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S E Richmond

Publications and source records attributed to S E Richmond.

5 recordsLinked to original sources

Exercise intensity and metabolic response in singles tennis.

The aim of this study was to determine exercise intensity and metabolic response during singles tennis play. Techniques for assessment of exercise intensity were studied on-court and in the laboratory. The on-court study required eight State-level tennis players to complete a competitive singles tennis match. During the laboratory study, a separate group of seven male subjects performed an intermittent and a continuous treadmill run. During tennis play, heart rate (HR) and relative exercise intensity (72 +/- 1.9% VO2max; estimated from measurement of heart rate) remained constant (83.4 +/- 0.9% HRmax; mean +/- s(x)) after the second change of end. The peak value for estimated play intensity (1.25 +/- 0.11 steps x s(-1); from video analysis) occurred after the fourth change of end (P< 0.005). Plasma lactate concentration, measured at rest and at the change of ends, increased 175% from 2.13 +/- 0.32 mmol x l(-1) at rest to a peak 5.86 +/- 1.33 mmol x l(-1) after the sixth change of end (P < 0.001). A linear regression model, which included significant terms for %HRmax (P< 0.001), estimated play intensity (P < 0.001) and subject (P < 0.00), as well as a %HRmax subject interaction (P < 0.05), accounted for 82% of the variation in plasma lactate concentration. During intermittent laboratory treadmill running, % VO2peak estimated from heart rate was 17% higher than the value derived from the measured VO2 (79.7 +/- 2.2% and 69.0 +/- 2.5% VO2peak respectively; P< 0.001). The %VO2peak was estimated with reasonable accuracy during continuous treadmill running (5% error). We conclude that changes in exercise intensity based on measurements of heart rate and a time-motion analysis of court movement patterns explain the variation in lactate concentration observed during singles tennis, and that measuring heart rate during play, in association with preliminary fitness tests to estimate VO2, will overestimate the aerobic response.

Adult↗

Reactivity and aggression in the rat: induction by alpha-adrenergic blocking agents injected ventral to anterior septum but not into lateral septum.

Intracranial injections were made bilaterally through permanently implanted cannulas ending in the lateral septum or in the region ventral to the anterior septum. The rats were first screened with injections of a local anesthetic, lidocaine, which blocks both synaptic and axonal conduction. Those animals that showed an increase in reactivity and aggression were then injected with a synaptic transmitter blocking agent. The results showed that transmitter blocking agents reproduced the effect of the local anesthetic only in the region ventral to the anterior septum and that alpha-adrenergic (phentolamine, tolazoline), but not beta-adrenergic (propranolol, hydralazine), cholinergic (atropine, hyocine), or dopaminergic (haloperidol) blocking agents were effective. These results suggest that synapses in the forebrain system controlling reactivity and aggression are alpha-asrenergic and are located in the region ventral to the anterior septum just lateral to the diagonal band of Broca. The septum itself may be involved only to the extent that it is traversed by fibers of passage.

Adrenergic alpha-Antagonists↗

Septal hyperreactivity: a comparison of lesions within and adjacent to the septum.

Following large septal lesions, male hooded rats were tested for reactivity 2, 7, and 14 days postoperatively. The results showed that lesions which destroyed the septal nuclei bilaterally caused a significant increase in reactivity above that of an operated control group. A similar increase in reactivity was produced by lesions which damaged the bed nucleus of the stria terminalis as well as the septum. A significantly greater level of reactivity was produced when the lesion destroyed the septum and in addition the area ventral to the anterior septum, including parts of the diagonal band of Broca and the accumbens nucleus. A second experiment examined the effectiveness of more restricted lesions ventral to the septum on reactivity. Ventral lesions which destroyed primarily the bed nucleus of the stria terminalis caused a small but significant increase in reactivity. With lesions ventral to the anterior septum the increase in reactivity was significantly larger. The increase in reactivity produced by the anterior-ventral lesions was also larger than that produced by lesions of the septum but it was not as great as that produced by combined lesions of the septum and the anterior-ventral area. These results suggest that several areas contribute to the hyperreactivity that is usually attributed to septal lesions.

Aggression↗