High blood pressure, or hypertension, receives massive amounts of attention within the medical, allied health, and fitness industries. Hypertension is considered a risk factor in development of heart disease. Heart disease is a causative agent leading to premature death, and has been for decades:

* Centers for Disease Control & Prevention Data

The relationship of high blood pressure to an increased risk of death from cardiovascular diseases has provided a great deal of motivation to find means to lower blood pressure through pharmaceutical intervention. As a result there have been at least fifty drugs developed to control, but not cure, hypertension.

Epidemiology of hypertension

In a recent scientific publication it was noted that 1.39 billion, or 31.1% of 2010 global population, are hypertensive (reviewed in Mills et al, Nature Reviews Nephrology 16: 223-237, 2020). If projected population growth and diagnostic patterns are actualized, that number of hypertensives within the population will be 1.89 billion in 2025.

Criteria for prescription of blood pressure control medication

The primary diagnostic criteria and rationale for prescription of blood pressure medications (anti-hypertensives) is simply sustained blood pressure elevation, measured in millimeters of mercury, or mmHg, detected through at least two repeated measurements of blood pressure by a clinical professional, where there is at least one week between the two measurements. There are presently a number of mildly differing opinions regarding the criteria in terms of the blood pressures for previously undiagnosed individuals. Within the public health literature regarding high blood pressure as a risk factor for developing heart disease, the threshold for diagnosis has evolved to become lower and lower over the decades:

• 1976 criteria 165/95 mmHg or higher
  (Alderman & Kano, American Journal of Medical Science 271(3): 343-349, 1976)

• 1983 criteria 170/105 mmHg or higher
  (Rastam et al, Scandinavian Journal of Primary Health Care 5(1): 9-12, 1987)

• 1993 criteria 160/90 mmHg or higher
  (Haynes et al, Canadian Medical Association Journal 149(4):409-418, 1993)

• 2010 criteria 140/90 mmHg or higher
  (Quinn et al, Canadian Journal of Cardiology 26(5): 241-249, 2010).

• 2017 criteria 130/80 mmHg or higher
  (Whelton et al, Journal of the American Medical Association 318(21): 2073-2074, 2017)

Note that the lower the threshold pressures are set, the larger the percentage of the population that is eligible for prescribed medication. These downward changes in diagnostic criteria make epidemiological conclusions about affected populations specious, with numbers appearing to be dramatically growing and dire but the changing definitions over time muddies the observed outcomes.

Normal blood pressure values for sedentary apparently healthy people

What exactly is a “normal” blood pressure? Is the less than 130/80 mmHg threshold appropriate and valid?

It depends, mostly on the population measured. If we look at “control groups” from a variety of research publications we can get a feel for common pressures noted experimentally and clinically as “average” or “normal”:

Table derived from data in: 

• • • Arsenault et al, Journal of the American College of Cardiology 55(1): 35-44, 2009
    • Daida et al, Mayo Clinic Proceedings 71(5): 445-452, 1996
    • Dimkpa & Ugwu, International Journal of Exercise Science 1(4): 142-152, 2008
    • Fei et al, Vascular Health Risk Management 1(1): 85-89, 2005
    • Mundal et al, Blood Pressure 6: 269-273, 1997
    • Shimizu et al, Experimental Physiology 106: 736-747, 2021

It appears that from the 20s to the 40s, systolic pressures in apparently healthy individuals, meaning individuals with no noted or diagnosed cardiovascular disease, tend to be under the 130 criteria. However, diastolic pressures generally are very near or over the 80 criteria for diagnosis of hypertension at every age. In the over 50 age groups both systolic and diastolic pressures regularly exceed the 130/80 threshold BUT it is common to add 10 mmHg to the diagnostic criteria specifically because older populations have higher blood pressures. This divergence in diagnostic criteria is a bit of a conundrum. Why are pressures between >130/80 and 140/90 dangerous to otherwise healthy younger populations but not to less robust, but still healthy, older populations?

