Brain Research 887 (2000) 199–202
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Short communication
Effect of long-term swimming exercise on somatosensory evoked
potentials in rats
a , b a a c
¨
¨
*
¨
¨
Umit Kemal Senturk
, Berrin Aktekin , Oktay Kuru , Filiz Gunduz , Necdet Demir ,
d
Mehmet R. Aktekin
a
Department of Physiology, School of Medicine, Akdeniz University, 07070, Antalya, Turkey
b
Department of Neurology, School of Medicine, Akdeniz University, 07070, Antalya, Turkey
c
Department of Histology and Embryology, School of Medicine, Akdeniz University, 07070, Antalya, Turkey
d
Department of Public Health, School of Medicine, Akdeniz University, 07070, Antalya, Turkey Accepted 3 October 2000
Abstract
The study investigated whether long-term swimming exercise prevents age-related changes in rat somatosensory evoked potentials (SEPs) and somatosensory cortex (SC) morphology. A total of 25 9-month-old rats were assigned to an exercise or control group. The exercise group swam 1 h / day five times weekly for 1 year. The results showed that long-term exercise prevented age-related changes in SEPs and SC morphology. 2000 Elsevier Science B.V. All rights reserved.
Theme: Development and regeneration
Topic: Sensory systems
Keywords: Evoked potential; Physical training; Aging; Somatosensory cortex
Most biological functions deteriorate with age. Even SEPs as age advances [4,9]. On the structural side, light though life expectancy appears to be universal and ge- microscopy investigations have revealed approximate but netically determined in all species, it can be modified by reliable information about morphological changes in the rat external factors such as stress, nutrition, environmental cortex with aging [13,14,16].
conditions and physical activity [2,10]. In recent years, To our knowledge, the effects of short- and long-term research has focused on the identification of contributing training on SEPs have not yet been studied in the rat. Our factors that potentially alter the rate and extent of de- aim was to find out whether long-term physical training generative change in aging. Findings have suggested that delays the onset of age-related changes in SEPs and regular exercise may reduce age-related degenerative somatosensory cortex (SC) morphology in this animal changes in neurological parameters such as cognitive model. We also sought to determine whether short-term function, electroencephalographic (EEG) activity, reaction exercise produces electrophysiological effects.
time and event-related potentials (ERPs) [2–5]. The mech- The study was approved by the university’s Committee anisms by which physical exercise affect the age-related for the Use of Animals in Research and followed the changes of CNS structure and function are undoubtedly guidelines established by the European Communities complex and are not well understood. Council Directive. A total of 25 9-month-old male Wistar The recording of somatosensory evoked potentials albino rats weighing 250–350 g were randomly assigned to (SEPs) yields valuable information about CNS function, either the control (n513) or the exercise (n512) group. and studies have shown that reliable changes occur in Standard rat chow and tap water were provided ad libitum, the animals were housed at 23628C under a 12 / 12-h dark / light cycle, and both groups were handled equally *Corresponding author. Tel.:190-242-227-4483; fax: 1
90-242-227-often. The exercise group swam 1 h / day (always between 4495.
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E-mail address: [email protected] (U.K. Senturk). 09:00 and 11:00 h) five times weekly over 1 year. The
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200 U.K. Senturk et al. / Brain Research 887 (2000) 199 –202
swimming was done in two 100350350-cm tanks of tap Cresyl Violet. The three anatomically and physiologically water that were kept at 32–348C. distinct regions of the rat primary SC (parietal 1 (Par 1), SEP recordings were done at three time points in both forelimb (FL) and hind limb (HL)) [20] were examined groups, namely, before the exercise program started using a monitorised Zeiss-Axioplan light microscope. A (baseline), at 3 months and at 12 months. In the exercise total of five sections from each rat’s brain were quantita-group, the recordings at 3 and 12 months were done 48 h tively analyzed by counting the neurons and glial cells in after swimming. All animals were deprived of food for 24 the cortical layer (I–VI) in an unbiased counting frame
2
h prior to SEP recordings. Ether anesthesia was used, and (2500mm ) under the340 objective [13,19]. The neuron-all recording data were collected within 15 min after the to-glial cell ratio (N : G) was calculated by dividing the loss of the corneal reflex and pain response. Rectal total number of neurons by the total number of glial cells. temperatures were maintained between 35 and 378C, by Statistical analysis was performed using the SPSS for keeping the animals warm using a heating table when Windows software package. The data were distributed
necessary. normally and are presented as means6S.D. We used
Cortical SEPs were recorded from a needle electrode Student’s t-test to compare the two groups’ data, and the inserted subcutaneously over the hind limb projection area paired t-test to make comparisons within the groups. We of the somatosensory cortex. The active electrode was also applied 2 (swimming and control groups) 33 (data placed 9 mm anterior and 2 mm lateral to the bregma [12]. sets collected at three time points) repeated measures A reference electrode was placed 20 mm anterior to the analysis of variance. P-values less than 0.05 were consid-bregma at the midline, and the grounding electrode was ered significant.
