# RKS: EXERCISE CAN SPELL HEALTHY MORTAL LIVING OR MORTALITY

BE WARNED OF THE FITNESS FANATICISM

1st April 2024

DISSECTING THE ART OF PHYSICAL FITNESS - A FINE-TUNED CRAFT

THE PITFALLS ANALYZED BEHIND RECENT CALAMITIES

Dear Reader,
Over the past decades, we have witnessed an increasing proportion of society engaging in ultra-endurance events, which are well in excess of the health-promoting exercise recommendations.
Table: Names of some popular celebrities who passed away whilst gymming.
In recent times, there has been a hue and cry regarding the reported drastic rise in gym-related deaths each year, with the majority being attributed to sudden cardiac arrest (SCA). In fact, 80-85% of all sudden deaths are heart-related - sudden cardiac deaths (SCD). In today's context, SCD is become the most common cardiac concern amongst all heart ailments.
Graph: Incidences of SCD vs other cardiac maladies.
It would be intriguing to analyze the bare underlying reasons for such a catastrophe and adapt preventive measures such that all the fitness freak are not dis-enthused with such alarming reported incidents.

HEART
It is necessary to understand the heart basics to grasp regarding the irregular heart beating (arrhythmia) which is ultimately attributable to SCD.
The heart has 2 upper cavities called atria and 2 lower chambers known as ventricles.
Right atrium
Left atrium
Right ventricle
Left ventricle
Fig: The heart structure.

The heart has 4 valves which are like taps that open to allow blood to flow inside to or outside from a particular chamber and close so as to prevent backflow of blood to the previous chamber during contraction.
Tricuspid valve: allow blood to flow from right atrium to right ventricle.
Bicuspid or mitral valve: allow blood to flow from left atrium to left ventricle.
Pulmonary valve: allow blood to flow from right ventricle to lungs for purification.
Aortic valve: allow blood to flow from left ventricle to aorta - the biggest artery which carries purified blood to all parts of the body.
For the blood circulation to be facilitated, the heart has a strong and significant layer of muscles called myocardium; the cells of the heart muscles are known as myocytes. To ensure that the blood continues to flow within the 4 chambers, the heart muscles undergo:
Systole - contraction: ventricular (right and left) systole & atrial (right and left) systole
Diastole - relaxation: ventricular (right and left) systole & atrial (right and left) diastole
The contraction and relaxation facilitating filling and emptying of heart chambers is done by opening and closing valves and the latter are operated by papillary muscles which are the smaller offshoots of the myocardium.

ELECTRICAL ACTIVITY OF HEART
Normally the heart beating - both rate and rhythm - is dictated by the electrical impulses generated by the sinoatrial (SA) node from where it spreads to the two atria, another junction in between atria and ventricles called atrioventricular (AV) node, and thereafter the electrical activity spreads to each and every muscle, including papillary muscles, in both the ventricles.

Fig: Electrical activity of heart.

The electrical current generated by the SA node spreads via the defined circuit to reach the ventricles, and the number of times the left ventricle contracts determines the frequency of heart beats per minute. Normal heart rate ranges between 60 to 100 beats per minute. If the frequency of beating differs, then it is labelled as:
Bradycardia: Heart rate less than (<)60 beats per minute
Tachycardia: Heart rate more than (>)100 beats per minute
If the heart beats 60 times in a minute it means that every 1 second it is contracting. If the beating occurs at irregular intervals then it is labelled as arrhythmia. If the rate is beyond the normal range PLUS it is irregular then it is referred to as either:
Bradyarrhythmia: Bradycardia + Arrhythmia
Tachyarrhythmia: Tachycardia + Arrhythmia
It is not necessary to have an abnormal heart rate accompanying arrhythmia; even a heart beating at a normal rate of 60-100 beats per minute can be arrhythmic. For example, there could be a very few additional contractions in between normal beat - this is known as extrasystoles (which could be, depending on the location of its origin, atrial extrasystoles or ventricular extrasystoles).