Further, if we consider the standard deviations within the published data we see that the mean (average) values presented have quite a bit of variation around them. Data from the MESA and ERIC study populations indicated that apparently healthy individuals of an average age of 62 had a mean 124mmHg systolic pressure (range of results = 111-140) and 125mmHg systolic pressure (range of results = 114-138) respectively (Jaspers et al, European Heart Journal 41(11): 1190-1199, 2019). Another study showed that apparently healthy individuals displayed an average blood pressure of 120/78 mmHg with a standard deviation around the mean of +/- 13/9 mmHg (Sabbahi et al, Journal of Human Hypertension 35(8): 685-695, 2022). Such data distributions suggest that a significant portion of the subjects, healthy subjects, had blood pressure values that exceeded the 130/80 diagnostic criteria.

Further, detailed descriptions of the apparently healthy subjects included in research are often at odds with reality. One such example can be seen where some “apparently healthy” subjects included were currently taking prescribed beta and/or calcium channel blockers (Arena et al, Journal of Cardiovascular and Pulmonary Prevention 29(4): 248-254, 2010). Having anti-hypertensive medications administered to what should be a control or normal reference group, even if there are only a few, undoubtedly skews the resulting “average” pressures artificially downward rendering any conclusions or recommendations from such a study moot.

We can also explore the validity of hypertension diagnostic criteria by looking at athletic blood pressures. Athletes tend to be quite healthy, often looked upon as exemplars of health. Do current diagnostic criteria reflect this assumption?

One recent paper measured resting blood pressures in recreationally trained exercisers (2-3 training sessions per week), competitive natural bodybuilders, and competitive triathletes. Theirs and other’s results indicate that the 130/80 mmHg diagnostic criteria forwarded in 2017 may be too aggressive:

Table derived from data in:

• • • Jurasz et al, Biology 11(5): 643, 2022
    • Mahjoub et al, American Journal of Physiology: Heart and Circulatory Physiology 317(4): H685-H694, 2019
    • Varga-Pinter et al, Kidney and Blood Pressure Research 34(6): 387-395, 2011

There are thousands of papers on blood pressure that utilize different intervention methodologies, measurement methods, subject populations, and post-experimental statistical procedures. As such the variation in “average” or “normal” blood pressure values published is large. This spectrum of grey data, coupled with individual variation in biological and social circumstances, means that creating a singular value threshold indicative of pathologic hypertension is extraordinarily difficult, if not impossible. The small section of tabular data above on trained individuals and resting blood pressure shows that even the most fit of us appear to be hypertensive according to the present 130/80 criteria. Five out of the six exerciser/athlete categories are apparently hypertensive in diastolic pressure and two out of six groups exceed the systolic hypertension threshold.

If we further look at standard deviations (the cluster and spread of individual data points around a mean/average). We can see that in most of the studies that close to 50% of the “control” or “normal” subject values are higher than the mean. This suggests that a quite large and significant number of subjects, healthy and fit subjects, have blood pressures exceeding the 130/80. This is further evidence that the current criteria are too low and may lead to healthy individuals being prescribed unwarranted pharmaceutical interventions by virtue of being “false positives”.

Common blood pressure medications outcomes and side effects

There are four basic categories of anti-hypertensives, each with distinct effects on blood pressure reduction and potential collateral or unintended effects:

Calcium Channel Blockers

Estimated to reduce resting systolic blood pressure by 7 to 9 mmHg (Flynn et al, Journal of Pediatrics 145(3): 353-359, 2004). Possible side effects include; constipation, dizziness, tachycardia, fatigue, headache, nausea, lower leg and foot edema.

Beta Blockers

Estimated reduction in resting systolic blood pressure of 8 mmHg (Wong & Wright, Cochrane Database Systematic Review 2: CD007452, 2014). Possible side effects include; fatigue, dizziness, cold digits (fingers and/or toes), insomnia, erectile dysfunction, nausea.

Angiotensin II Receptor Blockers

Olmesartan 20mg/day reduces resting blood pressure by 13/7 mmHg (+/- 15/10) (Raguki et al, Hypertension Research 45(5): 824-833, 2022). Valsartan 160mg/day lowers resting pressures by 13/10 mmHg (+/- 14/9) (Ruilope et al, Lancet 375: 1255-1266, 2010). Possible side effects include; dizziness, hyperkalemia, edema.

Angiotensin Converting Enzyme Inhibitor

Reduction in pressures estimated at 1.7/1.2 mmHg in 4-54 weeks (Wang et al, Cochrane Database of Systematic Reviews 10: CD012569, 2020). Possible side effects include; hyperkalemia, cough, anemia, reduced taste sensation, skin rash.

