I am studying four aspects of cardiorespiratory control in the human: the first breath of exercise; the way the beating heart affects respiratory airflow and gas mixing; how heart beat may affect the timing of the start and end of expiration in exercising humans; and the influence of the left vagus on cardiac activity.  All my current research is on human subjects.

My previous research included studying CO₂-sensitive receptors in the airways of birds.  This led to the effects of CO₂, hypoxia and K⁺ on the mammalian carotid body and subsequently to the effects of CO₂ and hypoxia on pulmonary blood vessels mounted on a myograph.  The myograph was also used to study small cerebral arteries and human radial arteries.  I have also investigated the respiratory side of the 'diving reflex' (in which facial cooling increases the drive to breathe while depressing cardiovascular function) and developed expertise in writing computer programs that look at interactions between, and cooperative actions of, the respiratory and cardiovascular systems.

Current Research Programme

Presently I am studying four aspects of cardiorespiratory control in the human.

The first breath of exercise

Krogh and Lindhard's observation in 1913 that the increase in minute ventilation that occurs with muscular exercise can “coincide absolutely with the beginning of work” is widely quoted evidence that central command, or cortical irradiation, provides a significant drive to breathe, but this observation has never been more than cursorily quantified.  Its separate components (latency, TI, TE, VT, airflow, etc) have not been properly studied and they have not been related to the activity of the respiratory rhythm generator.  In collaboration with Professor Abe Guz (Imperial College, London) and pairs of undergraduate dissertation students,  We believe that this will shed light on the way in which central command interacts with the rhythm generator.

The effect of the beating of the heart on respiratory air flow and gas mixing 

Each beat of the heart displaces air in the lungs around it and in most people this shows up as a small perturbation superimposed on airflow recorded at the mouth.  I am doing this by triggering about 100 consecutive stretches of pneumotachogram off the r-wave of the ECG to isolate cardiac influences from other perturbations.  This is akin to the isolation of excitatory postsynaptic potentials (EPSPs) on neuronal cell bodies generated in response to an action potential.

The most striking and consistent component of the summed waveform is a sharp inspiratory movement of air which appears to be associated with the expulsion of blood from the thorax, but there is frequently a second clear waveform (not unlike the dicrotic blood pressure wave) and sometimes a third and these can all change in exercise.  The origins of the second and third waveforms are not at all clear but they may well involve aspects of gas exchange so accounting for them may have clinical relevance – either in detection of the early stages of disease, or in assessing the disease state.

The possible effect of the heart beat on the timing of the start and end of expiration in exercising humans 

Since cardiac ejection is associated with a small sharp expansion of the lungs, the resulting increase in pulmonary stretch receptor discharge might influence the timing of ventilatory efforts.  In other words, it is possible, especially in exercise when the Hering-Breuer reflex becomes active in man, that the heart has some influence on the timing of breaths.  I am studying this by looking at the frequency distribution of r-waves around the I-E and E-I boundaries.  Some subjects studied so far have non-uniform distributions of r-waves with respect to the respiratory cycle that cannot be accounted for by sinus-arrhythmia.

The influence of the left vagus on cardiac activity

Sinus arrhythmia – the coupling, by the right vagus, of the behaviour of the sinoatrial node to ventilatory efforts – has been exhaustively studied, but the coupling of the behaviour of the atrioventricular node to ventilation by the right vagus has, to my knowledge, not been studied.  I have therefore put together a computer program that can focus at high temporal resolution (a few ms) on the p-q interval - i.e. on the a-v nodal delay.  In some subjects the p-q interval shortens during inspiration in a way very similar to the r-r interval (which is under the influence of the sinoatrial node).  This should prove to be a way to investigate the effect of the left vagus on the heart and it may have clinical relevance.  For example, in some patients the intact left vagus is stimulated because its effects on the brain relieves pain, but the stimulation must also excite the conducting tissue of the heart and the effects of this do not appear to have been studied.

I have done some work on computerised ECG analysis that is intended to be used to highlight spikes generated by artificial pacemakers, in response to a meeting with Dr Keith Johnston (Cardiac Dept, John Radcliffe Hospital).

Piers Nye