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This study examined the control of ventilation during repetitive bouts of isometric exercise in simulated sailing. Eight male sailors completed four successive 3-min bouts of similar isometric effort on a dinghy simulator; bouts were separated by 15-s rest intervals. Quadriceps muscle integrated electromyograph activity (iEMG) was recorded during each bout and expressed as a percentage of activity during maximal voluntary contraction (%iEMGmax). From the first to the fourth bout, the 3-min mean averages for ventilation and for %iEMGmax increased from 19.8 (SEM 1.1) to 37.5 (SEM 3.0) l.min-1 and from 31 (SEM 4) to 39 (SEM 4)% respectively; also, ventilation and %iEMGmax over each minute throughout the four bouts were significantly correlated (r = 0.85; P < 0.05). Progressive hyperventilation reduced the mean end-tidal partial pressure of carbon dioxide from 5.0 (SEM 0.3) kPa during bout 1 to 4.3 (SEM 0.4) kPa during bout 4 [37.7 (SEM 2.0) to 32.4 (SEM 3.0) mmHg]. From the first to the fourth bout the end-of-bout blood lactate concentration did not increase significantly although the concentration from the third bout onwards was significantly greater than at rest. The results suggested that the development of muscle fatigue, which was enhanced by the insufficiency of recovery during the 15-s intervals and mirrored in the progressive increase in iEMG, was linked with stimuli causing progressive hyperventilation. Though these changes in ventilation and iEMG could not be associated with changes in blood lactate concentration, they could both have been related to accumulating metabolites within the muscles themselves.

The rapidity and extent of hypoxic relaxation of vascular smooth muscle (VSM) from different systemic vessels is relevant to the study of mechanisms of vasodilatation in different vascular beds. Variations between sites may also assist understanding of the link between oxygen tension and mechanical activity, which has been shown not to be a simple deprivation of aerobic processes.Strips of rat portal vein (RPV), rabbit ear artery (REA) and rabbit common carotid artery (RCC) were studied under isotonic conditions, contracted by 10-6 noradrenaline (NA). Reduction of P02 to less than 3KPa during NA contraction led to relaxation which was rapid and 90 (, complete Preliminary 1-2 hour exposure to hyperoxia diminished the subsequent relaxant effect of hypoxia. Inhibition of glycolysis (iodoacetic acid) had no effect on normoxic NA contraction or on hypoxic relaxation, but prevented or diminished the subsequent recovery on reoxygenation. Low oxygen tension appears to act in VSM as though it interferes with net influx or utilisation of external calcium.A decrease in mechanical and electrical activity of isolated systematic vessels in response to hypoxia has been reported by many workers [inter alia Carrier, Walker and Guyton, 1964;Smith and Vane, 1966; Bohr, 1968, 1972;Namm and Zucker, 1973; Grubb and Coburn, 1976; Gurevich, Bershtein and Evdokimov, 1976; Hellstrand, Johansson and Norberg, 1977]. The last two accounts included a description of the response of isolated rat portal vein strips as 'rapid', but the precise time course and the P02 at which responses begin are not clear. The rapidity of response is relevant to the understanding of underlying mechanisms, and also to situations in vivo when a direct local action of P02 on smooth muscle is proposed to account for short latency effects. Cerebral vasodilatation in response to inhalational hypoxia, for example, can occur as rapidly as a chemoreceptor reflex response, but appears to be