Efficacy and safety of very early mobilisation within 24 h of stroke onset (AVERT): a randomised controlled trial
Early exercise improves cerebral blood flow through increased angiogenesis in experimental stroke rat model
So what is the fucking time to start rehab?
AbstractThe effectiveness of the rehabilitative benefits of physical exercise appears to be contingent upon when the exercise is initiated after stroke. The present study assessed the hypothesis that very early exercise increases the extent of apoptotic cell death via increased expression of proapoptotic proteins in a rat stroke model. Adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2 hr using an intraluminal filament and assigned to four nonexercise and three exercise groups. Exercise on a Rota-Rod was initiated for 30 min at 6 hr (considered very early), at 24 hr (early), and at 3 days (relatively late) after reperfusion. At 24 hr after exercise, apoptotic cell death was determined. At 3 and 24 hr after exercise, the expression of pro- and antiapoptotic proteins was evaluated through Western blotting. As expected, ischemic stroke significantly increased the levels of apoptotic cell death. Compared with the stroke group without exercise, apoptotic cell death was further increased (P < 0.05) at 6 hr but not at 24 hr or 3 days with exercise. This exacerbated cell injury was associated with increased expression of proapoptotic proteins (BAX and caspase-3). The expression of Bcl-2, an antiapoptotic protein, was not affected by exercise. In ischemic stroke, apoptotic cell death was enhanced by very early exercise in association with increased expression of proapoptotic proteins. These results shed light on the time-sensitive effect of exercise in poststroke rehabilitation. © 2016 Wiley Periodicals, Inc.
The molecular underpinnings of apoptotic cell death following cerebral ischemia are well established. During periods of reduced oxygen delivery, proapoptotic proteins, such as caspase-3 and BAX, become upregulated and are one of the major causes of neuronal death during ischemia/reperfusion injury (Wu et al., 2003). Conversely, Bcl-2 is an antiapoptotic protein that plays a critical role in cellular survival by acting as a repressor of apoptosis (Korsmeyer, 1995). Thus, the aim of the present study was to determine the effect of physical exercise therapy on apoptotic cell death and the expression of associated pro- and antiapoptotic proteins. We directly compared the effect of poststroke exercise on brain injury at 6 hr, 24 hr, and 3 days after reperfusion with the corresponding nonexercise group. Following a 2-hr middle cerebral artery occlusion (MCAO), we evaluated the extent of apoptotic cell death and the expression of proapoptotic (caspase-3 and BAX) and antiapoptotic (Bcl-2) protein