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Insulin resistance is a major contributor to the neuroplasticity deficits observed in patients with metabolic disorders. However, the relative contribution of peripheral versus central insulin resistance in the development of neuroplasticity deficits remains equivocal. To distinguish between peripheral and central insulin resistance, we developed a lentiviral vector containing an antisense sequence selective for the insulin receptor (LV-IRAS). We previously demonstrated that intra-hippocampal injection of this vector impairs synaptic transmission and hippocampal-dependent learning and memory in the absence of peripheral insulin resistance. In view of the increased risk for the development of neuropsychiatric disorders in patients with insulin resistance, the current study examined depressive and anxiety-like behaviors, as well as hippocampal structural plasticity in rats with hippocampal-specific insulin resistance. Following hippocampal administration of either the LV-control virus or the LV-IRAS, anhedonia was evaluated by the sucrose preference test, despair behavior was assessed in the forced swim test, and anxiety-like behaviors were determined in the elevated plus maze. Hippocampal neuron morphology was studied by Golgi-Cox staining. Rats with hippocampal insulin resistance exhibited anxiety-like behaviors and behavioral despair without differences in anhedonia, suggesting that some but not all components of depressive-like behaviors were affected. Morphologically, hippocampal-specific insulin resistance elicited atrophy of the basal dendrites of CA3 pyramidal neurons and dentate gyrus granule neurons, and also reduced the expression of immature dentate gyrus granule neurons. In conclusion, hippocampal-specific insulin resistance elicits structural deficits that are accompanied by behavioral despair and anxiety-like behaviors, identifying hippocampal insulin resistance as a key factor in depressive illness.

OMNI ratings of perceived exertion (RPE) and physiological responses in children (n=7 boys, 8 girls, 11.1±1.0 years) were examined during estimation (graded exercise test [GXT] and steady-state) and production (steady-state) trials on a cycle ergometer. Peak oxygen consumption (VOpeak) was determined via a GXT with RPE estimated every 30 s. Later, two 6-min trials were completed: Participants 1) estimated RPE at ~75% of VOpeak, 2) produced a level of exertion corresponding to their RPE at ~75% of VOpeak during the GXT. Data analysis included a one-way MANOVA and a paired t-test. The target intensity during the GXT corresponded to 74.2±2.5% of VOpeak; the steady-state estimation and production trials were performed at 76.5±2.7% and 68.5±14.1% of VOpeak, respectively (p>0.05). Mean RPE at ~75% of VOpeak during the GXT and production trial was 6.7±1.5; during the steady-state estimation trial RPE was 5.8±2.0 (p>0.05). There were no differences (p>0.05) in the physiological responses. Participants estimated RPE similarly at ~75% of VOpeak during both graded and steady-state exercise, but when asked to produce a given RPE, marked variability was observed in physiological responses. These findings may have implications in optimizing exercise prescriptions for children.

HRR and HRV findings suggest there are no differences in autonomic function during recovery from maximal exercise in lean and obese 8- to 12-year old children.