Engagement in more light physical activity and less sedentary time does not protect against age-related declines in cerebrovascular reactivity in healthy older adults

Abstract

Decreased resting cerebral blood flow and cerebrovascular reactivity (CVR) are important age-related factors associated with an increased risk of stroke or dementia. However, these declines may be exaggerated by a sedentary lifestyle or blunted by engaging in more aerobic-based physical activity. The objective of the present project was to explore differences in resting middle cerebral artery velocity (MCAv), CVR, moderate-to-vigorous intensity physical activity (MVPA), light-intensity physical activity, and sedentary time between healthy younger and older adults. Transcranial Doppler assessed resting right MCAv, and repeated breath hold-derived CVR between 15 younger (27 ± 10 years, 11 females) and 14 older adults (67 ± 9 years, 9 females). Habitual activity was assessed via a thigh-worn activPAL monitor worn 24-h/day for (6.0 ± 0.8 days). As expected, younger adults had higher resting MCAv (65 ± 11 versus 40 ± 22 cm/s, p = 0.003) and CVR (5.2 ± 3.2 versus 2.0 ± 0.7 cm/s/mmHg, p = 0.004). Older adults engaged in less habitual MVPA (202 ± 103 versus 269 ± 81 min/week, p = 0.05) and sedentary time (10.2 ± 2.7 versus 12.2 ± 1.8 h/day, p = 0.048) but accrued more light physical activity (575 ± 91 versus 402 ± 89 min/week, p = 0.015). Despite engaging in more habitual light physical activity and less sedentary time, older adults still exhibited lower MCAv and CVR compared with their younger peers.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1007/s11357-025-02061-2.

Introduction

Cerebrovascular disease is the fifth leading cause of death in the United States, 75% of which occurs in adults over the age of 65 [1–3]. Key factors in the early detection of cerebrovascular disease, stroke [4], and dementia [5] are insufficient resting cerebral blood flow (CBF) and poor cerebral arterial function, including age-related reductions in cerebrovascular reactivity (CVR) [4, 6, 7]. Older adults consistently display attenuated middle cerebral artery blood flow velocity (MCAv) and CVR responses compared with their younger peers [8–10]. However, these age-related decreases in cerebral vascular function may be lessened with more engagement in aerobic-based physical activities and/or exercise [11].

Important modifiable risk factors for cerebrovascular disease are physical inactivity and sedentary time (ST) [12]. Older adults engage in less habitual moderate-to-vigorous physical activity (MVPA) and more ST compared with younger adults [13]. Adults who engage in excessive ST (> 8 h/day) have worsened cerebrovascular functioning and increased risk of developing cerebrovascular diseases compared with those who engage in < 8 h/day of ST [14, 15]. Engagement in sufficient aerobic-based physical activity is effective in preventing the development of cerebrovascular disease [16–19]. It was previously documented in 81 healthy younger (≤ 30 years) and older males (≥ 60 years) that lifelong physical activity levels attenuated age-related declines in MCAv and CVR [20]. However, other work has reported no age-related declines in either resting MCAv or CVR (via stepped hypercapnia) in younger and older adults who engaged in ≥ 150 min of structured moderate physical activity per week [21]. However, limitations of this study were that habitual physical activity levels were measured subjectively and neither the impact of between-group differences in physical activity intensities or habitual ST were considered. This poses a limitation given the potential for measurement bias (e.g., misinterpretation, deliberate changes) and difficulty in participants recalling activities, possibly leading to an over- or under-estimation of true habitual activity [22, 23].

A prospective cohort study demonstrated that an increase of 30 min/week of MVPA was associated with a decreased risk of all-cause dementia [24]. Engaging in 2 h of additional light physical activity (LPA) per day was linked with healthy aging, categorized as survival to 70 years with no major chronic disease and no impairment performing activities of daily living (e.g., climbing a flight of stairs, carrying groceries, walking a mile, etc.) [25]. Understanding the benefits of engaging in LPA on age-related health outcomes is important given the decrease in functionality and mobility with aging, making engaging in MVPA more difficult with increasing age.

