Background Sedentary behaviour is associated with impaired cognition, whereas exercise can acutely improve cognition.
Objective We compared the effects of a morning bout of moderate-intensity exercise, with and without subsequent light-intensity walking breaks from sitting, on cognition in older adults.
Methods Sedentary overweight/obese older adults with normal cognitive function (n=67, 67±7 years, 31.2±4.1 kg/m2) completed three conditions (6-day washout): SIT (sitting): uninterrupted sitting (8 hours, control); EX+SIT (exercise + sitting): sitting (1 hour), moderate-intensity walking (30 min), uninterrupted sitting (6.5 hours); and EX+BR (exercise + breaks): sitting (1 hour), moderate-intensity walking (30 min), sitting interrupted every 30 min with 3 min of light-intensity walking (6.5 hours). Cognitive testing (Cogstate) was completed at four time points assessing psychomotor function, attention, executive function, visual learning and working memory. Serum brain-derived neurotrophic growth factor (BDNF) was assessed at six time points. The 8-hour net area under the curve (AUC) was calculated for each outcome.
Results Working memory net AUC z-score·hour (95% CI) was improved in EX+BR with a z-score of +28 (−26 to +81), relative to SIT, −25 (−79 to +29, p=0.04 vs EX+BR). Executive function net AUC was improved in EX+SIT, −8 (− 71 to +55), relative to SIT, −80 (−142 to −17, p=0.03 vs EX+SIT). Serum BDNF net AUC ng/mL·hour (95% CI) was increased in both EX+SIT, +171 (−449 to +791, p=0.03 vs SIT), and EX+BR, +139 (−481 to +759, p=0.045 vs SIT), relative to SIT, −227 (−851 to +396).
Conclusion A morning bout of moderate-intensity exercise improves serum BDNF and working memory or executive function in older adults, depending on whether or not subsequent sitting is also interrupted with intermittent light-intensity walking.
Trial registration number ACTRN12614000737639.
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Contributors MJW, DJG, KAE, EC, LHN, RL, PW, C-JB, NTL, BK, GL, NO and DWD contributed to the design of the study. MJW coordinated the trial and data collection and is the study guarantor. IH and JL assisted with recruitment and data collection. NE assisted with biochemical analysis. MJW and EC wrote the statistical analysis plan. MJW, DJG and DWD wrote the paper. KAE, EC, IH, LHN, RL, PW, C-JB, JL, NE, NTL, BAK, GL and NO reviewed and edited the paper. All authors approved the final version of the manuscript.
Funding This work was funded by a project grant from the National Health and Medical Research Council of Australia (1062338) and supported in part by the Victorian Government’s OIS Program. MJW is supported by The University of Western Australia and the Baker Heart and Diabetes Institute. DJG is supported by an NHMRC Principal Research Fellowship (APP1080914). EC is supported by an ARC Future Fellowship (ARC FT140100085). IH is supported by the University of Turku, Hospital District of Southwest Finland and the Juho Vainio Foundation. DD is supported by an NHMRC Senior Research Fellowship (NHMRC APP1078360). GL is supported by an NHMRC Senior Research Fellowship (APP1042492). The laboratory of GL has recently received research funding from Medtronic, Abbott (formerly Solvay) Pharmaceuticals, Servier Australia and Allergan. GL has acted as a consultant for Medtronic.
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval Ethical approval was obtained from the Alfred Hospital Ethics Committee (181-14) and The University of Western Australia Human Research Ethics Committee (RA/4/1/6990).
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement The data that support the findings of this study are available from the corresponding author upon reasonable request.
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