Cost of pharmacologic blood pressure treatment

In 2021, sales and prescription data indicated that there were 3.3 doses delivered per every 10 persons in the population, a dramatic increase from decades earlier consumption of 1.8 doses per every 10 person in the population (Jayawardana et al, PLOS Global Public Health 4(9):e0003698, 2024). Although costs are greatly variable, the average cost per year per person for one anti-hypertensive drug is approximately $3,950 (Mira Health data 2024). This calculates to $10.82 per daily dosage. Given this representative cost and use data, the total expenditure for single drug treatment in the USA can be estimated at:

There is no current consensus on the average age of hypertensive onset (Suvila et al, Current Hypertension Reports 22: 68, 2020) and there is no curative endpoint for pharmaceutical interventions. This suggests that individual patient expenditures on pharmacological treatments can span decades. This is a significant financial burden on individuals. It is an unwarranted burden if diagnostic criteria are set so low that national, international, and Olympic level athletes with no disease or symptoms present are considered diseased according to poorly supported diagnostic guidelines.

* Note that it is fairly common for multiple drugs to be prescribed so expenditures are likely much higher. Additionally, initial and continuing diagnostic costs, insurance premiums, and intermediary processing costs may indirectly decrease, or more likely increase, realized cost of medications charged to consumer.

Is there an effective alternative to medication?

There always has been a preferable alternative in most cases, weight loss. Weight loss that is diet driven, exercise driven, or driven by both has long been recommended to the public as a therapy to reduce blood pressure or completely cure the condition. But this is where public health efforts have failed. More than a half century of public resistance to starting and staying with any program of diet, physical activity, or exercise has left physicians a rather limited route to treating hypertension, one dependent on pharmaceuticals. It appears that the general population would rather pay the $3,950 per year for a drug than to modify their diet or begin exercising. It is this resistance, this convenience-and-ease-is-best mind-set that needs to be defeated in some manner to break drug dependency (not referent to addiction).

Everyone knows, from the mass of public messaging available, that simple changes in eating habits can produce anti-hypertensive effects. There are many dozens of popular or clinically recommended dietary approaches, with many improving blood pressure status:

• The Mediterranean Diet (with no caloric restriction) can reduce blood pressure by about 2.4/1.2 mmHg (Estruch et al, New England Journal of Medicine 368: 1279-1290, 2013).
• The Paleo Diet can reduce systolic blood pressure by about 3.1 mmHg (Frassetto et al, European Journal of Clinical Nutrition 63: 847-955, 2009).
• The Atkins Diet can produce about a 5.1/3.3 mmHg reduction in blood pressure (Ge et al, British Medical Journal 369: m696, 2020).

Long term participation in exercise also reduces resting blood pressure, with various exercises and exercise types producing variable beneficial effects:

Data adapted from a meta-analysis by Cornelissen & Smart, Journal of the American Heart Association 2(1): e004473, 2013.

 It is extremely common for diet and exercise to be simultaneously recommended by a clinician or be undertaken by an individual independent of advice. The effect of dietary manipulation independently or in concert with exercise has been investigated in a fairly large set of research publications. Results have been quite diverse but are generally positive in direction (meaning a reduction in pressures):

Data adapted from Meckling & Sherfey, Applied Physiology, Nutrition, and Metabolism 32(4): 743-752, 2007.

Comparing the improvements in blood pressure of single drug therapy versus diet versus exercise versus diet and exercise indicates that all have moderate beneficial effects:

First Order Operation – Obesity

While the clinical community continues to state that obesity is a contributor to hypertension, they often focus on correlating body fat to lipid build-up inside blood vessels, atherosclerosis, as the primary cause of hypertension. They largely ignore the direct effects of lipid accumulation outside of the circulatory system.

Simply adding subcutaneous fat is associated with increases in blood pressure. In a recent study of weight gain over an 8 week period, it was noted that there was a significant, 4/1.2 mmHg, post-weight-gain increase in blood pressure over a period of 24 hours continuous monitoring (Covassin et al, Mayo Clinic Proceedings 93(5): 618-626, 2019). Another study assessed abdominal subcutaneous fat quantity effects on systolic blood pressure and their data produces a very tight correlation of 0.96 (a 1.0 is perfect correlation):

Data adapted from Yano et al, Hypertension 68(3): 576-583, 2016

With subcutaneous fat accumulations, the body gets bigger around. The skin stretches to expand and accommodate the added fat mass. We can easily measure and estimate subcutaneous fat content of the body using a variety of methods (skin-fold caliper, bioimpedence, plesthmography, dual emission x-ray absorptiometry). However, the same cannot be said of fat mass accumulations that occur on the inside of the rib cage. Only imaging can be used to determine amounts present and as such, outside of research settings, we generally don’t have a grasp on how much we have inside our bodies.