The impact of habitual aerobic-based physical activity intensity and ST have on age-related declines in CBF and CVR has yet to be investigated. Given the conflicting results presented in the literature surrounding the impact of physical activity on age-related reductions in cerebrovascular regulation, the primary objective of the present study was to determine differences in resting MCAv and CVR, while considering differences in objectively measured habitual physical activity, ST and aerobic fitness between healthy younger and older adults.

Methods

Participants

Fifteen younger (27 ± 10 years, 11 females) and 14 older, healthy (67 ± 9 years, 9 females) adults completed this study. All were non-hypertensive [i.e., resting seated systolic blood pressure (SBP) < 139 mmHg and diastolic blood pressure (DBP) < 89 mmHg], nonsmokers (i.e., had not smoked nicotine or marijuana-containing cigarettes ≥ 4 days/week within the previous 6 months), nonobese (body mass index < 30 kg/m²), and not prescribed medications that impacted cardiovascular or cerebrovascular function (e.g. statins, sildenafil, or hormone replacement therapy) in the 6 months before study entry. All premenopausal females were not pregnant or breastfeeding and tested during the early-follicular phase of a natural menstrual cycle (i.e., Days 1–5 following the onset of menstruation, n = 2), or during the placebo/inactive phase of oral combined contraceptive pill use (n = 9). All protocols and procedures conformed to the Declaration of Helsinki, except registration into a database, and were approved by the Dalhousie University Health Sciences Research Ethics Board (File# 2023–6585). Participants were informed of the methods and study design verbally and in writing before providing written informed consent.

Measurement of MCAv

The right MCAv was recorded via transcranial Doppler (Multigon Industries Inc., Neurovision, Elmsford, NY, USA) using a 2-MHz probe positioned over the trans-temporal window. The MCAv signal was identified and recorded according to standardized criteria guided by signal depth and velocity [26]. The optimal signal depth, sample volume, and power remained constant throughout the testing session by a member of the research team. The MCAv signal was recorded at 400 Hz using a dedicated data acquisition system (PowerLab, ADInstruments) and analyzed offline (LabChart, Version 8, ADInstruments, Sydney, Australia).

Assessment of resting cardiorespiratory function

Continuous heart rate (HR) was calculated from successive cardiac intervals obtained from lead II of a standard bipolar electrocardiographic recording. Beat-by-beat blood pressure was recorded using non-invasive finger photoplethysmography (Finometer Model 2; Finapres Medical Systems, Amsterdam, The Netherlands). The electrocardiogram (1000 Hz) and Finometer (200 Hz) recordings were sampled continuously (PowerLab, ADInstruments) and analysed offline (LabChart, Version 8, ADInstruments, Sydney, Australia). A ‘physiological calibration’ of the Finometer blood pressure waveform was performed using the average of 3 consistent brachial SBP and DBP values (i.e., < 2 mmHg differences between successive readings) recorded from a semi-automated vital signs monitor (Carescape v100, General Electric Healthcare, Mississauga, ON, Canada). Finometer-derived SBP and DBP values were determined as the maximum and minimum within beat values, respectively. Mean arterial pressure (MAP) was calculated as ⅓SBP + ⅔DBP.

Participants were fitted with a facemask (7450 Series Silicone V2 Oro-Nasal Mask, Hans Rudolph) attached to a commercial gas analyzer (ML206 Gas Analyzer, ADInstruments, Sydney, Australia) for the continuous determination of breath-by-breath F_ECO₂, as well as a respiratory belt (TN1132/ST Respiratory Belt Transducer, ADInstruments, Sydney, Australia) to determine breathing rate and confirm breath-hold durations (both signals sampled at 20 Hz). The P_ETCO₂ was calculated as F_ECO₂ × Barometric Pressure (mmHg). Once stable signals were attained, baseline recordings were performed for ~ 5-min while breathing spontaneously before starting the CVR assessment.

Assessment of cerebrovascular reactivity

The CVR protocol began with 30-s of paced breathing (16 breaths/min) guided by an auditory metronome. Participants held their breath for 20-s at the end of tidal expiration, followed by a forced maximal exhalation. An additional 30-s paced breathing period followed. This pattern was repeated until the participant completed a total of 8 breath holds. Peak P_ETCO₂ was determined following each breath hold and subtracted from the average of the previous 2 paced breaths [8, 27, 28]. The MCAv and P_ETCO₂ responses to the final 6 breath holds were averaged [8, 27, 28]. The first 2 breath holds were used to familiarize participants with the task [27]. Cerebrovascular reactivity was then calculated (ΔMCAv/ΔP_ETCO_2, cm/s/mmHg). To account for perfusion pressure-mediated changes in MCAv, cerebrovascular conductance index (CVCi) was also calculated (MCAv/MAP, cm/s/mmHg).

