Feng Lin1, Ping Ren2, Kelly Cotton3, Anton Porsteinsson4, Mark Mapstone5, Kathi L Heffner4. 1. School of Nursing, University of Rochester Medical Center, Rochester, NY; Department of Psychiatry, University of Rochester Medical Center, Rochester, NY. Electronic address: Vankee_lin@urmc.rochester.edu. 2. School of Nursing, University of Rochester Medical Center, Rochester, NY; Department of Brain and Cognitive Science, University of Rochester, Rochester, NY. 3. Department of Brain and Cognitive Science, University of Rochester, Rochester, NY. 4. Department of Psychiatry, University of Rochester Medical Center, Rochester, NY. 5. Department of Neurology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY.
Abstract
OBJECTIVES: Adaptive physiological stress regulation is rarely studied in mild cognitive impairment (MCI). Here we targeted mental fatigability (MF) as a determinant of altered high frequency heart rate variability (HF-HRV) reactivity in individuals with MCI, and examined frontobasal ganglia circuitry as a neural basis supporting the link between MF and HF-HRV reactivity. METHODS: We measured mental fatigability and HF-HRV during a 60-minute cognitive stress protocol in 19 individuals with MCI. HF-HRV responses were modeled using a quadratic equation. Resting state functional connectivity of intra- and inter-network frontobasal ganglia circuitry was assessed using blood-oxygen-level-dependent magnetic resonance imaging among seven of the participants. RESULTS: Lower MF was associated with faster and greater rebound in U-shape HF-HRV reactivity, which linked to a stronger connectivity between right middle frontal gyrus and left putamen. CONCLUSIONS: Results suggest that MF may contribute to abnormal physiological stress regulation in MCI, and fronto basal ganglia circuitry may support the link.
OBJECTIVES: Adaptive physiological stress regulation is rarely studied in mild cognitive impairment (MCI). Here we targeted mental fatigability (MF) as a determinant of altered high frequency heart rate variability (HF-HRV) reactivity in individuals with MCI, and examined frontobasal ganglia circuitry as a neural basis supporting the link between MF and HF-HRV reactivity. METHODS: We measured mental fatigability and HF-HRV during a 60-minute cognitive stress protocol in 19 individuals with MCI. HF-HRV responses were modeled using a quadratic equation. Resting state functional connectivity of intra- and inter-network frontobasal ganglia circuitry was assessed using blood-oxygen-level-dependent magnetic resonance imaging among seven of the participants. RESULTS: Lower MF was associated with faster and greater rebound in U-shape HF-HRV reactivity, which linked to a stronger connectivity between right middle frontal gyrus and left putamen. CONCLUSIONS: Results suggest that MF may contribute to abnormal physiological stress regulation in MCI, and fronto basal ganglia circuitry may support the link.
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