RESUMO
The aim of this study was to investigate the effects of either normoxic or hypoxic recovery condition on post-exercise hemodynamics after sprint interval leg cycling exercise rather than hemodynamics during exercise. The participants performed five sets of leg cycling with a maximal effort (30 s exercise for each set) with a 4-min recovery of unloaded cycling between the sets in hypoxia [fraction of inspired oxygen (FiO2) = 0.145]. The load during pedaling corresponded to 7.5% of the individual's body weight at the first set, and it gradually reduced from 6.5 to 5.5%, 4.5, and 3.5% for the second to fifth sets. After exercise, the participants rested in a sitting position for 30 min under normoxia (room-air) or hypoxia. Mean arterial pressure decreased over time during recovery (p < 0.001) with no condition and interaction effects (p > 0.05). Compared to pre-exercise values, at 30 min after exercise, mean arterial pressure decreased by 5.6 ± 4.8 mmHg (mean ± standard deviation) during hypoxic recovery, and by 5.3 ± 4.6 mmHg during normoxic recovery. Peripheral arterial oxygen saturation (SpO2) at all time points (5, 10, 20, and 30 min) during hypoxic recovery was lower than during normoxic recovery (all p < 0.05). The area under the hyperemic curve of tissue oxygen saturation (StO2) at vastus lateralis defined as reperfusion curve above the baseline values during hypoxic recovery was lower than during normoxic recovery (p < 0.05). Collectively, post-exercise hypotension after sprint interval leg cycling exercise was not affected by either normoxic or hypoxic recovery despite marked differences in SpO2 and StO2 during recovery between the two conditions.
RESUMO
beta-Hydroxyisovalerylshikonin (beta-HIVS), which was isolated from the plant, Lithospermum radix, induces apoptosis in various lines of human tumor cells. To identify genes involved in beta-HIVS-induced apoptotic process, we performed cDNA array analysis and found that beta-HIVS suppresses the expression of the gene for a polo-like kinase 1 (PLK1) that is involved in control of the cell cycle. When U937 and HL60 cells were treated with 10(-6) M beta-HIVS for 0.5 h, both the amount of PLK1 itself and the kinase activity of this enzyme were decreased. By contrast, Bcr-Abl-positive K562 cells were resistant to the induction of apoptosis by beta-HIVS and this compound did not suppress the kinase activity of PLK1 in these cells. However, simultaneous treatment of K562 cells with both beta-HIVS and STI571, which selectively inhibits the protein tyrosine kinase (PTK) activity of Bcr-Abl, strongly induced apoptosis. Moreover, beta-HIVS increased the inhibitory effect of STI571 on PTK activity. Treatment of K562 cells with antisense oligodeoxynucleotides (ODNs) specific for PLK1 sensitized these cells to the beta-HIVS-induced fragmentation of DNA. These results suggest that suppression of the activity of PLK1 via inhibition of tyrosine kinase activity by beta-HIVS might play a critical role in the induction of apoptosis.