Assessment of aerobic fitness

Aerobic fitness was assessed using an incremental, maximal exercise test on an electromagnetically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands). The ergometer seat was adjusted to a comfortable position while ensuring that a slight knee bend (~ 10–20 degrees knee flexion) was achieved at the lowest pedal position. Participants were also equipped with a chest strap-based HR monitor (Polar H9, Kempele, FI) and a breathing mask (7450 Series Silicone V2 Oro-Nasal Mask, Hans Rudolph) attached to a commercial metabolic system (TrueOne 2400, Parvomedics Inc., Sandy, UT). The volume rates of oxygen consumption (V̇O₂), carbon dioxide production (V̇CO₂) and the respiratory exchange ratio (V̇CO₂/V̇O₂) were recorded.

Following a 5-min warm-up period of light-intensity cycling (50W), the workload was increased to 1 W/kg body mass and gradually increased by 15 W/min among older adults and 20 W/min among younger adults until voluntary exhaustion. Strong verbal encouragement was provided throughout the testing period. The test was terminated when: 1) a pedalling rate of 40 revolutions/min could not be maintained for ≥ 15-s, 2) there was a sudden decrease in HR of > 30 beats/min, or 3) when requested by the participant. Upon test completion, the intensity was reduced to the warm-up power output for a 5-min cool-down period. Ratings of perceived exertion were determined every ~ 2-min using the Borg 6–20 scale [29].

All data were averaged every 15-s and V̇O₂peak values determined from the greatest consecutive 30-s average. The final workload achieved was considered as the peak aerobic power. The primary criterion for the attainment of a V̇O₂max was a plateau (i.e., an increase in absolute V̇O₂ ≤ 150 ml/min or relative V̇O₂ < 2.1 ml/kg/min between successive 15-s averaged timepoints). In the absence of a plateau, a V̇O₂peak was ascribed if at least 2 of the following criteria were achieved: 1) a peak rating of perceived exertion score ≥ 18 on the Borg 6–20 scale [29], 2) a peak HR ≥ 95% of age-predicted (208 – (0.7 × age)) [30], and/or 3) a peak respiratory exchange ratio ≥ 1.15. Considering that only 7 participants achieved a V̇O₂max, but all achieved a V̇O₂peak, the latter term will be used throughout.

Assessment of habitual activity

Habitual physical and sedentary activity outcomes were recorded by an activPAL accelerometer and inclinometer (activPAL4, Pal Technologies Ltd.®, Glasgow, UK) worn 24 h per day for an average of 6.0 ± 0.8 days. The activPAL was waterproofed using a nitrile finger cot and transparent medical adhesive (Tegaderm™, 3 M, London, ON, Canada) secured to the midline of the right thigh, one-third of the way between the hip and knee [31]. Participants completed a self-report sleep log to help confirm activPAL-derived sleep time versus sedentary time. As per recommendations for valid habitual activity data [31], only participants with ≥ 4 days of activPAL data were included for analysis. The activPAL data were analyzed using a customized MATLAB program (MATLAB 2020, MathWorks, USA) to quantify total ST and standing time. Further analyses were conducted using a customized LabVIEW program (LabVIEW 2020, National Instruments, Austin, TX, USA) to determine habitual LPA, moderate-intensity physical activity (MPA), and vigorous-intensity physical activity (VPA), using height-adjusted step-rate thresholds for younger adults [32], or body mass index-adjusted step-rate thresholds for older adults [33].

