While the Wingate test is traditionally administered with the restriction that the subject stay seated, competition cyclists generally rise out of the saddle when sprinting. The purpose of this investigation, therefore, was to determine whether the results of Wingate tests are different if they are obtained when the subject is in a seated compared to a standing position. A group of 12 male cyclists, competing at the college level, performed four 30 s Wingate tests over the course of 2 weeks. Two practice tests were first administered, one with the subjects standing on the pedals and one with them seated, followed by two similar tests for the record in a randomized order. Each test was performed on a friction-loaded ergometer (resistance: 8.5% body mass, starting cadence 60 rpm). For the standing tests, the participants rose out of the saddle when the load was applied and remained standing throughout. Power was computed using a commercially available software/ hardware package that accounted for both the load on the flywheel, and the flywheel and crank system acceleration. Power values in the standing and seated trials for the [mean (SD)] 1 s peak [19.4 (1.4) W x kg(-1), 17.9 (1.7) W x kg(-1)], 5 s peak [16.8 (0.9) W x kg(-1), 15.7 (1.1) W x kg(-1)], 30 s average [11.0 (0.4) W x kg(-1), 10.4 (0.6) W x kg(-1)], and 5 s minimal power [8.3 (0.5) W x kg(-1), 7.5 (0.6) W x kg(-1)] were all significantly greater in the standing compared to the seated trials (P < 0.01). However, the fatigue index was not significantly different [51 (5)% standing. 52 (5)% seated; P = 0.25]. Since greater power output was achieved when the subjects were standing on the pedals, it may be more appropriate to test cyclists when they are in the standing position to gain a better representation of their capability to exert maximal power.

No abstract

Three weeks of strenuous swimming caused a prolonged Hcy increase, which was accompanied by changes in vitamin B12 and folate. The magnitude of these effects was not influenced by the training intensity.

Postnatal skeletal muscle growth in humans is generally ascribed to enlargement of existing muscle fibres rather than to cellular proliferation. Some evidence of muscle fibre division or splitting was provided in the nineteenth century. This evidence has more recently been supported by fibres obtained from regenerating muscle, and from muscle which has undergone stress-induced growth. Numerous investigators have reported indirect evidence for exercise-induced hypertrophy and hyperplasia. These findings are largely founded on secondary observations of fibre size or number differences expressed relative to muscle cross-sectional area. Since these observations in humans are open to methodological criticism, researchers have developed 3 animal models to represent exercise-induced human muscle growth. These include compensatory hypertrophy, stretch-induced hypertrophy, and weight lifting in trained animals. The results and criticisms of the experiments which have used these models are discussed in this review. In studies of muscle cross-sectional area, errors are created by fibres terminating intrafascicularly. Longitudinal growth of such fibres result in an overestimation of fibre number, and with the use of penniform muscles where fibres do not run parallel to the longitudinal axis of the muscle, the error is compounded. It was concluded that hyperplasia is not yet substantiated, and that new fibres, if present, may be the result of the development of satellite cells. Further experiments are required before a definitive answer can be provided. It is suggested that rigidly controlled exercise studies using contralateral control, fusiform muscles with analysis of individually teased muscle fibres be performed.