The aerobic training reduces the artery stiffness and systolic blood pressure. The anaerobic training such as resistance training, however, is associated with higher artery stiffness. We hypothesized that low-intensity circuit training might improve the large artery stiffness. The purpose of this study was to determine the effects of long-term low-intensity circuit training on artery stiffness in sedentary women. Twenty healthy women divided into two groups (training group and control group). In the training group, subjects asked to perform the resistance exercises consisted of arm curls, bench presses, lateral pull-downs, leg presses and squats 3 days per week for 2 months. They conducted 5 sets at 30% of their 10RM. Aerobic capacity (ventilatory threshold [VT]), muscle strength, resting blood pressure, and arterial stiffness index (brachial-ankle Pulse Wave Velocity [baPWV]) were evaluated before and after training period. After the low-intensity circuit training, work rate at VT was significantly increased (108.6±25.6W to 128.1±24.3W). The baPWV was significantly decreased (988.7±80.5cm · sec^-1 to 895.7±62.6cm · sec^-1). In control group, however, there were no significant differences during same duration. These results suggested that long-term low-intensity circuit training attenuates the large artery stiffness in healthy women. This kind of exercise may have great potential to lower the risks of circulatory illness in aged men.

It was reported that nerve fibers were present in the inner part of lumbar intervertebral discs from patients with discogenic pain. Because there are no nerve fibers in the inner part of annulus fibrosus in normal condition, this finding suggests nerve ingrowth into the disc may be a cause of discogenic pain. Disc degeneration is often asymptomatic, thus, to understand the differences between symptomatic and asymptomatic disc, it is necessary to understand the pathogenesis of discogenic pain. We recently revealed that over 90% of the nociceptive dorsal root ganglion (DRG) neurons innervating the disc are sensitive to nerve growth factor (NGF), which is related to inflammatory pain. This indicates that discogenic pain is closely related to inflammation and NGF may play a key role. The increase of inflammatory mediators in symptomatic discs has been reported; we therefore studied the effects of disc inflammation and found that it induces sensitization of disc-innervating neurons and nerve ingrowth into the disc. More recently, it was shown that annular rupture induces nerve ingrowth, an increase of inflammatory mediators in the disc, and upregulation of calcitonin gene-related peptide, a pain-related molecule in DRGs. These findings led us to believe that annular rupture triggers inflammation and nerve ingrowth, inflammatory mediators then further promote nerve ingrowth into the disc and sensitization of disc-innervating neurons, and discogenic pain finally becomes chronic. NGF, found in symptomatic discs, may act as a key factor in generating chronic discogenic pain by sensitizing disc-innervating neurons and stimulating nerve ingrowth into the disc.
Calcitonin Gene-Related Peptide ; Diagnosis-Related Groups ; Ganglia, Spinal ; Humans ; Inflammation ; Intervertebral Disc ; Intervertebral Disc Degeneration ; Nerve Fibers ; Nerve Growth Factor ; Neurons ; Rupture ; Up-Regulation

Objective: Atopic dermatitis (AD) is one of the known risk factors for Staphylococcus aureus infection. The authors report the case of a patient with cervical spondylosis and AD who developed delayed surgical site infection after posterior cervical instrumented surgery.Patient: A 39-year-old male presented to our hospital with paralysis of the left upper extremity without any cause or prior injury. He had a history of severe AD. We performed C3–C7 posterior decompression and instrumented fusion based on the diagnosis of cervical spondylotic amyotrophy. One year after surgery, his deltoid and bicep muscle strength were fully recovered. Nevertheless, his neck pain worsened 2 years after surgery following worsening of AD. One month after that, he developed severe myelopathy and was admitted to our hospital. Radiographic findings showed that all the screws had loosened and the retropharyngeal space had expanded. Magnetic resonance imaging and computed tomography showed severe abscess formation and destruction of the C7/T1 vertebrae.Result: We diagnosed him with delayed surgical site infection. Methicillin-resistant Staphylococcus aureus was identified on abscess culture. The patient responded adequately to treatment with antibiotic therapy and two debridements and the infection subsided.Conclusion: We should consider the possibility of delayed surgical site infection when conducting instrumented spinal surgery in patients with severe AD.