Experimental design

Height and weight were measured using a calibrated stadiometer and physician’s scale (Health-O-Meter, McCook II, USA) to the nearest 0.5 cm and 0.1 kg, respectively. Body mass index was then calculated (kg/m²). All participants completed aerobic fitness testing and transcranial Doppler MCA assessment over 1–2 sessions. Specifically, the aerobic fitness test was either completed after the MCA assessment on the same day or on a later visit. Participants were always equipped with the activPAL monitor following the aerobic fitness test. Participants abstained from MVPA for 24-h, avoided foods high in saturated fats, caffeinated products, chocolate, citrus fruits, alcohol, and antioxidant supplements for 12 h, and fasted for a minimum of 6 h prior to all assessments, and confirmed they adhered to guidelines upon arrival to the laboratory. All assessments were conducted in a thermoneutral room (~ 21 °C). Barometric pressure (mmHg) was noted at the beginning of the MCA assessment for calculation of P_ETCO₂.

Statistical analysis

All dependent variables were assessed for normality using a Shapiro–Wilk test. Age, systolic blood pressure, relative V̇O₂peak, peak ratings of perceived exertion, age-predicted HR_max, peak HR, peak aerobic power, and peak P_ETCO₂ were not normally distributed and assessed using non-parametric testing. Participant characteristics, aerobic fitness, habitual activity, cardiorespiratory fitness and cerebral hemodynamic outcomes were compared between younger and older adults using an independent samples t-test (or non-parametric: Mann–Whitney U tests). Exploratory linear regressions were run to determine the effect of age on MCAv and CVR with respect to specific postures (i.e., ST, standing time), exercise intensities (i.e., LPA, MVPA), and cardiorespiratory fitness. All statistical analyses were performed using R version 4.4.0 (R Foundation for Statistical Computing, Vienna, Austria).

Results

All participant characteristics, aerobic fitness and habitual activity outcomes are presented in Table 1. No between-group differences in height, weight, or body mass index differences were observed (all, p > 0.591). There were also no differences for absolute V̇O₂peak, peak aerobic power, or peak ratings of perceived exertion (all, p > 0.09). Younger adults accumulated more ST (p = 0.048; Fig. 1A). While older adults performed more habitual LPA (p = 0.015; Fig. 1B), younger adults engaged in more MVPA (p = 0.050; Fig. 1C). There were no differences in standing times between age-groups (p = 0.201).

Table 1.

Participant descriptive characteristics, aerobic fitness and habitual activity outcomes

	Younger Adults	Older Adults
Descriptive Characteristics
Participants (females)	15 (11♀)	14 (9♀)
Age (years)	27 ± 10 (20–50)	67 ± 9 (55–83)*
Height (cm)	169.9 ± 9.3 (157.1–191.2)	170.3 ± 11.6 (147.0–193.3)
Weight (kg)	70.8 ± 15.4 (49.9–104.4)	73.8 ± 15.0 (53.3–108.8)
Body Mass Index (kg/m2)	24.4 ± 3.8 (20.1–31.2)	25.4 ± 4.0 (20.7–34.7)
Aerobic Fitness
Absolute V̇O2peak (L/min)	2.72 ± 1.04 (1.69–5.15)	2.23 ± 0.86 (1.17–3.76)
Relative V̇O2peak (ml/kg/min)	38.1 ± 9.5 (26.7–65.5)	29.4 ± 9.4 (15.6–43.6)*
Peak RER (V̇CO2/V̇O2)	1.24 ± 0.15 (1.08–1.63)	1.22 ± 0.17 (1.01–1.64)
Peak HR (beats/min)	187 ± 12 (170–205)	164 ± 18 (130–194)*
Percent Age-Predicted HR (%)	99 ± 6 (87–111)	101 ± 10 (86–125)
Peak Aerobic Power (watts)	240 ± 25 (138–432)	199 ± 22 (88–336)
Peak RPE (6–20 scale)	19 ± 1 (16–20)	19 ± 1 (16–20)
Habitual Activity
Sedentary Time (hours/day)	12.2 ± 1.8 (9.0–15.3)	10.2 ± 2.7 (7.1–16.0)*
Standing Time (hours/day)	5.7 ± 1.3 (4.0–8.2)	6.6 ± 1.6 (4.1–8.2)
Sleeping Time (hours/day)	8.7 ± 1.0 (7.3–10.5)	8.4 ± 1.0 (4.1–8.2)
LPA (mins/week)	402 ± 89 (222–520)	575 ± 191 (365–859)*
MPA (mins/week)	269 ± 81 (93–381)	202 ± 103 (54–389)*
VPA (mins/week)	60 ± 73(4–222)	67 ± 45(5–126)
MVPA (mins/week)	269 ± 81 (93–381)	202 ± 103 (54–389)*

