Abstract
Physical exercise is one of the best interventions for improving traumatic brain injury (TBI) outcomes. However, an argument has been raised regarding the timing at which physical exercise should be initiated. In this study, male Wistar rats were subjected to stab wounding of the right hemisphere to develop a TBI model and were forced to walk once on a treadmill at a 5-m/min pace at 24h or 48h after TBI for 10min. Injured brain tissue was dissected after TBI to evaluate the effects of exercise. Behavioral abnormalities and motor impairment were assessed by various behavioral tests between 2 and 3 weeks after TBI. Exercise did not affect the circulating corticosterone levels and the weight of the adrenal glands. Exercise particularly that at 24h, worsened the motor impairment of the left forelimbs. Quantitative reverse-transcription polymerase chain reaction showed that exercise at 24h increased proinflammatory cytokines and chemokines on the third day while suppressing the proinflammatory reactions on the fourth day. Exercise at both time points decreased expression of transforming growth factor (TGF) β1 and its receptor TGFβR1. Exercise at 24h increased phosphorylation of IκB kinase on the fourth day, which may be correlated with the decreased effects of TGFβ1. Even a low-intensity exercise activity could cause deleterious effects when it is initiated within 48h after the onset of severe TBI, probably because of the resulting proinflammatory effects. Therefore, rehabilitation exercise programs should be initiated after 48h of TBI onset.
Highlights
Traumatic brain injury (TBI) causes more than one-third of all injury-related deaths (Majdan et al, 2016)
The present one-time exercise model involved a forced, slow, 10min walk on a treadmill, and it did not cause either the elevation of plasma corticosterone levels or changes in adrenal gland weight, the continuous forced exercise increases corticosterone levels in circulation (Hayes et al, 2008; Nishioka et al, 2016) or in feces (Svensson et al, 2016)
It has not been settled whether the effects of increased corticosterone level caused by forced exercise are beneficial or not
Summary
Traumatic brain injury (TBI) causes more than one-third of all injury-related deaths (Majdan et al, 2016). TBI is one of the leading causes of incurable neurological disability and/or psychological problems affecting several million people worldwide every year (Corps et al, 2015; Gyoneva and Ransohoff, 2015). The sequelae following TBI include personality changes, deficits in learning and memory, an increased risk of neurodegenerative changes, such as Alzheimer’s disease in addition to chronic traumatic encephalopathy (Griesbach, 2011; McKee et al, 2013). The incidence of TBI has increased in recent years, partly due to the growth of the elderly population (Ramanathan et al, 2012). Despite the serious pathological conditions and intensive research, established interventions to ameliorate the outcome of TBI are limited. Rehabilitation exercise programs may exert the best ameliorative effects (Griesbach, 2011; Rimmer et al, 2010)
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