Patients with asthma have exaggerated bronchoconstriction of their airways in response to certain indirect (e.g. cold air, allergens, dust, exercise) or direct (e.g. inhaled methacholine) stimuli. This 'hyper-reactivity' usually co-exists with airway inflammation, although the pathophysiological mechanisms underlying these changes are not fully understood. It is likely that this hyper-reactivity is associated with abnormal autonomic nervous system (ANS) control. In particular, the parasympathetic (vagal) component of the ANS appears to be implicated in the pathogenesis of asthma. In addition, several studies have suggested the existence of differential alteration in ANS function following exercise in asthmatics compared with non-asthmatic individuals. Several early studies suggested that the altered autonomic control of airway calibre in asthma might be reflected by a parallel change in heart rate. Cardiac vagal reactivity does indeed appear to be increased in asthma, as demonstrated by the cardiac response to various autonomic functions tests. However, other studies have reported a lack of association between bronchial and cardiac vagal tone, and this is in accord with the concept of system-independent ANS control. This review provides a discussion of cardiovascular-autonomic changes associated with either the pathophysiology of asthma per se or with asthma pharmacotherapy treatment. Previous investigations are summarised suggesting an apparent association between altered autonomic-cardiovascular control and bronchial asthma. The full extent of autonomic dysfunction, and its clinical implications, has yet to be fully determined and should be the subject of future investigation.

Breathing rates during physical exercise suggest that, during these conditions, the high-frequency (HF) bandwidth of heart rate variability (HRV) analysis should be extended beyond conventional guidelines. However, there has been little investigation of the most appropriate choice of HF bandwidth during exercise. HRV analysis was performed in 10 males and six females during progressive bicycle exercise. Cardiac cycle (RR) interval and breath-by-breath respiratory data were simultaneously recorded. HRV powers were determined for the band-limited ranges 0.04-0.15 Hz [low-frequency (LF)], 0.15-0.4 Hz (HF 0.4) and 0.15-bf Hz (HF bf, where bf represents maximum breathing frequency). Mono-exponential functions described the relationship between HRV and work rate for each bandwidth (r=0.92-0.95) and were used to calculate the "HRV decay constant" (work rate associated with a 50% reduction in HRV power). The HRV decay constants for each bandwidth were linearly related to maximal work rate (r>0.71; P<0.001) and were substantially greater in males than in females (P<0.001). There was a significant difference between the HRV decay constants for HF 0.4 and HF bf (P<0.005) in both genders. The HRV decay constants for the LF and HF bf bandwidths appear to provide an indication of work capacity from submaximal exercise, without prior assumption regarding heart rate and its relationship with work rate.

Sample entropy (SampEn) is a measure of the complexity of data. Few studies have compared the SampEn of electrocardiographic cardiac interval (RR) data (SampEn-RR) during differing physiological states, and none have examined SampEn for the corresponding QT interval (SampEn-QT). The aim of this study was to quantify SampEn-RR and SampEn-QT during rest and for a range of exercise workloads. Specific objectives were to assess both the utility of SampEn for discriminating between physiological states and the relationship of SampEn-RR with traditional measures of heart rate variability (HRV). Twelve males of similar age, mass and aerobic fitness participated. A three-lead ECG was recorded continuously during pre-exercise, progressive bicycle exercise and recovery, and beat-to-beat RR and QT intervals were quantified for sinus beats. SampEn and HRV were calculated within consecutive 1 min periods throughout. Consistent estimation of SampEn-RR and SampEn-QT was possible with an appropriate choice of SampEn parameters. SampEn-RR was sensitive to differing physiological conditions, but its discriminating ability was poorer than that of linear HRV indices. SampEn-RR was also negatively correlated with normalized LF and LF/HF parameters. We interpret changes in SampEn for RR and QT data in terms of the altered autonomic nervous system (ANS) control of either the atrial or the ventricular myocardium (or both) during discrete physiological states. We speculate that greater complexity in QT data might be explained by a direct ANS influence on the ventricular myocardium.