BASIS OF ARRHYTHMIA
The myocytes have a transmembrane potential meaning that these operate like a battery providing power and also transmit signals to other heart muscle cells via the electrical current generated. To maintain the transmembrane potential, there is a need for a balanced presence of sodium ions (Na+), potassium ions (K+) and calcium ions (Ca++). There is also a Na+ - K+ pump within the cell wall of the myocyte that pushes out K+ in exchange for Na+ for generating electrical current.
If any part of the circuit in the heart itself generates an electrical impulse independently, then it is an arrhythmia - irregularity in heart contraction. Depending on which portion of the heart the irregularity originates it is termed as:
Atrial arrhythmias - originating from either right or left atrium
Nodal arrhythmias - originating from AV node
Ventricular arrhythmias - originating from either right or left ventricle
The tachyarrhythmias are the culprits in 65-80% of the cases, whilst bradyarrhythmias are causative for only 5-20% of SCD incidences. The tachyarrhythmias are further segregated as:
Tachycardia: rate >150 and <250 beats - atrial tachycardia / ventricular tachycardia (V-tach)
Flutter: rate >250 and <350 beats - atrial flutter / ventricular flutter
Fibrillation: rate >350 and usually <500 beats - atrial fibrillation / ventricular fibrillation (V-fib)
In addition, asystole or SCA, another cause of SCD, is an entity wherein the heart's electrical system fails entirely, and causes the heart to stop pumping. Asystole is also known as “flat-line” or “flat-lining”.

EXERCISE-RELATED CATASTROPHES

INCIDENCE

There are over to 92,000 gymnasiums (gyms) in India but only 50 lakh Indians do gymming - i.e. 0.3% of the population. 52% of Indians do not find time to exercise, 36% lack the motivation to join a fitness centre whilst 14% are clueless about where to begin their fitness journey. Overall, irrespective of the cause or excuse, 53% lack the discipline to stay fit! The risk of sudden death during vigorous activity is equally low, at 1 per 1.51 million episodes for men and 1 in 36.5 million hours of exertion for women.

There are 2 or 3 such cardiac death incidents seen per 1,00,000 older individuals annually. Data has demonstrated that 1.9% of the SCA instances in adults aged around 65 are linked to activities like exercise, including cycling, working out at the gym, running, or playing tennis or golf and other similar.

THE REASONS - WHY??

People who have suffered a SCD during sports activity, or within one hour of the activity, are categorized as having a sports-related SCA.
There are 2 primary causes why a SCD occurs:
Mechanical - 10%: The blood progression to the heart is suddenly blocked by an embolism (- a clot that has travelled from some other part of the body), cardiac tamponade (abnormal collection of fluid outside heart and pressing upon it) or a ruptured cholesterol plaque (fatty deposit in artery causing narrowing and compromising blood flow).
Electrical - 90%: V-tach and V-fib are the two most commonest precipitators of SCD. It is of course essential to fathom that higher the rate of beating the lesser the time available for blood to fill up the concerned chamber of the heart, and hence more diminished is the quantity of blood pumped out with resultant starving of the various body cells of oxygen and nutrients. Imagine a ventricle pumping blood at 450 beats a minute - it means that in one second it has to contract 7.5 times! where is the time available to fill it adequately with blood or even the opportunity to adequately be able to force blood out effectively!
As far as mechanical causes are concerned, the incidence of embolism is 2% whilst that of cardiac tamponade is a mere 0.02%. Plaque rupturing in various heart arteries has been documented to vary from 8% to 42%. [Circ 2012; 106(7): 804-808]
The common electrical activity disturbing conditions, that have potential to cause SCD, include HOCM (hypertrophic obstructive cardiomyopathy - enlarged heart size with thicker muscles), valvular heart disease and myocarditis (inflammation of myocardium). HOCM is the most significant precipitant of an irregularity in heart rate and there are 2.4 million Indians having this disease either known to the patients or present (as silent predator) in an undiagnosed form. The incidence of valvular heart disease, another important cause of causing heart rate rhythm disturbances, is 2.5%, whilst that of myocarditis is 10%.
What triggers the electrical instability is emotions, electrolyte alterations, certain drugs and physical exertion.

