, as well as Modelflow®-derived parameters such as cardiac output, total peripheral resistance, and stroke volume, while adjusting for potential confounders. Results: Sarcopenia was associated with diminished recovery of mean arterial pressure during the 10–20 s period post-standing (β −0.67, p < 0.001). It also resulted in a reduced ascent to peak (0–10 s) and recovery from peak (10–20 s) of cardiac output (β −0.05, p < 0.001; β 0.06, p < 0.001). Furthermore, sarcopenia was associated with attenuated recovery (10–20 s) of total peripheral resistance from nadir (β −0.02, p < 0.001) and diminished recovery from peak (10–20 s) of stroke volume (β 0.54, p < 0.001). Notably, heart rate did not exhibit a significant association with sarcopenia status at any time interval post-standing. Conclusion: The compromised BP recovery observed in sarcopenia appears to be driven by an initial reduction in the peak of cardiac output, followed by attenuated recovery of cardiac output from its peak and total peripheral resistance from its nadir. This cardiac output finding seems to be influenced by stroke volume rather than heart rate. Possible mechanisms for these findings include cardio-sarcopenia, the impact of sarcopenia on the autonomic nervous system, and/or the skeletal muscle pump. [ABSTRACT FROM AUTHOR]

Background Sarcopenia and orthostatic hypotension are growing age-related health burdens associated with adverse outcomes, including falls. Despite a possible pathophysiological link, the association between the 2 disorders is not well elucidated. We sought to investigate this relationship in The Irish Longitudinal Study on Ageing (TILDA). Methods Data from 2 858 participants at wave 3 of TILDA were analyzed. Probable sarcopenia was defined as per the European Working Group on Sarcopenia in Older People revised definition cutoffs (hand grip strength [HGS] <27 kg in men, <16 kg in women, and/or 5-chair stand test [5CST] time >15 seconds). Participants underwent an active stand orthostatic test with continuous blood pressure (BP) monitoring. Multilevel mixed-effects models, controlling for possible confounders, were used to assess the effect of probable sarcopenia by HGS and 5CST criteria on the change in BP after standing. Results HGS- and 5CST-defined probable sarcopenia were independently associated with an attenuated BP recovery at 10–20 seconds poststand (systolic BP: β −0.54, p <.001; β −0.25, p <.001). On average, those meeting HGS probable sarcopenia criteria had a significantly lower BP at 20, 30, and 40 seconds (differences in systolic BP: −5.01 mmHg, −3.68 mmHg, −2.32 mmHg, p <.05 for all). Those meeting 5CST probable sarcopenia criteria had a significant difference in systolic BP at 20 seconds (−1.94 mmHg, p =.002) but not at 30 or 40 seconds. Conclusion Probable sarcopenia had a significant association with delayed orthostatic BP recovery, with HGS-defined probable sarcopenia having a stronger association than 5CST-defined probable sarcopenia. Results support a modest but significant pathophysiological link between probable sarcopenia and orthostatic hypotension. [ABSTRACT FROM AUTHOR]

Cognitive reserve supports cognitive function in the presence of pathology or atrophy. Functional neuroimaging may enable direct and accurate measurement of cognitive reserve which could have considerable clinical potential. The present study aimed to develop and validate a measure of cognitive reserve using task‐based fMRI data that could then be applied to independent resting‐state data. Connectome‐based predictive modelling with leave‐one‐out cross‐validation was applied to predict a residual measure of cognitive reserve using task‐based functional connectivity from the Cognitive Reserve/Reference Ability Neural Network studies (n = 220, mean age = 51.91 years, SD = 17.04 years). This model generated summary measures of connectivity strength that accurately predicted a residual measure of cognitive reserve in unseen participants. The theoretical validity of these measures was established via a positive correlation with a socio‐behavioural proxy of cognitive reserve (verbal intelligence) and a positive correlation with global cognition, independent of brain structure. This fitted model was then applied to external test data: resting‐state functional connectivity data from The Irish Longitudinal Study on Ageing (TILDA, n = 294, mean age = 68.3 years, SD = 7.18 years). The network‐strength predicted measures were not positively associated with a residual measure of cognitive reserve nor with measures of verbal intelligence and global cognition. The present study demonstrated that task‐based functional connectivity data can be used to generate theoretically valid measures of cognitive reserve. Further work is needed to establish if, and how, measures of cognitive reserve derived from task‐based functional connectivity can be applied to independent resting‐state data. [ABSTRACT FROM AUTHOR]

