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Hypertension Exercise Program

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ECG, electrocardiogram; echo, echocardiogram.

ECG, electrocardiogram; echo, echocardiogram.

Table 4 Factors affecting cardiac hypertrophy

Factors leading to hypertrophy

Factors reducing or preventing hypertrophy

24 h cardiac work Ventricular wall stress Sodium intake Sympathetic activity Angiotensin II Insulin-like growth factor Growth hormone Genotype

Nitric oxide Bradykinin can cause cardiac hypertrophy and a low salt intake allows resolution. The increased size of the heart is a response that decreases the wall stress of the ventricle and is a compensatory phenomenon. The cardiac hypertrophy with hypertension is concentric in nature, with sarcomeres laid down in the myocytes in parallel (Figure 7). The increased thickness of the myocytes together with associated fibrosis of the interstitium means that the oxygen diffusion pathway is increased and this may lead to precipitation of arrhythmias and sudden death. In cardiac hypertrophy associated with exercise the sarcomeres are laid down in series, and with this 'eccentric' hypertrophy there is no increased mortality.

In addition to cardiac hypertrophy in hypertensive patients there is significant impairment of diastolic relaxation. This may result from poor oxygen delivery to the mitochondria and thus a retarded reuptake of calcium into cell organelles. Thus, there is a dynamic aspect to diastolic dysfunction which may be reversible. However, in addition the laying down of fibrous tissue in the heart contributes to stiffness and poor diastolic filling. The poor diastolic function may occur prior to any increase in cardiac size. The poor diastolic filling due to reduction in left ventricular compliance may explain the subnormal stroke volume seen in hypertensive patients during exercise. In these circumstances the increased pulse rate means that there is insufficient time for a stiff left ventricle to fill adequately.

Figure 7 The diffusion distance in normal and eccentric hypertrophy is not increased. In concentric hypertrophy there is often associated fibrosis; this leads to a longer extracellular diffusion distance as well as a longer intercellular pathway. Thus, oxygen delivery to mitochondria is poor, the reuptake of calcium (an energy-dependent process) is sluggish, and 'functional' relaxation is slow, leading to impaired diastolic filling.

Figure 7 The diffusion distance in normal and eccentric hypertrophy is not increased. In concentric hypertrophy there is often associated fibrosis; this leads to a longer extracellular diffusion distance as well as a longer intercellular pathway. Thus, oxygen delivery to mitochondria is poor, the reuptake of calcium (an energy-dependent process) is sluggish, and 'functional' relaxation is slow, leading to impaired diastolic filling.

Early in the development of hypertension in spontaneously hypertensive rats and in humans total peripheral resistance is elevated. In rats changes in the resistance vessels are seen early. In borderline and mild hypertension in humans there may be little increase in total peripheral resistance at rest, but the total peripheral resistance does not fall to normal levels during conditions when maximal vasodilatation would be expected (e.g., exercise, heating, autonomic blockade). This probably indicates that structural changes occur early in the disease and the failure to dilate adequately may in part explain the excess rise in blood pressure seen in hypertensive patients during exercise.

Increased peripheral resistance is not evenly distributed across all regional vascular beds and the resistance in the kidney frequently appears to be increased, resulting in a reduction of about 10% in renal blood flow. In contrast, in prehypertensive people an increase has been reported in renal blood flow. Whether this has any pathogenic significance is not known. However, the reduced blood flow could result from activation of the tubuloglomerular feedback response due to altered sodium reabsorption in the proximal tubule.

The coronary flow in hypertensive patients is of importance. These people already may have an increased oxygen demand. The flow at rest is usually normal but even in patients with no evidence of coronary artery disease the flow reserve is impaired. In normal people the coronary artery rapidly dilates to meet the increased oxygen demand but in hypertensive patients this dilation is sluggish and does not reach the same maximal flow. The reason is complex and is possibly a combination of structural change and an impaired endothelial response.

The Sympathetic Nervous System

Many investigators have postulated that hypertension may result from impaired central control and this is mediated via the sympathetic nervous system. The increased cardiac output and heart rate seen in many people with early or incipient essential hypertension could be explained by excess sympathetic activity. However, it has been difficult to demonstrate that there is increased sympathetic activity because many of the techniques are relatively crude. It has been reported that plasma noradrena-line levels correlate with cardiac index and peripheral resistance in mildly hypertensive patients. It is difficult to know if increased sympathetic activity is primary, but in adolescents who later develop hypertension there is an increased blood pressure rise associated with mental or physical stress, which supports the concept of a dysregulatory neurogenic component. Sympathetic activity may also be altered by changes in sodium or potassium intake, and thus the 'prime' cause of hypertension remains to be elucidated.

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