Effects of induced local ischemia during a 4-km cycling time trial on neuromuscular fatigue development

The present study analyzed the effects of local ischemia during endurance exercise on neuromuscular fatigue (NMF). Nine cyclists performed, in a counterbalanced order, two separate 4-km cycling time trials (TT) with (ISCH) or without (CONTR) induced local ischemia. NMF was characterized by using isometric maximal voluntary contractions (IMVC), while central [voluntary activation (VA)] and peripheral fatigue [peak torque of potentiated twitch (TwPt)] of knee extensors were evaluated using electrically-evoked contractions performed before (PRE) and 1 min after (POST) the TT. Electromyographic activity (EMG), power output (PO), oxygen uptake (V̇O2) and rating of perceived exertion (RPE) were also recorded. The decrease in IMVC (-15±9% vs -10±8 %, P=0.66), VA (-4±3% vs -3±3%, P=0.46), and TwPt (-16±7% vs -19±14%, P=0.67) were similar in ISCH and CONTR. Endurance performance was drastically reduced in ISCH condition (512±29 s) compared to CONTR (386±17 s) (P<0.001), which was accompanied by lower EMG, PO, and V̇O2 responses (all P<0.05). RPE was greater in ISCH compared to CONTR (P < 0.05), but the rate of change was similar throughout the TT (0.016±0.005 and 0.020±0.006 RPE·s-1, respectively; P>0.05). These results indicate that similar end-exercise NMF levels were accompanied by impaired endurance performance in ISCH compared to CONTR. These novel findings suggest that the local reduced oxygen availability affected the afferent feedback signals to the central nervous system, ultimately increasing perceived effort and reducing muscle activity and exercise intensity in order to avoid surpassing a sensory tolerance limit before the finish line.

Local and Remote Postconditioning Decrease Intestinal Injury in a Rabbit Ischemia/Reperfusion Model

Intestinal ischemia/reperfusion (I/R) injury is a significant problem that is associated with high morbidity and mortality in critical settings. This injury may be ameliorated using postconditioning protocol. In our study, we created a rabbit intestinal I/R injury model to analyze the effects of local ischemia postconditioning (LIPo) and remote ischemia postconditioning (RIPo) on intestinal I/R injury. We concluded that LIPo affords protection in intestinal I/R injury in a comparable fashion with RIPo by decreasing oxidative stress, neutrophil activation, and apoptosis.

The Roads to Mitochondrial Dysfunction in a Rat Model of Posttraumatic Syringomyelia

The pathophysiology of posttraumatic syringomyelia is incompletely understood. We examined whether local ischemia occurs after spinal cord injury. If so, whether it causes neuronal mitochondrial dysfunction and depletion, and subsequent energy metabolism impairment results in cell starvation of energy and even cell death, contributing to the enlargement of the cavity. Local blood flow was measured in a rat model of posttraumatic syringomyelia that had received injections of quisqualic acid and kaolin. We found an86±11% reduction of local blood flow at C8 where a cyst formed at 6 weeks after syrinx induction procedure(P<0.05), and no difference in blood flow rate between the laminectomy and intact controls. Electron microscopy confirmed irreversible neuronal mitochondrion depletion surrounding the cyst, but recoverable mitochondrial loses in laminectomy rats. Profound energy loss quantified in the spinal cord of syrinx animals, and less ATP and ADP decline observed in laminectomy rats. Our findings demonstrate that an excitotoxic injury induces local ischemia in the spinal cord and results in neuronal mitochondrial depletion, and profound ATP loss, contributing to syrinx enlargement. Ischemia did not occur following laminectomy induced trauma in which mitochondrial loss and decline in ATP were reversible. This confirms excitotoxic injury contributing to the pathology of posttraumatic syringomyelia.