EXERCISER'S HEART IS A PROARRHYTHMIC HEART

4% of the older population who exercise experience short periods of rapid, irregular heartbeats during exercise, typically lasting from three to six heartbeats, and at a rate hovering around 175 beats per minute. The athlete’s heart, a heart that adapts so magically to cope with the demands of exercise, harbours many structural and functional changes that have accrued over years and these, by themselves, predispose to arrhythmia development. Maximal oxygen consumption during exercise correlates strongly and directly with the eccentric cardiac remodelling and the increase in left ventricular mass and dimensions. When the myocardium is not able to pump blood efficiently, the condition of the heart is called as cardiomyopathy. The changes that can occur in such cases are of 2 types:

Hypertrophic cardiomyopathy: Chamber size is decreased and diastole is impaired but systole force is maintained.
Dilated cardiomyopathy: Chamber size is increased and systole is impaired.

During ‘low/moderate/high-intensity’ aerobic exercise training (AET) the maximal oxygen uptake (VO2max) is 35% / 35%-70% / 70%-100%. Hence, to cope p with the same the myocardium undergoes initially hypertrophy. When the heart weighs over 500 gms in hypertrophic cardiomyopathy, it is not compatible with life.

Fig: Heart structure as it differs in cardiomyopathy.

Increase in wall thickness by 10-20% is known as hypertrophy and enlargement of chamber by 10-15% is clinically labelled as dilatation. Historically, the focus during exercise has been the left ventricle but it is the right ventricle that is most stressed (30-folds more) during strenuous physical activity.

The relation between sports and arrhythmias can be understood along three lines:

Sports as arrhythmia trigger on top of an underlying problem;
Sports as arrhythmic substrate promotor; and
Sports as substrate inducer.

Anything which is pivotal in causing arrhythmia, as in the case of heart, is known as a substrate or the 'raw material'. Curiously, 30 min of low-intensity exercise 5 days per week achieves the threshold for causing right ventricular dilatation, whilst for upper limits to be adhered to if left ventricular dysfunction is to be kept at bay is engaging for <60 minutes of low-intensity physical activity upto 5 times weekly.

EXERCISE-INDUCED ARRHYTHMIA DUE TO UNDERLYING HEART DISEASE

Sudden heart attack causing SCD in the young during exercise is usually caused in the backdrop of undiagnosed heart diseases like dilated cardiomyopathy, (arrhythmogenic) ventricular dysplasia (fibrous tissue replacing muscles of heart). Hypertrophic cardiomyopathy is reported as the most prevalent underlying condition in athletes dying suddenly.

EXERCISE-INDUCED ARRHYTHMIA DUE TO SUSBTRATE INDUCER

Hormones and ionic imbalances within heart muscle cells promote arrhythmias in those exercising. When engaged in exercising the heart is subject to extreme physiological stresses, both during the physical activity period itself and paradoxically also at rest. The high adrenergic tone (following enhanced liberation of adrenaline hormone), potential for deficiency in blood and oxygen supply, ionic (pertaining to especially sodium-potassium) disturbances, as well as high vagal tone, low heat rate and dispersion of repolarization (the resetting of the electrochemical gradients of the heart cell) at rest are the outcome of high wall stress during physical activity.

The adrenaline-rush during exercising can interfere with repolarization and thereby cause spurts of extrasystoles.
In an ischemic heart, the extrasystoles progress to arrhythmias. This is oxygen deprived cells have a lower content of calcium (hypocalcemia) within the myocyte. Intracellular hypocalcemia can cause fatal arrhythmias.
During exercising, the myocytes utilize phosphocreatine (PCr) as an immediate source of calories for coping with the increased energy needs of the myocardium during a workout. When the PCr breaks down there is a rise in intracellular K+ which is nondiffusible and hence cannot be pushed out by the normal Na+ - K+ pump of the myocyte. This results in increased K+ levels (hyperkalemia) within the myocytes, and this hyperkalemia is responsible for the vast majority of clinical arrhythmias.