Data are presented as means ± standard deviations (ranges). V̇O₂peak, peak volume rate of oxygen consumption; V̇CO₂, volume rate of carbon dioxide production; HR, heart rate; RER, respiratory exchange ratio; RPE, rating of perceived exertion (Borg 6–20 scale); LPA, light-intensity physical activity; MPA, moderate-intensity physical activity, VPA, vigorous-intensity physical activity. Between-group differences assessed via independent samples t-tests or Mann–Whitney U tests. ^*, p < 0.05 versus Younger Adults

Fig. 1.

Between-group comparisons for: A) total sedentary time (Younger: 12.2 ± 1.8 h/day, Older: 10.2 ± 2.7 h/day, p = 0.049), B) light-intensity physical activity (LPA, Younger: 402 ± 89 min/week, Older: 575 ± 191 min/week, p = 0.015), and C) moderate-to-vigorous intensity physical activity (MVPA, Younger: 269 ± 81 min/week, Older: 202 ± 103 min/week, p = 0.050). Data presented as means ± standard deviations, with individual data points. Males are shown in closed symbols, while females are depicted by open symbols. *, p < 0.05 versus Younger Adults

All hemodynamic variables are outlined in Table 2. Both groups had similar DBP and MAP (both, p > 0.390). Older adults had a lower resting HR (p = 0.007) and higher SBP (p = 0.015). Furthermore, older adults had reduced resting MCAv and lower CVCi (all, p < 0.004) (Table 2 and Fig. 2). Resting P_ETCO₂ was similar between groups (p = 0.343).

Table 2.

Resting hemodynamic and cerebrovascular reactivity outcomes

	Younger Adults	Older Adults
Resting Hemodynamics
Heart Rate (beats/min)	67 ± 9 (56–85)	57 ± 9 (45–71)*
Systolic Blood Pressure (mmHg)	118 ± 9 (96–131)	126 ± 6 (118–137)*
Diastolic Blood Pressure (mmHg)	69 ± 8 (55–80)	70 ± 9 (52–85)
Mean Arterial Pressure (mmHg)	81 ± 8 (66–96)	83 ± 9 (63–97)
MCAv (cm/s)	65 ± 11 (51–86)	40 ± 22 (18–89)*
CVCi (cm/s/mmHg)	0.86 ± 0.15 (0.57–1.06)	0.42 ± 0.09 (0.26–0.49)*
PETCO2 (mmHg)	40 ± 6 (31–54)	38 ± 4 (30–45)
Cerebrovascular Reactivity
Peak Mean Arterial Pressure (mmHg)	96 ± 8 (85–108)	98 ± 8 (92–109)
Peak MCAv (cm/s)	85 ± 22 (50–118)	56 ± 20 (31–98)*
Peak CVCi (cm/s/mmHg)	0.94 ± 0.26 (0.47–1.39)	0.50 ± 0.07 (0.42–0.58)*
Peak PETCO2 (mmHg)	43 ± 4 (37–51)	41 ± 6 (29–48)
CVR (cm/s/mmHg)	5.2 ± 3.2 (1.1–12.2)	2.0 ± 0.7 (1.1–3.7)*

Data presented as means ± standard deviations (ranges). MCAv, middle cerebral artery blood velocity; CVCi, cerebrovascular conductance index; P_ETCO₂, partial pressure of end-tidal carbon dioxide; Cerebrovascular Reactivity was calculated as the increase in MCAv divided by the increase in P_ETCO₂ between breaths holds and the average of the previous 2 paced breaths. The average of the final 6 of 8 breath holds were used for analysis. Between-group differences assessed via independent samples t-tests or Mann–Whitney U tests. *, p < 0.05 versus Younger Adults

Fig. 2.

