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The magnitude of improvement in peak oxygen uptake (V(o)(2peak))) and performance to an exercise training regime is related to the V(o)(2) of prior accumulated exercise training bouts. However, it is unclear whether constant rate training (CRT) or interval training (INT) preferentially alters the V(o)(2) of running exercise. Therefore, the purpose of this study was to compare the acute V(o)(2) response to constant, and interval training sessions. Consequently, this study compared the mean average V(o)(2) of 17 moderately trained participants to a 20-min CRT and two different 20min INT treadmill runs. Participants completed three treatments (twice) in random order over 3 weeks. In 1min INT participants completed 10x1min efforts at the velocity corresponding to V(o)(2peak) (V(peak)) interspersed with 10x1min efforts at 0.5V(peak). In the 2min INT, participants completed 5x2min efforts at the V(peak) interspersed with 5x2min efforts at 0.5 at V(peak). In CRT participants ran at a velocity equivalent to the mean velocity of INT (75% V(peak)). Mean average V(o)(2) for 2min INT, 1min INT and CRT were, respectively, 3200+/-661; 3076+/-6041; 2909+/-584mlmin(-1). Both INT sessions resulted in a significantly higher mean average V(o)(2) than CRT. Furthermore, 2min INT resulted in 90% of V(o)(2peak) being exceeded more frequently than 1min INT. We conclude that INT serves as a more potent stimulus for improvement in V(o)(2peak) and subsequent endurance performance than CRT. [ABSTRACT FROM AUTHOR]

When physical performance is monitored with an ergometer, random error arising from the ergometer combines with biological variation from the subject to limit the precision of estimation of performance changes. We report here the contributions of ergometer error and biological variation to the error of measurement in a performance test with two popular cycle ergometers (air-braked King-cycle, mobile SRM crankset) and a relatively new inexpensive mobile ergometer (PowerTap hub). Eleven well-trained male cyclists performed a familiarization trial followed by three 5-min time trials within 2 wk on a racing cycle fitted with the SRM and PowerTap and mounted on the Kingcycle. Mean power output in each trial was recorded with all ergometers simultaneously. A novel analysis using mixed modelling of log-transformed mean power provided estimates of the standard error of measurement as a coefficient of variation and its components arising from the ergometer and the cyclists. The usual errors of measurement were: Kingcycle 2.2%, Powerlap 1.5%, and SRM 1.6% (90% confidence limits ± 1.3). The components of these errors arising purely from the ergometers and the cyclists were: Kingcycle 1.8%, Powerlap 0.9%, SRM 1.1%, and cyclists 1.2% (± 1.5). Thus, ergometer errors and biological variation made substantial contributions to the usual error of measurement. Use of the best ergometers and of test protocols that reduce biological variation would improve monitoring of the small changes that matter to elite athletes. [ABSTRACT FROM AUTHOR]

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For centuries the scientific basis of contraceptive methods has consisted almost entirely in the cognition that the male ejaculate contained a factor essential for fertilization. Methods were therefore evolved for preventing the entrance of semen into the higher levels of the female productive tract, principally barriers and spermicides of various kinds. The scientific basis for more effective contraceptive techniques broadened only in the twentieth century with the identification of many of the intricate steps involved in conception. In particular, knowledge of hormonal factors involved in the female sexual cycle has led to the development of highly reliable means of ovulation inhibition. Increased understanding promises to offer many other possibilities of controlled interference at critical stages of reproductive events. There is, of course, enormous variation in the effectiveness of different methods. The article presents a table abstracted from the Report of the IPPF, 1964 and from a review in "Family Planning and Population Programs." The wide variations reported are due to differences in the geographical locations of the studies, the methods of obtaining data, the social classes of the people studied, their motivation, and so forth.

The release of sympathin in response to periarterial nerve and ventral auricular nerve stimulation in the isolated perfused rabbit ear has been measured by bioassay of the perfusate on the electrically stimulated rat colon and, in some experiments, by bioassay on a second perfused ear. The output was extremely small, the maximum amount of sympathin recorded being 9.7 pg. per pulse. In a number of preparations, sympathin was not detected in the perfusate. Loss of noradrenaline by re-uptake into storage sites is probably not the major factor responsible for the difficulty in detecting sympathin, since injected noradrenaline showed only a small loss during its passage through the ear and the output remained low in the presence of phenoxybenzamine and cocaine. The possibility is considered that the small quantities of sympathin detected in the perfusate reflect either a small overflow of transmitter or a genuinely low output of sympathin in the ear vessels compared with tissues such as heart, spleen and intestine. Attention is drawn to the ability of the central artery alone to reproduce much of the resistance to perfusion observed in the whole ear in response to periarterial stimulation and to noradrenaline. [ABSTRACT FROM AUTHOR]