We do know that there is a relationship between internal fat accumulation and hypertension, but most fat mass-obesity research lumps all body fat masses together. But let’s consider a simple explanation of how non-subcutaneous fat quantity increases can produce a simple but profound effect on blood pressure, not through a biological function but one driven by physics.

The thoracic cavity as a modified pressure vessel

How much fluid can fit inside a 16 ounce glass? 16 ounces. If you put in a two 1.5”x1.5”x1.5” cubes of solid ice into the glass then pour fluid in, how much fluid now fits? About 12 ounces. If you try to put the full 16 ounces in, the fluid will overflow the glass. Adding extraneous mass to an open container of a fixed volume reduces the amount of fluid that can be added without exceeding capacity and inducing overflow.

The thoracic cavity (the area bounded by the rib cage above and the diaphragm below) differs from the glass example above as this anatomical structure is a membrane sealed container. You can’t simply pour or place extraneous materials, such as fat, inside. Fat is deposited within the thoracic cavity via circulatory transport of lipid precursors to cells and tissues inside the chest. Those precursors are assembled in the cells of the organs and tissues present and deposited in the fluid filled spaces surrounding the structures within the thoracic cavity. In this instance, extraneous fat mass is added to a relatively fixed volume container. This is unlike the ice example above as the glass has no lid which provides an easy exit of excess added fluid (overflow). With no easy and rapid exit of newly included excess materials, the thoracic cavity becomes somewhat affected by the same principles as a pressure vessel.

A pressure vessel is a sealed container intended to hold fluids or gases and maintain them at a specific pressure or range of pressures. Two of the easiest examples of this are a SCUBA tank and an automobile tire, where as you pump more and more air into the tank or tire, the higher the internal pressure goes.

Anatomically and physiologically, if you blow all the air out of your lungs and do not follow up with an immediate inhalation, heart rate and blood pressure will slightly decrease. This is in large part a function of increased available and unoccupied volume within the chest due to lung deflation. Lower pressure enables the heart to contract less forcefully and less quickly and still deliver blood as required. But what happens if we insert big globules of fat into the thoracic cavity, depositing them around the heart and throughout the inside of the thoracic cavity?

The circulatory system is pressure driven. The ventricles produce the highest pressures during systole, pressures that push blood into the slightly lower pressured arterial vessel network. Pressure continues to drop as blood proceeds through the venous network until returning blood is drawn into the atria where the lowest pressures are found. Essentially, blood must follow a pressure gradient from high to low. Anything that disrupts that pressure gradient has the potential to disrupt the efficiency of heart and vascular function.

The addition of more fat mass inside the pericardium, epicardium, and thoracic cavity, can produce an increase in intrathoracic pressure. Added intrathoracic volume pushes the ribs outwards and towards their expansive limit. We do know that the chest walls expand and retract, as this requisite to breathing. In general there can be about 4 to 7 centimeters of expansion or retraction of the chest wall (Sharma et al, Journal of the Japanese Physical Therapy Association 7:23-28, 2004). This native volume compliance allows for early fat deposits to be muted in overt pressure effects and functional compromise, as the rib cage remains able to expand and contract roughly within its normal expansive limits. However as added fat mass is deposited, the functional limits of the chest wall are approached and further chest wall expansion and retraction is less possible. This continued addition of more intrathoracic fat mass exerts a stronger elevating effect on pressures within the chest cavity. And this is where we see downstream events begin to manifest.

Some research appears to demonstrate a dose response between intrathoracic fat mass and a variety of anatomical and physiological correlates to health, including blood pressure:

(Cetin et al, Journal of Cardiology 61(5): 359-364, 2013)

So, we see from this study of obese individuals that as the amount of fat around the heart (pericardial element of intrathoracic fat) increases, blood pressures also increase.

