Abstract
PurposeSedentary behaviour is negatively associated with mood and cognition, yet how acute sitting contributes to these overall associations is unknown. Since sitting heightens inflammation and impairs cerebrovascular function, this study investigated the hypothesis that these sitting-induced changes are related to impaired mood and cognition.MethodsTwenty-five healthy desk workers (18 male, 28.3 ± 7.5 years, BMI: 24.2 ± 3.3 kg∙m−2) were recruited. During laboratory visit one, participants were familiarised with cognitive performance tests measuring executive function, attention and working memory. During laboratory visit two, participants completed 6 h of continuous, uninterrupted sitting. At baseline and after 6 h, serum markers of inflammation, middle cerebral artery blood flow velocity (MCAv), cerebrovascular carbon dioxide reactivity (CVR), dynamic cerebral autoregulation (CA), cognitive performance and mood (positive and negative affect, alert, contented and calm) were assessed. Data were analysed using paired-samples t tests and correlation analyses.ResultsFollowing sitting, C-reactive protein (∆-1.0 µg/ml) and tissue plasminogen activator (∆-360.4 pg/ml) decreased (p < 0.05), MCAv reduced (∆-2.9 cm∙s−1, p = 0.012) and normalised gain increased in the very low frequency range, indicating impaired CA (∆ + 0.22%·mmHg−1, p = 0.016). Positive affect (∆-4.6, p < 0.001), and alert (∆-10.6 p = 0.002) and contented (∆-7.4, p = 0.006) mood states also decreased following sitting. No significant changes in interleukin-6, tumour necrosis factor-alpha, von Willebrand factor, CVR or cognitive performance were observed (p > 0.05). The observed changes in inflammation and cerebrovascular function were not related to changes in mood (p > 0.05).ConclusionAlterations in inflammation or cerebrovascular function following six hours of prolonged, uninterrupted sitting are not related to the observed reductions in mood, indicating other mechanisms underlie the relationship between acute sitting and mood disturbances.
Highlights
cerebral autoregulation (CA) Cerebral autoregulation cerebral blood flow (CBF) Cerebral blood flow CVR Cerebrovascular carbon dioxide reactivity CVC Cerebrovascular conductance common carotid artery (CCA) Common carotid artery heart rate (HR) Heart rate high frequency (HF) High frequency high-sensitivity c-reactive protein (hs-CRP) High-sensitivity c-reactive protein IL-6 Interleukin-6 low frequency (LF) Low frequency mean arterial pressure (MAP) Mean arterial pressure middle cerebral artery blood flow velocity (MCAv) Middle cerebral artery blood flow velocity Positive and Negative Affect Schedule (PANAS) Positive and negative affect schedule PETCO2 Pressure of end tidal CO2 sedentary behaviour (SB) Sedentary behaviour tissue plasminogen activator (t-PA) Tissue plasminogen activator
HR in the supine (p = 0.022, d = 0.48) and seated (p = 0.003, d = 0.49) postures were significantly reduced at posture and all other measurements were repeated (POST) compared to PRE (Table 2)
There was no significant difference between PRE and POST supine (p = 0.365) or seated (p = 0.306) PETCO2 (Table 2)
Summary
CA Cerebral autoregulation CBF Cerebral blood flow CVR Cerebrovascular carbon dioxide reactivity CVC Cerebrovascular conductance CCA Common carotid artery HR Heart rate HF High frequency hs-CRP High-sensitivity c-reactive protein IL-6 Interleukin-6 LF Low frequency MAP Mean arterial pressure MCAv Middle cerebral artery blood flow velocity PANAS Positive and negative affect schedule PETCO2 Pressure of end tidal CO2 SB Sedentary behaviour t-PA Tissue plasminogen activator.
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