On the Nervous Factors Controlling Respiration and Circulation during Exercise Experiments with curarization

Asmussen, Erik; Johansen, Søren; Jørgensen, Mogens; Nielsen, Marius

doi:10.1111/j.1748-1716.1965.tb04073.x

Cited by 134 publications

(68 citation statements)

References 10 publications

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“…It has been suggested that during exercise in the heat, central fatigue can occur with progressive hyperthermia, which can reduce arousal and the brain's ability to maintain exercise (30,31). Given that RPE reflects changes in brain activity during prolonged exercise in the heat (33), the increase in V E in this study could in part reflect an increase in central command (1). These thermal and nonthermal factors may operate together during prolonged exercise with progressive hyperthermia and lead to hyperventilation.…”

Section: Discussionmentioning

confidence: 85%

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Tsuji

Honda

Fujii

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Nishiyasu T. Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat. Am J Physiol Regul Integr Comp Physiol 302: R94 -R102, 2012. First published September 28, 2011 doi:10.1152/ajpregu.00048.2011.-We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (Tes). Initial Tes was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). Tes after the water immersion was significantly higher in the Preheating trial (37.5 Ϯ 0.3°C) and lower in the Precooling trial (36.1 Ϯ 0.3°C) than in the Control trial (36.9 Ϯ 0.3°C). In the Precooling trial, minute ventilation (V E) showed little change until Tes reached 37.1 Ϯ 0.4°C. Above this core temperature threshold, V E increased linearly in proportion to increasing Tes. In the Control trial, V E increased as Tes increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, V E increased from the initially elevated levels of Tes (from 37.6 to 38.6°C) and V E. The sensitivity of V E to increasing Tes above the threshold for hyperventilation (the slope of the Tes-V E relation) did not significantly vary across trials (Precooling trial ϭ 10.6 Ϯ 5.9, Control trial ϭ 8.7 Ϯ 5.1, and Preheating trial ϭ 9.2 Ϯ 6.9 L·min Ϫ1 ·°C Ϫ1 ). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.hyperpnea; hyperthermia; thermoregulation; precooling; preheating WHEN HUMANS ARE EXPOSED TO a hot environment, heat dissipation through cutaneous vasodilation and sweating increases in response to rising body core and skin temperatures. In addition to these thermoregulatory responses, Haldane found in 1905 that an increase in ventilation is also induced by a rise in body core temperature (13). Since that early report, many studies have confirmed the existence of hyperthermia-induced hyperventilation (5, 9 -11, 16, 26, 32, 38, 43) although its characteristic and significance remain unclear.When ventilation is expressed as a function of core temperature in passively-heated humans at rest, there is no significant change until core temperature reaches a temperature threshold for hyperventilation, ϳ37.8 -38.5°C. Above this threshold, ventilation increases linearly in proportion to increasing core temperature with minimal change in oxygen consumption (5, 10). As in resting subjects, metabolic factors contribute minimally to ventilation during prolo...

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Section: Discussionmentioning

confidence: 85%

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Tsuji

Honda

Fujii

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…That part of the response initiated from the moving limbs undoubtedly receives an important contribution from the muscle receptors (Alam & Smirk, 1937, 1938 Korner, 1952; Lind, McNicol & Donald, 1966;Coote et al 1971;. Some workers consider that it is the muscle mechanoreceptors that are responsible (Granit, Skoglund & Thesleff, 1953; Gauthier, Lacaisse, Pasquis & Dejours, 1964;Asmussen et al 1965), but there is a strong body of evidence against this (Laporte, Leitner & Pages, 1962; Senapati, 1966;Hodgson & Matthews, 1968; Hnik, Hudlicka, Kucera & Payne, 1969;Coote & Perez-Gonzalez, 1970; Perez-Gonzalez & Coote, 1972;, some of which indicates that it is the small myelinated and unmyelinated nerve fibres of the muscle that are involved.…”