Between-group comparisons for: A) resting middle cerebral artery blood velocity (MCAv, Younger: 65 ± 11, Older: 40 ± 22, p = 0.003) and B) cerebrovascular reactivity (Younger: 5.2 ± 3.2, Older: 2.0 ± 0.7, p = 0.004). Data presented as means ± standard deviations, with individual data points. Males are shown in closed symbols, while females are depicted by open symbols. *, p < 0.05 versus Younger Adults

During the breath hold protocol, older adults had lower peak MCAv and CVCi responses (both, p < 0.002), but no between-group differences were observed for peak P_ETCO₂ or MAP (both, p > 0.466; Fig. 2). Finally, CVR was lower in older adults (p = 0.004; Fig. 2).

Age was inversely associated with both MCAv and CVR when considering each postural outcome (i.e., ST, standing time), physical activity intensity (i.e., LPA, MVPA), and cardiorespiratory fitness (i.e., relative V̇O₂peak) (all, p < 0.03) and are presented in Supplementary Figs. 1 & 2.

Discussion

The primary objective of this study was to compare resting MCAv, CVR, habitual physical activity and ST between younger and older healthy adults. Cardiorespiratory fitness (Table 1), total ST (Fig. 1A), MVPA (Fig. 1C), resting MCAv (Fig. 2A) and CVR (Fig. 2B) were lower in older adults despite engaging in more LPA (Fig. 1B). These results suggest that engagement in more habitual LPA, as well as less ST, were insufficient at preventing age-related declines in CBF and CVR.

The present study demonstrates the impact of ageing on cerebrovascular function outcomes, aligning with previous work. Specifically, Ainslie et al. [34] assessed resting MCAv in a group of aerobically-trained versus untrained males (n = 307, 18–79 years) [34]. They demonstrated age-related declines in resting MCAv, regardless of training status [34]. While the exact mechanisms of this decline remain unknown, it may be attributed to impaired regulation of vascular tone and endothelial-dependent vasodilation consequent to cerebral arterial stiffening [8, 35–37]. Thomas et al. [10] compared CVR responses between younger adults (n = 9, 27 ± 4 years, 4 females), Masters athletes (n = 10, 75 ± 6 years, 3 females, 40.6 ± 2.0 ml/kg/min) and inactive older adults (n = 10, 75 ± 6 years, 2 females, 23.4 ± 1.7 ml/kg/min). They determined that CVR was lower in both the Masters athletes and inactive older adults versus younger adults [10], outlining similar age-related attenuation in CVR responses demonstrated in the present study. Furthermore, Klein et al. [8] compared resting MCAv and CVR outcomes (via repeated breath holds) between younger (n = 20, 24 ± 4 years, 9 females) and older adults (n = 20, 71 ± 7 years,11 females). Similar to the present study, they reported that older adults had reduced resting MCAv and CVR responses [8]. Finally, both our study and that by Klein et al. [8] observed attenuated baseline and breath hold-induced peak MCAv in older adults. The observed age-related differences in CVR that were observed in this study could be attributed to the reduced peak MCAv responses in older adults, as there were no between-group differences in peak P_ETCO₂.

Although the age-associated reductions in MCAv and CVR we observed align with previous literature, none of the studies mentioned above considered the potential impact of both habitual physical activity levels and cardiorespiratory fitness. The 24-h Canadian movement guidelines suggest engaging in at least 150 min/week of MVPA [38]. Meeting these MVPA guidelines has been shown to improve peripheral vascular functioning among older adults [39], although it remains unclear whether this remains true among cerebral vessels. Bailey et al. [20] demonstrated that engaging in ≥ 150 min per week of MVPA attenuated the age-related decline in aerobic fitness, MCAv and CVR among healthy males, although this was not measured objectively [20]. On average, our older adults exceeded this threshold, although they still engaged in less MVPA compared with the younger adults (Table 1, Fig. 1C). Considering the results demonstrated by Bailey et al. [20] in conjunction with the results from this study, it could be hypothesized that while meeting MVPA guidelines may attenuate the age-related decline in MCAv and CVR, it may not be sufficient in restoring function to that of a younger adult. This hypothesis is further confirmed by the results of Miller et al. [21] who demonstrated lower CVR responses in older adults who met these MVPA guidelines compared with younger adults. The present study confirms the findings of Miller et al. [21] but is strengthened by having objectively measured habitual activity outcomes, eliminating the measurement bias that accompanies measuring habitual activity subjectively [23]. Whether a threshold of weekly MVPA required to improve resting MCAv or CVR responses among older adults exists has yet to be established and provides grounds for future work.