In this study we investigated the association between information entropy in short length blood pressure signals and physical frailty status, in a group of patients aged 50+ recruited from the Falls and Syncope Unit at the Mercer's Institute for Successful Ageing in St James's Hospital, Dublin, Ireland. This work is an external clinical validation of findings previously derived in a population-based cohort from The Irish Longitudinal Study on Ageing (TILDA). The hypothesis under investigation was that dysregulation (as quantified by entropy) in continuous non-invasive blood pressure signals could provide a clinically useful marker of physical frailty status. We found that in the 100 patients investigated, higher entropy in continuously measured resting state diastolic blood pressure was associated with worse physical frailty score, as measured by the Frailty Instrument for primary care of the Survey of Health, Ageing and Retirement in Europe (SHARE-FI). Since physical frailty is defined as a pre-disability state and hence it can be difficult for clinicians to identify at an early stage, the quantification of entropy in short length cardiovascular signals could provide a clinically useful marker of the physiological dysregulations that underlie physical frailty, potentially aiding in identifying individuals at higher risk of adverse health outcomes. [ABSTRACT FROM AUTHOR]

Background: Frailty, expressed as accumulation of health deficits in older adults, could contribute to the risk of cognitive decline. We cross‐sectionally studied the brain connectivity signatures of frailty in The Irish Longitudinal Study on Ageing (TILDA). Method: We included participants from Wave 3 of TILDA who underwent resting‐state functional MRI. Connectivity maps were based on Shen's parcellation and connectome‐based predictive modeling was used to find associations between connectivity and frailty as measured by Frailty Index (FI) (Table 1). On each iteration of a 10‐fold cross‐validation the training folds were utilized to perform partial Spearman correlations (adjusted for age, sex, and mean framewise displacement) between each brain connection and FI scores. Connections with p<0.001 correlations were selected. Network strength was computed by summing the correlations across all connections selected and a linear model built using the network strength to predict FI score. After 10 folds are complete the performance was measured with linear R values between predicted and true FI scores. This process was repeated 1000 times (with random cross‐validation splits) and mean performance metrics obtained. A permutation test was employed in which the above procedure was repeated 1000 times, with FI scores shuffled each time. Significance of selected connections was calculated as the number of permutations scores that were equal to or greater than the proper mean score, divided by 1000. Result: 347 participants were included (mean age 67.7 (SD 7.3) and 51.6% men). We obtained a connectivity network that positively correlated with frailty ("frailty network") (R = 0.169, p = 0.006) and another that negatively correlated with frailty ("robustness network") (R = ‐0.193, p = 0.006); and are depicted in Figure 1. The "frailty network" was more widespread and showed higher connectivity from right occipital to both prefrontal cortices, subcortical and left temporal cortex, whereas the "robustness network" exhibited higher functional connectivity in subcortical to left parietal and bilateral temporal cortices. Conclusion: Functional brain connectivity could be influenced by frailty. Further research should study the relationship of brain connectivity and different tools for frailty and establish how different patterns of deficit accumulation affect brain health across lifespan. [ABSTRACT FROM AUTHOR]

Background: Cerebral autoregulation (CAR) systems maintain blood flow to the brain across a wide range of blood pressures. Deficits in CAR have been linked to gait speed (GS) but previous studies had small sample sizes and used specialized equipment which impede clinical translation. The purpose of this work was to assess the association between GS and orthostatic cerebral oxygenation in a large, community-dwelling sample of older adults.Method: Data for this study came from the Irish Longitudinal Study on Ageing. A near-infrared spectroscopy (NIRS) device attached to the forehead of each participant (n = 2 708) was used to track tissue saturation index (TSI; the ratio of oxygenated to total hemoglobin) during standing. GS was assessed using a portable walkway.Results: Recovery was impaired in slower GS participants with a TSI value at 20 seconds (after standing) of -0.55% (95% CI: -0.67, -0.42) below baseline in the slowest GS quartile versus -0.14% (95% CI: -0.25, -0.04) in the fastest quartile. Slower GS predicted a lower TSI throughout the 3-minute monitoring period. Results were not substantially altered by adjusting for orthostatic hypotension. Adjustment for clinical and demographic covariates attenuated the association between but differences remained between GS quartiles from 20 seconds to 3 minutes after standing.Conclusion: This study reported evidence for impaired recovery of orthostatic cerebral oxygenation depending on GS in community-dwelling older adults. Future work assessing NIRS as a clinical tool for monitoring the relationship between GS and cerebral regulation is warranted. [ABSTRACT FROM AUTHOR]