Section: Introductionmentioning

confidence: 99%

The contribution of articular receptors to cardiovascular reflexes elicited by passive limb movement

Barron¹,

Coote²

1973

The Journal of Physiology

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1. In decerebrate cats, passive movements of one hind limb led to increases in arterial blood pressure, heart rate and ventilation. When both limbs were moved the magnitude of the changes was approximately doubled. 2. Section of the nerves to the limb abolished the responses to movement. The responses are, therefore, dependent on a reflex originating in the moving limb. 3. The magnitude of the cardiovascular responses was significantly reduced following section of the sensory nerve fibres from the knee joint, in an otherwise partially denervated limb. This indicates that part of the reflex changes associated with limb movement arise from sensory endings in the joints. 4. Electrical stimulation of articular nerves led to similar cardiovascular responses. The afferent fibres involved were identified as those having conduction velocities below 18 m/sec, whose terminations are classified as the type IV joint receptors. The possibility that these subserve some other function than pain is discussed.

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“…In this regard, earlier experiments involving partial neuromuscular blockade (Ochwadt, Biicherl, Kreuzer & Loeschcke, 1959;Asmussen, Johansen, J0rgensen & Nielsen, 1965;Freyschuss, 1970;BondePetersen, Gollnick, Hansen, Hulten, Kristensen, Secher & Secher, 1975;Secher & Johansen, 1976;Hobbs, 1982) may be of special interest as decamethonium and tubocurarine may preferentially block white and red skeletal muscles, respectively (Paton & Zaimis, 1951;Zaimis, 1953;Jewell & Zaimis, 1954). Also, this preference seems to be valid for humans since a significant correlation has been demonstrated between the degree of curarization and the percentage of slow-twitch muscle fibres in m. vastus lateralis, soleus and gastrocnemius (Secher, Rube & Secher, 1982).…”

Section: Introductionmentioning

confidence: 99%

Partial neuromuscular blockade and cardiovascular responses to static exercise in man.

Leonard¹,

Mitchell²,

Mizuno³

et al. 1985

The Journal of Physiology

112

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SUMMARY1. In human subjects sustained static contractions of the quadriceps femoris in one leg were performed with the same absolute and the same relative intensity before and after partial neuromuscular blockade with either decamethonium or tubocurarine which reduced strength to about 50 % of the control value. During the contractions performed with the same absolute force, the magnitude of the cardiovascular responses (heart rate and blood pressure) was greater during neuromuscular blockade than during control contractions. During the contractions involving the same relative force the magnitude of the cardiovascular responses was almost the same with and without neuromuscular blockade. These findings were independent of the drug used.2. The metabolic part of the exercise pressor reflex was assessed by the application of an arterial cuff I min before cessation of exercise and for the following 3 min of rest. Although heart rate and blood pressure decreased after cessation of exercise, application of the tourniquet resulted in higher post-exercise values and this effect was seen both with and without neuromuscular blockade.3. Muscle biopsies from the subjects' m. vastus lateralis were analysed for fastand slow-twitch fibre composition showing 27-66 % slow-twitch fibres. No correlation was found between cardiovascular responses to static exercise, with or without neuromuscular blockade, and fibre type predominance. 4. The results suggest that the involvement of fast-or slow-twitch muscle fibres does not play a dominant role in the cardiovascular responses to static exercise in man. Both central command and reflex neural mechanisms are of importance, and it appears that these two control mechanisms are redundant and that neural occlusion may be operative. However, when partial neuromuscular blockade induces a disproportion between an increase in central command and a constant or decreasing muscle tension and metabolism, the larger signal arising from central command determines the magnitude of the cardiovascular responses.

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On the Nervous Factors Controlling Respiration and Circulation during Exercise Experiments with curarization

Cited by 134 publications

References 10 publications

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

The contribution of articular receptors to cardiovascular reflexes elicited by passive limb movement

Partial neuromuscular blockade and cardiovascular responses to static exercise in man.

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