Interestingly, the older adults in the present study engaged in more weekly LPA (Table 1, Fig. 1B) and less ST (Table 1, Fig. 1D). Engaging in LPA has been positively associated with the onset of chronic disease, physical function, medication use [40], as well as an increased odds of healthy aging [25]. While evidence exists to support the positive implications of engaging in increased LPA on health outcomes, our older adults engaged in more LPA but still had lower resting MCAv and CVR outcomes. This suggests that high levels of LPA may not be a sufficient stimulus to protect against the age-related declines in cerebrovascular functioning.

The 24-h Canadian movement guidelines also recommend that adults do not engage in more than 8 h of daily ST [38], a threshold that was exceeded by both age groups. Decreasing daily ST improves cerebrovascular regulation among older adults [41]. Although our older adults engaged in less ST than the younger adults (Table 1), their lower resting MCAv and CVR suggest that this was not protective against age-related declines in cerebrovascular outcomes. Whether meeting sedentary behaviour guidelines, in isolation or combined with all recommendations, provides a protective effect to the age-related declines in outcomes of cerebrovascular functioning should be more thoroughly investigated.

The present study is the first study to explore the relationship between habitual activity and sedentary patterns on cerebrovascular regulation outcomes. In addition, we considered cardiorespiratory fitness, as measured using the gold standard method of indirect calorimetry. However, investigating the direct impact of exercise training or changes in habitual activity through an interventional design would have further strengthened the study. Objective habitual physical activity was only assessed over one week, which may not provide a sufficient window for capturing true physical and sedentary activities. While previous work has outlined seasonal variations in PA levels, it remains unclear whether year-round fluctuations in PA engagement impact cerebrovascular function [42]. Future work should consider assessing habitual activity and cerebrovascular outcomes throughout the year to account for potential season-dependent changes in activity. Furthermore, the use of non-imaging TCD units only provides an indirect measure of CBF and cannot assess changes in lumen diameter. In addition, the measurement of MCAv via TCD is an outcome of oxygen delivery but does not provide insight into oxygen extraction or utilization.

In conclusion, older adults have worse cerebrovascular functioning outcomes than younger adults. Increased engagement in MVPA and corresponding improvements to cardiorespiratory fitness offer neuroprotective benefits and blunts age-related declines in cerebrovascular function [20]. Compared to LPS, MVPA generates larger hyperemic and shear stress responses, which would provide a greater stimulus for vascular endothelial adaptations [43]. In contrast, engagement in more habitual LPA (and less total ST) is unlikely to provide the hormetic stress required to increase aerobic fitness, improve endothelial vasodilatory function and subsequent cerebrovascular adaptations necessary to provide the same level of benefit in older adults. In younger healthy adults, we identified a positive relationship between habitual LPA and popliteal artery endothelial-dependent vasodilation [44]. It is unclear whether the benefit of engaging in more habitual LPA exists on peripheral vasculature health in older adults. The result of this study suggests that higher levels of daily LPA do not offer this protection to the cerebral vasculature in older healthy adults”.

As demonstrated by the results of this study, LPA may not serve as a sufficient stimulus to see improvements in cerebral vascular function in older adults. Whether achieving MVPA and/or ST guidelines provides a protective effect against these age-related declines in cerebrovascular functioning should be systematically investigated.

Supplementary Information

Below is the link to the electronic supplementary material.

Author contributions

Molly K Courish and Derek S Kimmerly contributed to the study conception and design. Material preparation, data collection and analysis were performed by Molly K Courish and Abigail V. Wickens. The first draft of the manuscript was written by Molly K Courish and all authors commented on all versions of the manuscript. All authors read and approved the final manuscript.

Funding

MKC was supported by a Level 2 Killam PreDoctoral Scholarship.

Data Availability

Data will be made available upon reasonable request.

Declarations

Ethics and consent to participate

All protocols and procedures conformed to the Declaration of Helsinki, except registration into a database, and were approved by the Dalhousie University Health Sciences Research Ethics Board (File# 2023–6585). Participants were informed of the methods and study design verbally and in writing before providing written informed consent.

Competing interests

The authors declare no conflicts of interest.