attached to the animal’s tail [6]. SEPs were recorded using From baseline to 12 months, the groups registered a Nihon Kohden (MEM-4104) Neuropack Four EMG / EP similar mean body and heart weight gains, but the mean measuring system, with a filter set to bandwidth 20–3000 heart weight-to-body weight ratio was significantly higher Hz. The contralateral posterior tibial nerve was stimulated in the swimming group (0.0031860.00058) than in the with a ring electrode anode distally. The stimulus duration control group (0.0027460.00052) (P,0.05).
was 0.2 ms, the repetition rate was 3 Hz, and we used an Table 1 lists all the measured latency and amplitude data intensity sufficient to produce a definite twitch of the big for each group. In the recordings done at baseline and at 3 toe (|2.4–5 mA). For each set of recordings we took the months, there were no significant differences in latency mean of 200 responses, and did this at least twice to ensure and amplitude findings between or within the groups, and response reproducibility. Hind limb transcutaneous stimu- the data for both time points were similar. However, at 12 lation evoked electrical activity with prominent first-posi- months the control group’s N1 latency was significantly tive (P1), first-negative (N1) and second-positive (P2) longer, and their N1-P1 and P1-N2 amplitudes signifi-components. A negative wave was expressed as an upward cantly lower than the values recorded previously. These deflection. Peak latency and peak-to-peak amplitude were findings also differed significantly from the exercise group measured for each component in order to quantify the results at 12 months. Apart from this, the control group P1 effects of exercise on neuronal responses to somatosensory and N2 latencies were similar to those in the first two data stimulation in the aging brain. sets. In the exercise group, none of the SEP component After the final SEP recordings were completed, each rat measurements at 12 months differed statistically from was euthanized with 1 g / kg urethane injected intraperito- previously recorded values.
neally. The brain was immediately removed, fixed, dehy- The results of the histologic examination of the somato-drated and embedded in paraffin. Serial sections (20-mm sensory cortex are summarized in Table 2. The N : G was thick) were then cut in the coronal plane and stained with significantly higher in the exercise group than in the
Table 1
a
SEP latencies and amplitudes of control (n513) and exercise (n512) groups
Control Exercise
Baseline 3 Months 12 Months Baseline 3 Months 12 Months
Latencies (ms)
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U.K. Senturk et al. / Brain Research 887 (2000) 199 –202 201 Table 2
The neuron : glia (N : G) ratios of parietal 1 area (Par 1), forelimb area (FL) and hind limb area (HL) in the cortical layer I–VI of control (n513) and
a
Values are mean6S.D., significant difference between groups * P,0.05, ** P,0.01, *** P,0.001.
controls in all regions except layer I in Par 1, layer I–II in density increase. The later could be due to the reduction of
FL and layer III in HL. synaptic density with age.
Our main aim was to investigate whether long-term The impact of physical exercise on age-related changes exercise delays the onset of age-related changes in SEPs in CNS structure and function is not well understood, but and SC morphology in rats. In addition, we looked at the several mechanisms have been proposed to explain this impact of short-term physical training on SEPs. Short-term complex relationship. Animal and human studies have both exercise produced no changes in either group’s SEP proven that aerobic exercise is associated with permanent recordings, but long-term physical training did prevent the structural changes in the brain [7,17], and with elevated age-related changes that have been documented in rat SEPs biogenic amine levels, enhanced oxygen transport and and SC morphology. Similar findings have been reported utilization [8,18]. These mechanisms are not mutually in human studies regarding short-term physical activity exclusive. Rather, these and other exercise-related
pro-[1,11]. cesses likely work together to decelerate neuronal
degene-Brain bioelectric activity measurements (EEG, ERPs ration.
and visual, somatosensory and auditory evoked potentials In line with other published evidence, our findings (Eps)) provide valuable information about aging [4,9]. suggest that a sedentary lifestyle contributes to physiologi-Research has proven that advancing age is accompanied by cal and structural CNS deterioration during aging. It seems slowing of dominant brain rhythms on EEG, and by that regular exercise may effectively slow the rate of prolonged latency and decreased amplitude in ERPs and functional decline as the body ages. It is currently unclear Eps [4,15]. These characteristic findings are considered to at what age range exercise effects on neuronal structure reflect a reduction in CNS inhibitory abilities, and may be and function are greatest. However longitudinal and cross-linked to lower neuron and synapse density, loss of over designed studies are necessary to clarify the effect of dendritic spines, impaired cerebral circulation, and changes life-long physical activity on age-related functional de-in neurotransmitter synthesis and degradation [2]. cline.
As expected, at 12 months we noted significant age-related changes in the control rats’ SEPs. Control N1 latency was longer, and the N1-P1 and P1-N2 amplitudes
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