Relationship of aerobic and anaerobic parameters with 400 m front crawl swimming performance

The aims of the present study were to investigate the relationship of aerobic and anaerobic parameters with 400 m performance, and establish which variable better explains long distance performance in swimming. Twenty-two swimmers (19.1±1.5 years, height 173.9±10.0 cm, body mass 71.2±10.2 kg; 76.6±5.3% of 400 m world record) underwent a lactate minimum test to determine lactate minimum speed (LMS) (i.e., aerobic capacity index). Moreover, the swimmers performed a 400 m maximal effort to determine mean speed (S400m), peak oxygen uptake (V.O2PEAK) and total anaerobic contribution (C_ANA). The C_ANA was assumed as the sum of alactic and lactic contributions. Physiological parameters of 400 m were determined using the backward extrapolation technique (V.O2PEAK and alactic contributions of C_ANA) and blood lactate concentration analysis (lactic anaerobic contributions of C_ANA). The Pearson correlation test and backward multiple regression analysis were used to verify the possible correlations between the physiological indices (predictor factors) and S400m (independent variable) (p < 0.05). Values are presented as mean ± standard deviation. Significant correlations were observed between S400m (1.4±0.1 m·s^-1) and LMS (1.3±0.1 m·s^-1; r = 0.80), V.O2PEAK (4.5±3.9 L·min^-1; r = 0.72) and C_ANA (4.7±1.5 L·O₂; r= 0.44). The best model constructed using multiple regression analysis demonstrated that LMS and V.O2PEAK explained 85% of the 400 m performance variance. When backward multiple regression analysis was performed, C_ANA lost significance. Thus, the results demonstrated that both aerobic parameters (capacity and power) can be used to predict 400 m swimming performance.     

Neocarzinostatin and auromomycin preferentially cleave simian virus 40 DNA and chromosomes at a number of discrete locations

Neocarzinostatin and auromomycin were shown to cleave simian virus 40 (SV40) DNA with preference for distinct regions of the viral genome. The positions cut by neocarzinostatin and auromomycin were similar, while micrococcal nuclease cleaved at positions other than those recognized by neocarzinostatin and auromomycin. Breaks were distributed throughout the viral genome and were not associated with any single type of genetic element. The limited number of locations in SV40 DNA that were preferentially cut by neocarzinostatin and auromomycin suggests that drug attack is directed by DNA structures other than the known trinucleotide sequence specificity of the drugs. Neocarzinostatin and auromomycin cut purified, cell-free, nuclear and intracellular chromosomal SV40 DNA at similar regions. The data indicate that there are regions in DNA that are hypersensitive to the drugs; the hypersensitivity may be determined by the microstructure of the DNA. The conformational change associated with the packing of the DNA into nucleosomes did not affect the microstructure of the sensitive region, nor did the shielding effect of nuclear proteins affect the drug's access to it. In addition, intracellular drug metabolism or other cellular factors did not alter the ability of drugs to interact at these sensitive regions.