Adequate stimuli of the carotid body: more than an oxygen sensor?

Animal and tissue studies have indicated that the carotid bodies are sensitive to glucose concentrations within the physiological range. This glucose sensitivity may modulate the ventilatory response to hypoxia, with hyperglycaemia suppressing the hypoxic response and hypoglycaemia stimulating it. This study was designed to determine whether hypo- and hyperglycaemia modulate the hypoxic ventilatory response in humans. In 11 normal research participants, glucose levels were clamped at 2.8 and 11.2 mmol l(-1) for 30 min. At the start and end of each clamp, blood was drawn for hormone measurement and the isocapnic hypoxic ventilatory response was measured. Because generation of reactive oxygen species may be a common pathway for the interaction between glucose and oxygen levels, the experiments were repeated with and without pretreatment for 1 week with vitamins C and E. Hypoglycaemia caused an increase in the counter-regulatory hormones, a 54% increase in isocapnic ventilation, and a 108% increase in the hypoxic ventilatory response. By contrast, hyperglycaemia resulted in small but significant increases in both ventilation and the hypoxic ventilatory response. Antioxidant vitamin pretreatment altered neither response. In conclusion, the stimulant effect of hypoglycaemia on the hypoxic ventilatory response is consistent with a direct effect on the carotid body, but an indirect effect through the activation of the counter-regulatory response cannot be excluded. The mechanisms behind the mild stimulating effect of hyperglycaemia remain to be elucidated.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2007.130112

The effects of hypo- and hyperglycaemia on the hypoxic ventilatory response in humans.

BACKGROUNDThe exercise-induced rise in arterial potassium concentration ([K+]a) may contribute to exercise hyperpnea and could play a role in exertional fatigue. This study was designed to determine whether the exercise-induced rise in [K+]a is altered in patients with chronic heart failure (CHF) and whether physical training affects K+ homeostasis.METHODS AND RESULTSWe evaluated 10 subjects with CHF (ejection fraction, 23 +/- 3.9%) and 10 subjects with normal left ventricular function (NLVF) who had undergone previous coronary artery graft surgery (ejection fraction, 63 +/- 8.6%). Subjects performed an incremental cycle ergometer exercise test before and after a physical training or detraining program. Changes in [K+]a and ventilation (VE) during exercise were closely related in both groups. Subjects with CHF did less absolute work and had reduced maximal oxygen consumption (VO2max) compared with subjects with NLVF (P < .01). Exercise-induced rises in [K+]a, VE, norepinephrine, lactate, and heart rate we...

Effect of physical training on exercise-induced hyperkalemia in chronic heart failure. Relation with ventilation and catecholamines.

The increase in ventilation caused by exercise is controlled by a combination of neural and chemical events, although the precise contribution and relative importance of these signals is still debated. It is generally agreed that the genesis of exercise hyperpnoea lies within the central nervous system and that peripheral reflexes, both chemical and neural, modulate central drive. Recently, attention has once again focused on the idea that circulating factors, in particular potassium, may play an important role in this modulation by stimulating known areas of peripheral chemoreception. Arterial chemoreceptors, muscle chemoreflex and slowly adapting pulmonary stretch receptors are all excited by hyperkalaemia. When potassium is raised to mimic exercise concentrations it increases ventilation in anaesthetised animals. This response is abolished by surgical denervation of the arterial chemoreceptors and is markedly reduced by chemical denervation with hyperoxia. Hypoxia enhances the ventilatory response to hyperkalaemia, and the stimulatory effects of potassium are further increased when combined with lactic acid or raised concentrations of noradrenaline. Hyperkalaemia can also increase the hypoxic sensitivity of the arterial chemoreflex in exercise. There is a close temporal relationship between potassium and ventilation during exercise, but changes in potassium are not proportionally related to changes in ventilation. When all data are taken together, there is good evidence that potassium has a supporting role in the control of exercise hyperpnoea, predominantly through modulation of the arterial chemoreflex.

Potassium and breathing in exercise.

The purpose of this study was to determine whether changes in arterial plasma potassium concentration [K+]a affect expired ventilation (VE) in euoxia, hypoxia and hyperoxia during rest and light exercise in humans. Three periods of ventilatory measurements were undertaken in eight healthy subjects at rest and in seven other subjects during cycle ergometry (70 W). The first period of measurement was before the ingestion of 64 mmol of potassium chloride (KCl), the second 20 min after ingestion of KCl when [K+]a levels were elevated, and the third 3 h after the ingestion of KCl when [K+]a had returned substantially to normal. During each period, end-tidal PO2 was cycled between euoxia, hypoxia and hyperoxia, whilst the end-tidal PCO2 was maintained constant. The acute ventilatory response to hypoxia (AHVR) was calculated as the difference in VE during hypoxia and hyperoxia within each period of measurement. Oral KCl produced a 1.3 +/- 0.2 mM (mean +/- S.E.M.) increase in [K+]a at rest and a 0.8 +/- 0.2 mM increase during exercise. There was no significant difference in ventilation during euoxia between the three periods of measurement at rest or during exercise. There was a significant increase in AHVR with the rise in [K+]a of 21 min-1 mM-1 at rest (arterial PO2 during hypoxia ca 57 Torr) and 10 l min-1 mM-1 during exercise (arterial PO2 during hypoxia ca 52 Torr). There was a significant difference in the absolute increase in AHVR with [K+]a between rest and exercise, but this difference was not significant if the increase in AHVR with [K+]a was expressed as a percentage of the initial AHVR. We conclude that changes in [K+]a of the order of 1 mM have little effect on euoxic ventilation at rest or during light exercise in humans. We also conclude that [K+]a changes of this order increase AHVR at rest and during light exercise and that increases in [K+]a contribute to the increase in AHVR with exercise in humans.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1994.sp020138

Effect of raised potassium on ventilation in euoxia, hypoxia and hyperoxia at rest and during light exercise in man.

Potassium is lost from exercising muscle into extracellular fluid and causes hyperkalaemia. Intravenous administration of KCl in anesthetized cats to produce similar levels of arterial hyperkalaemia causes peripheral chemoreceptor stimulation, which produces an increase in ventilation. Interactions of arterial PO2, PCO2, and (K+) as drives to breathing are discussed.

http://physiologyonline.physiology.org/content/nips/5/3/104.full.pdf

Potassium and Breathing

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Potassium and Breathing