Hidetaka Imagita

Evaluation of Rhodiola rosea supplementation on skeletal muscle damage and inflammation in runners following a competitive marathon

Adaptogens modulate intracellular signaling and increase expression of heat shock protein 72 (HSP72). Rhodiola rosea (RR) is a medicinal plant with demonstrated adaptogenic properties. The purpose of this study was to measure the influence of RR supplementation on exercise-induced muscle damage, delayed onset of muscle soreness (DOMS), plasma cytokines, and extracellular HSP72 (eHSP72) in experienced runners completing a marathon. Experienced marathon runners were randomized to RR (n=24, 6 female, 18 male) or placebo (n=24, 7 female, 17 male) groups and under double-blinded conditions ingested 600mg/day RR extract or placebo for 30days prior to, the day of, and seven days post-marathon. Blood samples were collected, and vertical jump and DOMS assessed the day before, 15min post- and 1.5h post-marathon. DOMS was also assessed for seven days post-marathon. Marathon race performance did not differ between RR and placebo groups (3.87±0.12h and 3.93±0.12h, respectively, p=0.722). Vertical jump decreased post-marathon (time effect, p<0.001) with no difference between groups (interaction effect, p=0.673). Post-marathon DOMS increased significantly (p<0.001) but the pattern of change did not differ between groups (p=0.700). Myoglobin (Mb), creatine phosphokinase (CPK), aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukin (IL)-6, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), granulocyte-colony-stimulating factor (G-CSF), C-reactive protein (CRP), and eHSP72 all increased post-marathon (all p<0.001), with no group differences over time (all p>0.300). In conclusion, RR supplementation (600mg/day) for 30days before running a marathon did not attenuate the post-marathon decrease in muscle function, or increases in muscle damage, DOMS, eHSP72, or plasma cytokines in experienced runners.

Relationship Between Muscle Strength Asymmetry and Body Sway in Older Adults

The purpose of this study was to investigate the relationship between muscle strength asymmetry and body sway while walking. We studied 63 older adult women. Strong side and weak side of knee extension strength, toe grip strength, hand grip strength, and body sway while walking were measured. The relationship between muscle strength asymmetry for each muscle and body sway while walking was evaluated using Pearsons correlation coefficient. Regarding the muscles recognized to have significant correlation with body sway, the asymmetry cutoff value causing an increased sway was calculated. Toe grip strength asymmetry was significantly correlated with body sway. Toe grip strength asymmetry causing an increased body sway had a cutoff value of 23.5%. Our findings suggest toe grip strength asymmetry may be a target for improving gait stability.

Tidal volume and diaphragm muscle activity in rats with cervical spinal cord injury.

[Purpose] The purpose of this study was to make an experimental model of cervical spinal cord injury (CSCI) using Wistar rats, in order to analyze the influence of CSCI on the respiratory function. [Subjects] Thirty-two male 12-week-old Wistar rats were used. [Methods] The CSCI was made at the levels from C3 to C7, and we performed pneumotachography and electromyography (EMG) on the diaphragm. Computed tomography was used to determine the level of spinal cord damage. [Results] After the operation, the tidal volume of the rats with a C3 level injury decreased to approximately 22.3% of its pre-injury value. In addition, in the same rats, the diaphragmatic electromyogram activity decreased remarkably. Compared with before CSCI, the tidal volume decreased to 78.6% of its pre-injury value in CSCI at the C5 level, and it decreased to 94.1% of its pre-injury value in CSCI at the C7 level. [Conclusion] In the rats that sustained a CSCI in this study, the group of respiratory muscles that receive innervation from the thoracic spinal cord was paralyzed. Therefore, the EMG signal of the diaphragm increased. These results demonstrate that there is a relationship between respiratory function and the level of CSCI.

Oxygen therapy may worsen the survival rate in rats with monocrotaline-induced pulmonary arterial hypertension

Although oxygen therapy rapidly improves arterial oxygen saturation in idiopathic pulmonary arterial hypertension, the effects of chronic administration of oxygen are unknown. The purpose of the present study was to investigate the effects of chronic oxygen therapy on the histological changes and survival rate in rats with idiopathic pulmonary arterial hypertension. Idiopathic pulmonary arterial hypertension was induced by monocrotaline injection. The rats were then randomly assigned to receive or not receive oxygen therapy (O2 group and non-O2 group, respectively). The rats in the O2 group were exposed to a high (90%) oxygen environment from day 17 following injection of monocrotaline, when hypoxemia was first observed. The pulmonary arteriole walls were significantly thicker in monocrotaline-injected rats than in saline-injected rats as vehicle on day 19 and were significantly thicker in the rats that received oxygen therapy than in the rats that did not. Right ventricular inflammations were significantly higher in monocrotaline-injected rats than in saline-injected rats on day 19 and were significantly higher in the rats that received oxygen therapy than in the rats that did not. By day 20 after injection of monocrotaline, the survival rate was significantly lower in the rats that received oxygen therapy than in those that did not. Superoxide dismutase activity in the lungs was higher in monocrotaline-injected rats than in saline-injected rats on day 19 after monocrotaline injection and was also higher in the saline-injected rats that received oxygen therapy than in the saline-injected rats that did not. No interaction was detected between monocrotaline injection and oxygen therapy. These results suggest that chronic oxygen therapy worsens the histological changes and survival rate in idiopathic pulmonary arterial hypertension. The fact that degradation of the histological changes and survival rate was accompanied by increase in superoxide dismutase activity suggests that antioxidant capacity may contribute to the degradation.

The time course and extent of motor neuron loss following spinal cord compression in rats

Motor deficits after spinal cord injury arise from damages to the descending spinal pathways and ventral motoneurons (VMN). In contrast to data on damages to the white matter or the descending spinal pathways, few quantitative data on damages to VMN after injury are available currently. The purpose of this study was to examine quantitatively the temporal and spatial pattern of VMN loss after spinal cord compression. Two groups of adult female Wistar rats were used in this study: rats which were subjected to spinal cord compression in short duration with an aneurysm clip (experimental group) and rats which were subjected to a sham-operation (control group). Using serial cross-sections of the spinal cord, VMN were counted up to the 7th day after surgical intervention at 0, 1, 2, and 3 mm rostral and caudal to the lesion epicenter (experimental group) or to the median of the serial sections (control group). At 15 minutes after the compression, VMN were lost only at the epicenter section and no VMN were observed there. By 8 hours, VMN loss had spread to next 1 mm rostral and caudal section to the epicenter. Virtually, no further loss was detected between 8 hours and later time points. This study showed that compression to the adult rat spinal cord in short duration led to VMN loss, which progressed acutely and expanded modestly. Our findings could be used to develop effective treatment and provide a better understanding of VMN loss after spinal cord injury.