Other Considerations For Heart Rate Monitoring Associated With Changes In Myocardial Performance

Figure 3.2 (see page 52) illustrates the optimisation of myocardial performance by the interaction between HR and ejection fraction, which is directly related to stroke volume (Conconi, et al., 1982; Pokan, et al., 1998). For the healthy individual, although stroke volume reaches a maximum at about 50 to 60% of VO2max, myocardial performance is preserved as HR continues to rise towards maximal levels. In cardiac patients, the right-hand panel of Figure 3.2 demonstrates a deterioration of ejection fraction as HR progresses towards maximum. In an attempt to preserve cardiac output, HR rises in an accelerating manner, which further decreases diastole and thus myocardial perfusion time. The risk of ischaemia is heightened and/or blood pressure does not rise to meet the circulation required for the aerobic demands of the muscles. Not only does the HR rate shorten diastole that can affect myocardial perfusion, but it can also reduce ventricular filling (Poulsen, 2001). Reduced ventricular filling leads to reduced stroke volume by way of the Frank-Starling mechanism, and hence myocardial performance may not match the circulatory needs of the exercise being performed. The change in rate pressure product has also been demonstrated to behave similarly to ejection fraction (as seen in Figure 3.2), where it begins to decrease at higher heart rates (Omiya, et al., 2004).

The rate pressure product turn point identified by Omiya, et al. (2004) is also correlated with both the ventilatory and lactate thresholds (the upper limit recommended for continuous aerobic exercise at which a training benefit is optimised). This finding corresponds with the original concept of the heart rate turn-point reported by Conconi, et al. (1982) (Figure 3.2). However, some debate exists over its merits as a means of estimating the lactate threshold because the relationship may be strongly dependent on the exercise testing protocol used (Bodner and Rhodes, 2000). Nevertheless, from a myocardial perspective, there is no doubt in all these reports that at higher intensities, HR does not continue to rise in a linear fashion, which provides the evidence of a decreased myocardial performance. For the practitioner this means that encouraging patients to work at high HR is not prudent in the early stages of CR. Although Ehsani, et al. (1982) did show that myocardial contractile improvements could occur from exercising at higher exercise intensities, this was with three to four days of training over a 12-month period. For a few cardiac patients, over many years of progressive overload aerobic training, higher heart rates can be attained and are safe (Thow, et al., 2004). Few studies have evaluated the physiological outcomes after years of CR exercise.

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