Contrasting the physiological effects of heliox and oxygen during exercise in a patient with advanced COPD

Summary of the physiological effects of heliox and oxygen breathing during exercise

Collectively the findings indicate that the increase in endurance time during heliox or oxygen breathing can be attributed to a number of physiological adjustments associated with improvements in respiratory, cardiovascular and muscle cellular metabolic responses. The improvement in ventilatory response was accompanied by lower dyspnoea and leg fatigue perceptions during both supplementations (table 1) and by a lower degree of reduction in respiratory (both inspiratory and expiratory) and locomotor muscle oxygen saturation compared with room air (figure 3). Increases in respiratory and locomotor muscle oxygen availability by heliox and oxygen administration were due to higher systemic oxygen delivery (figure 1) albeit for different reasons; namely, greater cardiac output and local muscle perfusion with heliox administration (figures 1 and 2) and higher arterial oxygen concentration with oxygen breathing (figure 1). In conclusion, along with the alleviation of ventilatory constraints by heliox and oxygen breathing compared with room air (table 1) [5], a common basis for enhanced endurance time by heliox or oxygen administration is the improved respiratory and locomotor muscle oxygen delivery and reduced metabolic acidosis and sensations of breathlessness and leg discomfort afforded by both interventions (figure 4) [4].

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Figure 4

A schematic representation conceptualising the acute physiological responses a patient with COPD exhibits during exercise breathing heliox or oxygen compared with exercise in room air. t_E: expiratory time; DH: dynamic hyperinflation; CO: cardiac output; O₂DEL: oxygen delivery; SVC: systemic vascular conductance; EMG: electromyography. ^#: profoundly in hypoxaemic patients. Figure partially created using BioRender.

Heliox and oxygen breathing on reducing dyspnoea during exercise

As far as dyspnoea is concerned, an interesting observation in this case is the fact that heliox and oxygen acted differently on the reduction of exertional dyspnoea. Specifically, during exercise, heliox increased V′_E (by shifting the operating lung volumes downward) but oxygen decreased V′_E compared with room air breathing (table 1) [4–9]. Nevertheless, during both interventions the patient reported less shortness of breath (table 1), either through making him breathe less (with oxygen) or making him breathe more but with less constraints (heliox). Indeed, heliox supplementation as an ergogenic strategy is based on the idea that a lighter gas mixture could be moved to and from the lung airways more easily than atmospheric air [6, 7]. Heliox reduces turbulent airway resistance and both inspiratory and expiratory pressures during exercise as compared with room air breathing [8, 9]. Due to these effects, the patient demonstrated higher V′_E, less dynamic hyperinflation (expressed as change in IC from rest) and improved cardiac function during exercise when compared to room air breathing (table 1 and figure 1) [4, 9–11].

However, it is known that oxygen administration primarily increases arterial oxygen concentration but also lessens V′_E (table 1) and ventilatory drive, potentially via inhibition of carotid bodies and/or improved metabolic conditions of the skeletal muscles (manifested by increases in intracellular pressure of oxygen and concentrations of phosphocreatine and a reduction in intracellular concentrations of inorganic phosphate) [5, 10, 12].The effects of oxygen supplementation on operating lung volumes (end-inspiratory and end-expiratory lung volumes), V_T, breathing pattern and exercise induced-dynamic hyperinflation might be more pronounced in hypoxaemic patients as compared to normoxic or to patients with mild arterial oxygen desaturation [13–15]. Furthermore, it has been postulated that patients who exhibit a reduction in dynamic hyperinflation in response to oxygen breathing appear to have greater airway obstruction, greater ventilatory constraints during exercise and poorer exercise performance with steeper dyspnoea/ventilation slopes as compared to their counterparts [12, 16]. Therefore, it can be argued that during exercise hypoxaemic patients might experience greater reduction in dyspnoea sensations in response to reductions in V′_E following oxygen administration [12, 15].

Heliox and oxygen breathing: central and local haemodynamic responses during exercise

The mechanisms orchestrating the ergogenic effect of heliox and oxygen breathing on exercise capacity were not limited to the alleviation of ventilatory constraints during exercise. The results from this case and other studies suggest that extrapulmonary improvements could potentially alleviate exercise induced-dyspnoea in patients with COPD [17, 18]. Furthermore, during heliox and oxygen breathing the patient exhibited improved respiratory and locomotor muscle metabolic condition as indicated by the smaller decrease in local muscle oxygenation that was accompanied by less lactic acidosis as compared with room air (figure 3). These beneficial effects are of critical importance when considering that exercise-induced respiratory and leg muscle fatigue can contribute to the increase in dyspnoea perceptions [19, 20]. Indeed, in the neurobiological model of dyspnoea proposed by Dempsey et al. [19] neural inputs that reach the somatosensory cortex and contribute to dyspnoea sensations originate from the locomotor and respiratory muscles via the group III–IV muscle afferents. During exercise in room air, a restriction in oxygen delivery to the respiratory and locomotor muscles occurs due to the inability of the circulatory system to fully satisfy their energy demands [21]. This, in turn, could exaggerate both respiratory and locomotor muscle fatigue and thus further increase dyspnoea perceptions during exercise. Furthermore, during heliox and oxygen breathing the greater increase in respiratory and locomotor muscle oxygen delivery compared with room air may have postponed exercise-induced skeletal muscle fatigue and thus alleviated muscle sensory afferent traffic in type III–IV nerves innervating the respiratory and locomotor muscle, also contributing to the reduction in dyspnoea sensations (table 1). In addition, reductions in ventilatory drive with oxygen breathing in patients with COPD during exercise have been associated with reduced peripheral chemoreceptor afferent activity [22]. Importantly, Gosselin et al. [23] demonstrated that oxygen supplementation can reduce quadriceps muscle electromyogram activity at any given work rate compared with exercise in room air.

In summary, the beneficial effects of supplemental heliox and oxygen on respiratory and locomotor muscle metabolic and muscle contractile function would be expected to delay the onset of lactic acidosis accompanied by improvements in dyspnoea, leg discomfort and exercise tolerance in patients with COPD. In support of this notion, significant associations between the improvement in respiratory muscle oxygen delivery and the lower lactic acidosis and dyspnoea perceptions reported during exercise while breathing heliox or oxygen compared with room air were recently demonstrated [24]. A conceptual representation of the effect of heliox and oxygen breathing during exercise is presented in figure 4.