Influence of inspired oxygen concentration on the dynamics of the exercise hyperpnoea in man.

Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans.

“…Supporting this hypothesis is the demonstration by Wasserman et al (1975) that, on average, subjects who had had both carotid bodies surgically resected increased their ventilation towards the steady-state during subthreshold square-wave exercise more slowly than did control subjects. The data of Griffiths et al (1986), however, suggested that not all of this hyperoxic-induced slowing of ventilatory kinetics could be attributed to the carotid bodies. With inspirates of 30% 02, these authors could discern no peripheral chemoreceptor component, as evidenced by 'Dejours' tests (Dejours, 1963); in subsequent tests, however, in which the inspirate was 100% 02, there was a further significant slowing of the ventilatory kinetics -associated with a further slowing of VC02.…”

Muscle sympathetic nerve activity and ventilation during exercise in subjects with and without chronic heart failure

“…One of these includes sensitization or greater stimulation of muscle mechanoreceptors (15) and metaboreceptors (13) during work, perhaps exacerbated by conversion from type I (slow twitch, aerobic) to type II (fast twitch, anaerobic) muscle fibres (26,27). Other mechanisms include increased sensitivity of peripheral and central chemoreceptors (20,28,29), and amplification of signals within the central nervous system originating from these several inputs (30). The relative contribution of central command, an important stimulus to ventilation at the onset of exercise (31)(32)(33), diminishes as exercise is sustained (34,35).…”

Dynamic asymmetries of cardiac output transients in response to muscular exercise in man.

“…This allows the mean capillary pressure to remain sufficiently high to provide the diffusional flux of oxygen (Brooks, 1985;Poole et al 1991;Wagner et al 1991). However, the known heterogeneities of skeletal muscle blood flow and of oxygen utilization during exercise, coupled with the evidence of precapillary (arteriovenous) 02 exchange (Duling & Berne, 1970;Van Lieuw, 1973;Meuer et al 1985) (Griffiths et al 1986;Paterson & Whipp, 1991). Furthermore, the oxygen uptake responses to sinusoidally varying workloads are themselves sinusoidal (Casaburi, Whipp, Beaver, Wasserman & Koyal, 1977;Miyamoto, Nakazono, Hiura & Abe, 1983) The time constant for the off-transient in Q was appreciably longer than that for its on-transient response, and although not considered in this regard, the phenomenon may also be seen in the results of Davies et al (1972), Miyamoto et at.…”

“…During the non-steady-state phase of exercise CV 02 was determined by the relative time constant for VO2 ('r,V) and Q (-r) Prampero & Cerretelli, 1972;Miyamoto, Hiura, Tamura, Nakamura, Higuchi & Mikami, 1982;De Cort, Innes, Barstow & Guz, 1991 It is important, with respect to tissue oxygenation, to know whether there is on-off symmetry for the Q kinetics, as has been demonstrated for V02 (Whipp, 1976;Griffiths, Henson & Whipp, 1986;Paterson & Whipp, 1991 and maximal oxygen uptake, 46-6 + 1P7 ml kg-l min-'.…”