Elevated blood pressure stems from the added fat volume into space limited in size by the rib cage, in turn pushing inwards on the heart and lungs, and downward onto the diaphragm. As a result of this there are several anatomical adaptations that occur naturally, where the body attempts to compensate for the added fat mass in order to maintain the low pressures in the heart and thoracic cavity. One adaptation of note is the enlargement of atrial dimensions (see left atrial diameter in table above). A larger chamber can produce a more net negative pressure and counter some pressure elevation from added fat mass. However, as obesity increases, anatomical changes cannot compensate and limit pressure increases.

Addition of intrathoracic fat can change the orientation of, physical space occupied by, and function of organs and tissues within the chest:

• It is frequently noted that the heart is moved from a diagonal orientation to a more horizontal orientation with obesity (Kurisu et al, International Journal of Cardiology: Metabolic and Endocrine 9: 61-65, 2015).
• The lungs experience a reduction in residual capacity (Jones & Nzekwu, Chest 130: 827-833, 2006), residual capacity being defined as the volume of the lung remaining inflated after normal expiration. This volume of unused lung space provides a means of responding to periods of increased demand for oxygen. The consequence of this latter occurrence, fat mass intruding into space normally occupied by the lung, is a functional limitation in the volume of air which can be moved in and out of the lungs during any exertion above rest.
• Added intrathoracic pressures are related to increased work required by the heart to successfully drive circulation (Alexander, Heart Disease and Stroke 2: 317-321, 1993).

So it appears that simple obesity produces significant derangement of cardiovascular function AND will, over time, produce maladaptation in both anatomical structures and metabolism. It thus follows that exiting obesity to a healthy bodyweight can reverse hypertension and improve any negative adaptations that occurred as a result of prolonged obesity. This is specifically of great interest for the exercise and fitness industry as it is the major health benefit which trainers can deliver, either by preventing obesity proactively or reducing it in customers who are obese.

Marketing health benefits is not as glamorous as other benefits of regular exercise at a gym. But we can use other related and very common motivations such as:

Look attractive
Have a firmer shape
Build muscle
Meet others
Have fun

Partial list from Soderstrom, Annals of Leisure Research 26(4): 521-544, 2021

Obesity, both intrathoracic and subcutaneous, can definitely affect an individual’s self-perceived attractiveness and firmness of shape (commonly referred to as appearing “toned”). In respect to intrathoracic fat, it is not directly apparent how one might link an internal accumulation of fat to outward appearance, but it is easily done. As the diaphragm is not a rigid bottom boundary between the thoracic and abdominal cavities, when fat is added into the thoracic cavity, it begins pushing downwards onto the viscera within the abdominal cavity. This in turn displaces abdominal contents down and forward, which along with added intra-abdominal fat enlarges the thoracic cavity and contributes to creating a protrusion of the abdomen (“pot gut”, “beer gut”, or similar slang). This means that even vanity led goals can be exploited to get people into the gym, where consistent exercise over time can both reduce obesity driven cardiovascular dysfunction and deliver desired vanity improvements, without utilization of pharmacological agents and invoking their exorbitant costs and side effects.

Another marketing point could be simple finance. Gym memberships generally range from about $25 per month (pay for access) to about $150 per month (pay for service), much less than the monthly total expenditure for a single blood pressure medication. The sooner we can get a sedentary individual into the gym and the longer that we can keep them returning, the more money they can retain in their pockets:

In the context of this article, we truly desire to deliver improvements in fitness and health in the gym, improvements that decrease obesity and blood pressure. While very important to many potential gym-goers, pointing out that adoption of a lifestyle that includes progressive exercise can enable individual retention of more money – money, previously destined for endless pharmaceutical control of blood pressure – may be more powerful of a motive. Coupling the wagon load of functional and health goals to the delivery of individual vanity goals may be more attractive to non-exercisers who are unfamiliar with and are uncaring about how exercise and fitness affect their quality of life in general. Regardless of the trainee’s specific goal or interest that led them to consider joining a gym or starting exercise, we can inform them fully regarding the good things that will happen to them as a result of long term and consistent training. This includes that the sweat equity gained from exercise can transform physical fitness into fiscal fitness where money saved can be spent on the modern penchant and socially driven concept of “lifestyle brand” consumption or in otherwise improving one’s life circumstances.