04 NOVEMBER 2009 ISSUE

Factoring BP into exercise equation

Chris Milne

Hypertension is a common problem in the population, so it follows there will still be a proportion of our active patients who either have established hypertension or develop this during the time they are under the care of their GP. This article is by no means comprehensive, but aims to give a brief overview of the important issues involved.

To begin with, it is important to consider the effect of exercise on blood pressure.

Blood pressure is a result of the interaction of the cardiac output and the total peripheral resistance.

The cardiac output, in turn, is a product of the stroke volume and heart rate.

Stroke volume increases progressively with acute exercise, and plateaus at about 50 per cent of maximum oxygen consumption (VO2 max).

In a normotensive individual, there is a dramatic rise in the cardiac output proportional to the exercise intensity, and the total peripheral resistance decreases.

This leads to an increase in the systolic blood pressure and mean arterial pressure, in direct proportion to increases in exercise intensity.

The acute effects of isometric exercise are rather different. There is a dramatic increase in blood pressure, and systolic blood pressures of between 200 and 300mmHg have been observed during weightlifting.

Effectively, weightlifting involves a Valsalva manoeuvre which dramatically increases the intrathoracic pressure and also the arterial pressure.

Peak blood pressure tends to occur during maximal lifts or near exhaustion. The American College of Sports Medicine guidelines recommend termination of an exercise test if the blood pressure exceeds 250/115mmHg.

With prolonged exercise training there are progressive adaptations. With aerobic training one can expect a drop in the resting blood pressure, with the systolic dropping by an average of 11mmHg and the diastolic by an average of 6mmHg.

There is usually an increase in chamber size within the heart, with only slight thickening of ventricular walls, and these training effects result in a markedly increased stroke volume with associated bradycardia at rest and mild left ventricular hypertrophy.

By contrast, repetitive weight training tends to lead to thickened left ventricular walls and may ultimately result in concentric left ventricular hypertrophy.

What are the effects of hypertension on the exercising athlete? It is important to have good control of blood pressure prior to participation in vigorous physical activity, as both aerobic exercise and weight training cause marked increases in blood pressure. Total peripheral resistance is known to be increased during aerobic and weight training in all grades of hypertension.

A warm-up is important for people who exercise, but even more important for the person with hypertension.

Monitor exercise programme

Those people with established cardiovascular disease need careful monitoring, particularly in the early phases of undertaking an exercise programme.

Another factor worthy of consideration is that people with hypertension do not shunt blood to the skin as effectively as normotensives. This means they need to take particular care when exercising in the heat.

The most comprehensive guidelines with regard to athletes with cardiovascular abnormalities were promulgated from the 36th Bethesda Conference in 2005. The taskforce recommended out-of-office measurements for individuals with a blood pressure above 140/90mmHg, to exclude “white coat hypertension”.

Those with sustained hypertension should have echocardiography. Athletes with a blood pressure of over 160/100mmHg at rest should be kept away from weight training or other sports with high static load until their blood pressure is well controlled.

What to do if one of your active patients is found to be hypertensive? First, assess them accurately, taking note of their blood pressure on several occasions, both sitting and standing. 

Second, look for evidence of postural hypotension. Those people with high aerobic fitness tend to exhibit enhanced vagal tone which makes them more prone to postural hypotension.  Look for secondary causes of hypertension, eg, by listening for a renal bruit and checking the urine for microalbuminuria or mild proteinuria.

Next, look for evidence of target organ damage. Once again, urine examination is relevant, as is an examination of the fundi, looking for increased light reflex or early A-V crossing changes. Retinal haemorrhages or exudates indicate advanced changes and specialist collaboration with supervision would be advised.

In terms of blood pressure control, it is important to optimise non-drug methods. This includes reducing life stressors, plus limiting salt intake in those who are known to be salt sensitive. In addition, alcohol consumption should be moderated, as this is known to contribute to hypertension.

If drug therapy is required, there is a wide range of drugs to choose from.

Ordinarily, diuretics or beta-blockers would be first-line agents for management of hypertension, but each of these has significant limitation in the exercising individual. Diuretics reduce plasma volume but cause little or no change in total peripheral resistance. Diuretics may, therefore, reduce maximal exercise capacity and make the athlete more prone to heat illness or cramping.
 
Beta-blockers reduce myocardial contractility and heart rate, and reduce aerobic performance.  In addition, non-cardioselective beta-blockers block glycogenolysis and this may result in hypoglycaemia, especially during or after intense exercise. They also mask the symptoms of hypoglycaemia.

ACE inhibitors first choice therapy

The drugs of choice for control of hypertension in the exercising individual would be ACE inhibitors. These drugs control blood pressure without an associated decrease in aerobic capacity. Occasionally, athletes may notice an exaggerated tendency to postural hypotension when they have an abrupt stop to intense endurance exercise; this is a good reason to cool down gradually, so there is sufficient return of blood to the right side of the heart to enable the person to remain upright without fainting. 

If your patient is not a candidate for an ACE inhibitor, then a calcium antagonist is a worthwhile alternative. These medicines lower the calcium concentration in vascular smooth muscle and, thereby, decrease total peripheral resistance. They do not cause any decrease in maximal aerobic capacity.

As experienced clinicians will be well aware, some calcium antagonists, particularly nifedipine, can cause pedal oedema.

In addition, nifedipine is associated with a reflex tachycardia in some cases. For those people who exercise in cold conditions, highly selective calcium antagonists, eg, felodipine, may be useful in enhancing peripheral blood flow, and thereby reducing a tendency to frostbite.

Another alternative for control of blood pressure would be alpha-blockers. These drugs have tended to fall from favour in the last decade or so due to perceived problems with tachyphylaxis, which was a particular problem with prazosin.

However, I have found them to be a useful agent, particularly in those people who experience side effects with either ACE inhibitors or calcium antagonists.

For the elite athlete with hypertension it is imperative to be aware of the fact both diuretics and beta-blockers are banned drugs in various sports and are, therefore, absolutely contraindicated for this small proportion of our exercising population.

All in all, unless it is severe, hypertension is not a contraindication to exercise and, in fact, aerobic exercise is known to be helpful in its control.

We are fortunate to have a wide variety of effective agents available.

In the rare case of an individual whose blood pressure is proving impossible to control with two or more agents, specialist advice should be sought from a physician or cardiologist.

Chris Milne is a sports physician practising in Hamilton  

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