Hypocalcemia causes tachyarrhythmias whilst hyperkalemia is responsible for bradyarrhythmias (like asystole) when these ionic disturbances occur within the heart muscle cell on account of exercising. Adrenaline causes tachyarrhythmias directly, or indirectly by precipitating hypokalemia. In fact, regular exercise exerts a significant effect on the expression and function of cardiac ion channels. The classical 'Q-T interval' prolongation is the commonest defect in electrocardiograms (ECG) noticed in those exercising.

EXERCISE-INDUCED ARRHYTHMIA DUE TO SUBSTRATE PROMOTER

In HOCM, there is replacement of overgrown heart muscles with fibrous tissue (also called as scar tissue since it forms the visible scars on skin following any damage) in few areas so as to compensate for the narrowing caused. In dilated cardiomyopathy, the over-stretched muscles of the affected chamber activate specific hormones and chemicals which facilitate fibrosis of the myocardium. What ultimately causes the heart to beat irregularly is the fibrous tissue which replaces the normal papillary muscles of the myocardium. The papillary muscles are important for the functioning of heart valves, and their replacing with scar tissue causes the well-known valvular heart disease - a known trigger for arrhythmias.

Fig: Right and left ventricles affected vs exercise levels and intensities.

The fibrous tissue interrupts the electrical circuit of the heart and thereby precipitates the arrhythmia. If the exerciser is an older individual, there is always present fibrous tissue in the myocardium as a result of replacing the destroyed cardiomyocytes with scar tissue.

SPORTS EXERCISING & LONG WORK-HOURS EQUALLY CHALLENGING FOR HEART AS GYMMING - Drs. BEWARE!

Table: Names of medical professionals who collapsed and passed away whilst engaging in outdoor / indoor activities other than gymming.

This list can never be comprehensive – there will be unreported many who could have ‘achieved’ exercise martyrdom.

CONCLUSIONS

The WHO (World Health Organization) recommends a minimum of 150 minutes of moderate-intensity exercise or 75 minutes of vigorous-intensity exercise per week. A meta-analysis in almost 900,000 individuals demonstrated that the physically active group had a 35% reduction in the risk of cardiovascular death and 33% reduction in all-cause mortality. It must thus be understood that exercising does not cause heart problems, diseases or deaths; it is vigorous exercising with undiagnosed diseases, or in an untrained body which might be harmful. So it is important to gradually build an exercise schedule, be regular in that, and supplement it with healthy diet and lifestyle habits.

Advices:

People who have been having a sedentary lifestyle for years must gradually build exercise schedule and routine.
Vigorous exercises may harm in an untrained body and it is advisable to build stamina and strength before trying to develop muscular mass.
Before engaging in extreme physical sports or vigorous physical activity and exercise, it is important to get checked for any possible undiagnosed structural heart diseases.
Arduous exercises should be refrained from if there is detected an underlying heart condition.
Many who have erratic heart rhythm but no underlying heart ailment can be told to continue with their exercising schedule with no any treatment being necessary except to maintain a constant periodical vigil.
If arrhythmias are precipitated because of gruelling workouts - 'overtraining syndrome’, and arrhythmias are precipitated, is desirable to temporarily halt and/or initiate partial detraining with follow-up on the reversibility of the sinus nodal function.

It must be understood that exercising does not PER SE cause heart problems, diseases or deaths; it is vigorous exercising with undiagnosed diseases, or in an untrained body which might be harmful.

People who have SCA with exercise tend to have fewer comorbidities and cardiovascular risk factors than people who have SCA not triggered by exercise. Taken together, the benefits of sports activity likely outweigh the risk of associated SCD risk.

DR R K SANGHAVI

Prophesied Enabler

Experience & Expertise: Clinician & Healthcare Industry Adviser

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Dr R K Sanghavi