title: Spatial memory is improved by aerobic and resistance exercise through divergent molecular mechanisms.
abstract: A growing body of scientific evidence indicates that exercise has a positive impact on human health, including neurological health. Aerobic exercise, which is supposed to enhance cardiovascular functions and metabolism, also induces neurotrophic factors that affect hippocampal neurons, thereby improving spatial learning and memory. Alternatively, little is known about the effect of resistance exercise on hippocampus-dependent memory, although this type of exercise is increasingly recommended to improve muscle strength and bone density and to prevent age-related disabilities. Therefore, we evaluated the effects of resistance training on spatial memory and the signaling pathways of brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1), comparing these effects with those of aerobic exercise. Adult male Wistar rats underwent 8 weeks of aerobic training on a treadmill (AERO group) or resistance training on a vertical ladder (RES group). Control and sham groups were also included. After the training period, both AERO and RES groups showed improved learning and spatial memory in a similar manner. However, both groups presented distinct signaling pathways. Although the AERO group showed increased level of IGF-1, BDNF, TrkB, and β-CaMKII (calcium/calmodulin-dependent kinase II) in the hippocampus, the RES group showed an induction of peripheral and hippocampal IGF-1 with concomitant activation of receptor for IGF-1 (IGF-1R) and AKT in the hippocampus. These distinct pathways culminated in an increase of synapsin 1 and synaptophysin expression in both groups. These findings demonstrated that both aerobic and resistance exercise can employ divergent molecular mechanisms but achieve similar results on learning and spatial memory.
authors.affiliation: Psychobiology and Exercise Research Center, CEPE, São Paulo, Brazil.
authors.forename: R C
authors.initials: RC
authors.lastname: Cassilhas
authors.forename: K S
authors.initials: KS
authors.lastname: Lee
authors.forename: J
authors.initials: J
authors.lastname: Fernandes
authors.forename: M G M
authors.initials: MG
authors.lastname: Oliveira
authors.forename: S
authors.initials: S
authors.lastname: Tufik
authors.forename: R
authors.initials: R
authors.lastname: Meeusen
authors.forename: M T
authors.initials: MT
authors.lastname: de Mello
mesh_terms: D000818:Animals; D015153:Blotting, Western; D019208:Brain-Derived Neurotrophic Factor / Q000502:physiology; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000096:biosynthesis; D003345:Corticosterone / Q000096:biosynthesis; D004797:Enzyme-Linked Immunosorbent Assay; D006624:Hippocampus / Q000378:metabolism / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008568:Memory / Q000502:physiology*; D051058:Oncogene Protein v-akt / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D017526:Receptor, IGF Type 1 / Q000502:physiology; D020813:Receptor, trkB / Q000096:biosynthesis / Q000502:physiology; D055070:Resistance Training; D015398:Signal Transduction / Q000502:physiology; D013028:Space Perception / Q000502:physiology*; D016704:Synapsins / Q000096:biosynthesis
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D016704:Synapsins; D007334:Insulin-Like Growth Factor I; D017526:Receptor, IGF Type 1; D020813:Receptor, trkB; D051058:Oncogene Protein v-akt; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D003345:Corticosterone