Hypertension in Athletes

Current UK guidance on hypertension in adults sets the clinic diagnostic threshold at 140/90 mmHg, but a single clinic reading is never enough. The recommended clinic sequence is to take a second measurement, take a third if the first two differ substantially, and record the lower of the final two. Where clinic blood pressure falls between 140/90 and 179/119 mmHg, measurement away from the clinic is offered to confirm the diagnosis, because the white coat effect is common. A reading of 180/120 mmHg or above follows the severe hypertension pathway rather than routine confirmation. Diagnosis is made when the clinic pressure is at least 140/90 mmHg and the average daytime ambulatory or home pressure is at least 135/85 mmHg.

Ambulatory blood pressure monitoring (ABPM) is the reference standard, and home blood pressure monitoring (HBPM) is the alternative where ambulatory monitoring is not tolerated. For home monitoring the standard protocol is two seated readings taken about a minute apart, twice a day in the morning and the evening, for between four and seven days, with the first day discarded and the remaining readings averaged.

Two athlete-specific patterns matter. Masked hypertension, where clinic readings are normal but out-of-office readings are raised, is easily missed, and out-of-office monitoring should be considered where it is specifically suspected, such as unexplained target organ changes or discordant clinic and exercise findings, rather than applied routinely to every athlete with a high-normal reading. An exaggerated blood pressure response to exercise is associated with future hypertension, but it is not itself a diagnosis of hypertension, there is no universally accepted athlete-specific threshold, and it should prompt out-of-office assessment and follow-up rather than automatic treatment. Technique also matters more than clinicians expect: an undersized cuff on a large muscular arm overestimates pressure, so cuff size should be matched to the athlete's arm before any label is applied.

A raised blood pressure in an athlete is the start of an assessment, not the end of one. Secondary causes deserve real consideration in young athletes, in whom primary hypertension is less expected: renal parenchymal and renovascular disease, coarctation of the aorta, primary hyperaldosteronism, phaeochromocytoma, thyroid disease and obstructive sleep apnoea all present this way. Radio-femoral delay and a difference between arm and leg pressures point toward coarctation and should be checked in a young athlete rather than assumed absent.

Substance use is an important and often missed contributor. Regular non-steroidal anti-inflammatory drugs taken for training niggles, sympathomimetic decongestants and anabolic androgenic steroids are particularly important, while caffeine, energy products and other stimulants can acutely raise blood pressure or confound the measurement. The history should ask about these directly rather than in general terms, since athletes often do not regard over-the-counter medicines or supplements as worth mentioning.

Standard assessment of target organ damage covers renal function, a urine albumin to creatinine ratio, an electrocardiogram and retinal examination, alongside formal estimation of cardiovascular risk using a validated tool within its validated age range. Athlete-specific cardiology assessment sits on top of this rather than replacing it: echocardiography to assess for left ventricular hypertrophy, and exercise testing to observe the blood pressure response, are selected according to age, severity, symptoms, electrocardiographic findings, the demands of the sport and specialist judgement, rather than being mandatory for every athlete with hypertension. One judgement recurs: distinguishing the physiological remodelling of athlete's heart, in which wall thickening is accompanied by proportionate enlargement of the ventricular cavity with preserved systolic and diastolic function, from hypertensive remodelling, which is more likely to be concentric with a relatively smaller cavity and may impair relaxation.

Management starts with the same lifestyle measures as in any patient, and athletes often have less room to improve here than expected, so attention usually turns to reducing sodium intake, moderating alcohol, and removing the pressor substances identified in the history. Exercise itself remains part of the treatment rather than something to be withdrawn. The treatment target for most adults under 80 is a clinic pressure below 140/90 mmHg with a home or ambulatory average below 135/85 mmHg.

Drug selection should still follow the standard UK algorithm, which takes account of age, ethnicity and comorbidity and proceeds in steps, while incorporating anti-doping status and performance effects into the choice. The practical rule in a tested athlete is to choose a permitted option from within the clinically appropriate class wherever possible, rather than treating sport as a reason to abandon the algorithm. In practice angiotensin converting enzyme inhibitors, angiotensin receptor blockers and calcium channel blockers are not prohibited and cover most of the standard first and second steps, so a compliant choice is usually available. These classes generally have less direct effect on exercise performance than beta blockers or diuretics, though individual adverse effects such as hypotension, dizziness, cough or ankle oedema still matter to a training athlete.

Two classes carry restrictions. Diuretics are prohibited at all times because they act as masking agents, so they should be avoided where a suitable permitted alternative exists; they are not medically forbidden, and if a diuretic is genuinely necessary the therapeutic use exemption (TUE) pathway must be followed before use. Beta blockers are prohibited only in listed sports, principally in-competition, with out-of-competition prohibition applying in some disciplines, because they reduce tremor and heart rate where steadiness is rewarded; they also blunt maximal heart rate and perceived exercise capacity. The list of affected sports is reviewed annually and does change, so the current list must be checked for the athlete's specific discipline rather than recalled from memory.

Athletes with controlled hypertension and no clinically important target organ damage can usually participate fully, and should be encouraged to do so. Severe or uncontrolled hypertension, evidence of target organ damage, or hypertension alongside other cardiovascular disease calls for individual sports cardiology assessment, with temporary modification of very high static load activity where appropriate while control is achieved, since these disciplines produce the largest acute pressure surges. Current sports cardiology recommendations favour individualised risk assessment over rigid or permanent disqualification.

Follow-up should be planned rather than opportunistic. Blood pressure is rechecked after any treatment change, then at least annually once stable, with periodic reassessment of target organ damage and cardiovascular risk. The athlete should understand why the drug was chosen, what the anti-doping position is, and that any new medicine or supplement should be checked before use. Documenting that conversation protects both the athlete and the clinician.

• •Diagnosis needs clinic pressure of at least 140/90 mmHg plus a daytime ambulatory or home average of at least 135/85 mmHg.
• •Clinic pressure of 180/120 mmHg or above follows the severe hypertension pathway rather than routine confirmation.
• •An exaggerated exercise blood pressure response is not itself diagnostic and has no agreed athlete-specific threshold.
• •Athlete's heart shows proportionate cavity enlargement with preserved function; hypertensive remodelling is more concentric and may impair relaxation.
• •Diuretics are prohibited at all times as masking agents; beta blockers are prohibited in listed sports only.
• •Follow the standard prescribing algorithm and select a permitted option from within the clinically appropriate class.