A training experiment was carried out to investigate the difference in training effects between power-up type and bulk-up type strength training exercises from the aspects of muscle histochemical properties and capillary supply. The subjects were eleven healthy males. The power-up type group (five males) performed knee extension exercise for 5 sets at 90% of 1 RM (one repetition maximum) with a 3-min rest between sets (repetition method) . The bulk-up type group (six males) performed the same exercise for 9 sets at 80-40% of 1RM with a 30-s or 3-min rest between sets (interval method, multi-poundage system) . Both programs were carried out twice a week for 8 weeks.
The main results were as follows ;
1. Percentages of fiber types showed no recognizable changes in either group.
2. Fiber area was significantly increased for all fiber types (Type I, Type IIA, Type JIB) in both groups. However, the rate of increase was greatest for type IIA fiber, followed by type JIB fiber and then type I fiber. Moreover, the rate of increase for all fiber types in the bulk-up group was higher than that in the power-up group.
3. Percentage of fiber area showed no recognizable changes for any fiber types in the powerup group. However, the percentage area of type II fibers, especially type IIB fiber, was significantly decreased in the bulk-up group.
4. CC (Type I), CC (Type IIA) and CC (Type IIB) (number of capillaries in contact with each fiber type) were significantly increased in both groups. However, in comparison with CC (Type I), CC (Type IIA · Type IIB) showed a higher rate of increase in the power-up group. On the other hand, in comparison with CC (Type IIA · Type JIB), CC (Type I) showed a higher rate of increase in the bulk-up group. Also, compared with the power-up group, the bulk-up group showed a signifi-cantly higher rate of increase of CC (Type I) .
5. C/Fiber area (Type I), C/Fiber area (Type IIA) and C/Fiber area (Type IIB) (number of capillaries supplying each fiber area) were decreased in both groups.
The above results show that power-up type exercise leads mainly to hypertrophy of type I, type IIA and type IIB fibers without any change in percentage fiber type or percentage fiber area, whereas bulk-up type exercise leads mainly to hypertrophy of each fiber type with decreases in percentage area of type II fibers, especially type JIB fiber. Also, power-up type exercise leads mainly to an increase in the number of capillaries around type II fibers, whereas bulk-up type exercise leads mainly to an increase in the number of capillaries around type I fiber. However, capillary development around all fiber types did not necessary coincide with muscle hypertrophy in either exercise.
The authors reported previously that power-up type exercise is effective mainly for improving muscular strength and anaerobic power, whereas bulk-up type exercise is effective mainly for induc. ing hypertrophy and anaerobic endurance. The results of this study may help to clarify these effects from the viewpoint of the adaptations of muscle fibers and the capillary supply.

Metastasis is the chief cause of mortality in cancer patients. Recently, chemokines and chemokine receptors were shown to play an important role in the metastasis of various cancers. We examined the role of chemokine receptor-mediated signaling in the invasion potential of human oral squamous cell carcinoma (OSCC) cell lines that were derived from 5 primary tumors and 6 cervical lymph node metastases. Comprehensive analysis of the mRNAs for human chemokine receptors showed that the OSCC cell lines had uniform expression patterns of chemokine receptors. Overall, there were no consistent differences in the expression of chemokine receptors between primary site- and lymph node metastasis-derived cell lines. However, a highly invasive OSCC cell line (SAS-H1) expressed up-regulation of CCR5, CCR6, CCR7, CXCR1, CXCR6 and CX3CR1 compared to a poorly invasive OSCC cell line (SAS-L1). Then we examined whether factors in the tumor microenvironment regulated chemokine receptor expression in SAS-H1 cells. Specifically, transforming growth factor (TGF) -β1 enhanced the expression of CCR5, CCR6, CCR7 and CX3CR1. Pretreatment of SAS-H1 cells with transforming growth factor (TGF) -β1 increased the expression of CCR7 and CX3CR1, and then enhanced CCL21- and CX3CL1-induced directional migration (1.5-fold enhancement as compared with untreated control). In addition, CX3CL1 increased the adhesion of SAS-H1 cells on uncoated tissue culture plates. Neither chemokine stimulated cell proliferation. Treatment of SAS-H1 cells with CX3CL1 activated the phosphotidylinositol-3-kinase (PI3K) and MEK signal transduction pathways. Our results suggest that chemokine receptor-mediated signaling is involved in the local invasion and metastasis of human OSCC.