In this study, the intensities of activity and movement patterns during men's basketball were investigated by videoing the movements and monitoring the heart rate and blood lactate responses of eight elite players during competition. The results are expressed according to 'live time', which is actual playing time, and 'total time', which includes live time as well as all stoppages in play. The mean (+/- S.D.) frequency of all activities was 997 +/- 183, with a change in movement category every 2.0 s. A mean total of 105 +/- 52 high-intensity runs (mean duration 1.7 s) was recorded for each game, resulting in one high-intensity run every 21 s during live time. Sixty percent of live time was spent engaged in low-intensity activity, while 15% was spent in high-intensity activity. The mean heart rate (HR) during live time was 169 +/- 9 beats min-1 (89 +/- 2% peak HR attained during laboratory testing); 75% of live time was spent with a HR response of greater than 85% peak HR. The mean blood lactate concentration was 6.8 +/- 2.8 mM, indicating the involvement of glycolysis in the energy demands of basketball. It is concluded that the physiological requirements of men's basketball are high, placing considerable demands on the cardiovascular and metabolic capacities of players.

The one-dimensional equations of flow in the elastic arteries are hyperbolic and admit nonlinear, wavelike solutions for the mean velocity, U, and the pressure, P. Neglecting dissipation, the solutions can be written in terms of wavelets defined as differences of the Riemann invariants across characteristics. This analysis shows that the product, dUdP, is positive definite for forward running wavelets and negative definite for backward running wavelets allowing the determination of the net magnitude and direction of propagating wavelets from pressure and velocity measured at a point in the artery. With the linearizing assumption that intersecting wavelets are additive, the forward and backward running wavelets can be separately calculated. This analysis, applied to measurements made in the ascending aorta of man, shows that forward running wavelets dominate during both the acceleration and deceleration phases of blood flow in the aorta. The forward and backward running waves calculated using the linearized analysis are similar to the results of an impedance analysis of the data. Unlike the impedance analysis, however, this is a time domain analysis which can be applied to nonperiodic or transient flow.

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The role of longitudinally and circumferentially oriented fibres in left ventricular wall motion was examined by digitising echocardiograms of the mitral ring (whose motion reflects long axis change) and of the standard minor axis in 36 healthy individuals, 36 patients with coronary artery disease, 16 with left ventricular hypertrophy, 44 with mitral valve disease (24 of whom had undergone mitral valve replacement). In the controls long axis shortening significantly preceded minor axis shortening (mean (1 SD) difference 25 (40) ms) so that the minor axis increased more during isovolumic contraction (0 25 v 0 09 cm), indicating that the left ventricle became more spherical. Changes in the long and short axes were synchronous at end ejection and in early diastole in the controls. Epicardial excursion preceded endocardial excursion by 50 (20) ms at its peak. These time relations were consistently disturbed in all patient groups, irrespective of the extent of fractional shortening of the minor axis. The onset of long axis shortening was delayed, and this was often associated with premature shortening of the minor axis, the normal spherical shape change during isovolumic contraction was lost, and peak epicardial and endocardial changes became more synchronous. In patients with coronary disease these changes are the expected consequence of ischaemic injury to longitudinally orientated subendocardial fibres. In left ventricular hypertrophy their presence consistently showed systolic dysfunction when orthodox measures were still normal. They were more pronounced after mitral valve replacement when the papillary muscles had been sectioned; long axis shortening was reduced during systole and prolonged into early diastole, while normal shortening of the minor axis was maintained only by abnormal epicardial excursion.Relations between long and short axis motion in healthy individuals are characteristic, and their loss is an early index of systolic ventricular disease. These disturbances precede changes in orthodox measures such as fractional shortening or peak velocity of circumferential fibre shortening.Anatomical studies'2 have shown longitudinal as well as circumferential fibres with a continuous variation in fibre angle across the left ventricular wall. The function of these longitudinal fibres has not been extensively studied. Because effective ventricular function during ejection and filling is likely to depend upon the coordinated action of all myocardial layers, we set out to study the timing and extent of changes in the long axis, comparing them with those of the minor axis in healthy controls and those with left ventricular disease. In addition, we investigated patients after mitral valve replacement where a component of the longitudinal fibres (the papillary muscles) had been sectioned. Patients and methods CONTROLS AND PATIENTSCross sectionally guided M mode echocardiograms were recorded and analysed in 36 patients with coronary artery disease, 16 with left ventricular hypertrophy, 44 patients with mitr...

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These data indicate that conduit artery distensibility is increased by acetylcholine and increased blood flow in healthy subjects but not in CHF patients, whereas the effects of adenosine and GTN on distensibility are preserved in CHF patients. This implies that EDRF-mediated increases in distensibility are impaired in CHF patients, thus adding to cardiac work.

Replicative senescence in human fibroblasts is absolutely dependent on the function of the phosphoprotein p53 and correlates with activation of p53-dependent transcription. However, no evidence for posttranslational modification of p53 in senescence has been presented, raising the possibility that changes in transcriptional activity result from upregulation of a coactivator. Using a series of antibodies with phosphorylation-sensitive epitopes, we now show that senescence is associated with major changes at putative regulatory sites in the N and C termini of p53 consistent with increased phosphorylation at serine-15, threonine-18, and serine-376 and decreased phosphorylation at serine-392. Ionizing and UV radiation generated overlapping but distinct profiles of response, with increased serine-15 phosphorylation being the only common change. These results support a direct role for p53 in signaling replicative senescence and are consistent with the generation by telomere erosion of a signal which shares some but not all of the features of DNA double-strand breaks.Normal human somatic cells (with the possible exception of stem cells) are capable of only a finite number of cell divisions, after which they enter a nondividing though viable state termed replicative senescence (22,55). The significance of this phenomenon for human health is two-edged. On the one hand, it imposes a natural obstacle to clonal expansion, which probably plays a vital part in limiting tumor development (2, 38, 59). On the other hand, in some tissues, notably skin and blood vessels, it may account for progressive functional abnormality with advancing age. This may result directly from loss of regenerative capacity but also indirectly through senescence-associated biochemical changes, a good example being the increased collagenase secretion by ageing dermal fibroblasts, which may be significant even when only a minority of cells are overtly senescent (11,34). Knowledge of the underlying mechanisms of cellular senescence is therefore central to both cancer and aging research.We and others have demonstrated that one key signal pathway mediating replicative senescence involves the phosphoprotein p53, more widely recognized for its role as a tumor suppressor, which is known to mediate growth arrest in response to a wide variety of cellular stress signals including DNA damage (31, 40). Experimental abrogation of p53 function prevents fibroblasts from entering senescence normally and indeed can reverse established senescence, demonstrating that p53, if not sufficient, is certainly necessary for this process (5,6,20). Furthermore, growth arrest in senescence is tightly correlated with switching on of the transcriptional transactivation function of p53, as revealed by the use of reporter constructs and by DNA binding assays (1,7,50).Nevertheless, senescence has not thus far been shown to lead to any of the range of posttranslational modifications of the p53 protein which bring about its activation in response to other signals such as DNA damage (19). ...

The determinants of aortic pressure and flow are generally studied using impedance methods, the results of which indicate that reflected waves are important, particularly during aortic flow deceleration. An alternative analysis of measured aortic pressure and velocity, using the method of characteristics to calculate the energy flux per unit area of the waves, suggests a different conclusion. We suggest that aortic deceleration is caused by a discrete expansion wave propagating from the left ventricle, and that energy thus recovered by the ventricle may be coupled to early filling of the ventricle.