Abstract

The global sport scenario is too much challenging where glory or defeat can depend on minor gaining or loosing of athlete's performance potentials. There's no limitation to what extend the world's best track & field athletes will do in training to improve their competition-day performance. Preparticipation, screening and the requirement for specialized training in cardiological interpretation in athletes, given the disparities between athletes and the general population, have significantly increased interest in sports cardiology. It's crucial to distinguish between disease and physiological changes that the heart and circulatory system go through in response to the exercise demands that are unique to the athletic heart. The purpose of the review-based article is to discuss the left ventricular morphological changes (cardiac remodeling) of male track and field athletes in relation to the different sports specific training programme and the importance of cardiac hypertrophy in modern sporting scenario.

Keywords

Cardiac hypertrophy, Cardiac remodeling, and Track and field Athletes.

Introduction

Track and field competitors compete in a variety of activities that date back to ancient Greece, including as running, throwing, walking, and leaping. Athletes must move more quickly in order to succeed, whether they are walking, sprinting, throwing, or jumping. The capacity to compete physically has become the foundation of modern sport, and technical advancements like digital equipment are encouraging this trend. In the Tokyo Olympics (2020) Selemon Barega Shirtaga of Ethiopian long-distance runner won the gold medal in the 10,000 metres,¹ Lamont Marcell Jacobs of Italy sprinted to Olympic gold in the men's 100-meter dash, finishing in 9.80 seconds and Javelin thrower Neeraj Chopra of India bagged the gold medal in javelin throw event. Depending upon the nature of the sporting excellence they all have trained differently, Niraj Chopra of India emphasizes medicine balls, cable pull workouts, and HIIT circuits while strengthening his upper and lower body and correcting his joints. Advanced training is frequently linked to morphological alterations in the heart, including enlargements of the left ventricle's mass, wall thickness, and size. "Athlete's heart" refers to the increase in left ventricular mass brought on by exercise.² Engaging in sports or physical activities with significant volume and intensity regularly can cause cardiac alterations that fit the description of left ventricular hypertrophy, particularly in highly trained individuals.^3-5 It was initially proposed by Morganroth et al.5 that there are two distinct physical forms of the athlete's heart: a heart trained for strength and a heart trained for endurance. As to their view, athletes who participate in high-dynamic sports like running primarily experience an increase in left ventricular chamber size, accompanied by a corresponding rise in wall thickness due to volume overload brought on by the high cardiac output of endurance training.   

Since isometric exercise, such as weightlifting, causes pressure overload in addition to the high systemic arterial pressure found in this type of exercise, athletes who have been trained in endurance sports are therefore assumed to exhibit eccentric left ventricular hypertrophy, which is characterized by an unchanged relationship between left ventricular wall thickness and left ventricular radius. Consequently, it is assumed that athletes who have received strength training have concentric left ventricular hypertrophy, which is defined by a greater wall-to-radius ratio. Despite numerous authors' investigations into the morphology of the athlete's heart and the effects of various sports on cardiac structure,^6-9 they have not been able to provide a satisfactory answer to the question of whether there are different types of athlete's hearts. The current research focuses on the fundamental types of exercise: combined dynamic and static (cycling and rowing), mainly static exercise (all sports involving the throwing and lifting of heavy items), and mainly dynamic exercise (long-distance running) and their relation with cardiac structure.  

Intensive physical activity is linked to both peripheral and central cardiovascular adaptations that improve the extraction of oxygen from working muscles for aerobic glycolysis and help produce a large and sustained cardiac output, respectively. The capacity to produce a high stroke volume is essentially dependent on an increase in heart size. Numerous echocardiographic studies including thousands of athletes have examined the athlete's heart over the past thirty years.^5-7,10,11 

Heart remodeling is generally understood to be a pathological or physiological state that can follow events like volume overload, pressure overload, idiopathic dilated cardiomyopathy, or myocardial infarction.12 With the following characteristics—an increase in maximal cardiac output, a rise in stroke volume, a decrease in resting heart rate, and electrocardiographic alterations in conduction and repolarization—the athlete's heart is a physiological state that results from systematic training.¹³ The heart undergoes a physiological state of cardiac remodeling as a result of many myocardial adaptations brought on by overtraining. Clinically, these morphological alterations are characterized by changes in heart size and shape brought on by a higher load, and they vary depending on the kind of training.¹⁴ 

The purpose of the review study is to highlight the distribution and structural remodeling of the left ventricle of the heart (concentric and eccentric hypertrophy), depending upon the different nature of athletic performances related demands.

Physiology of Remodeling

Clinically, cardiac remodeling is characterized by alterations in the size, shape, and function of the heart in response to an increase in stress or cardiac damage.¹² Heart remodeling can be brought on by several factors, including biochemical, molecular, and mechanical processes. According to Cohn JN, Ferrari R, and Sharpe N,¹² hemodynamic load, neurohumoral activation, and other variables including endothelin, cytokines, nitric oxide generation, and oxidative stress, all have a significant impact on the process of cardiac remodeling. According to Mihl C., W.R.M. Dassen, and H. Kuipers,¹⁴ athletes may experience physiological remodeling, which is a compensatory alteration in the size and operation of the heart. The cardiomyocyte is the specific heart cell that participates in the remodeling process. The heart hypertrophies in reaction to stretching brought on by an increase in hemodynamic stress. The synthesis of new contractile proteins and the parallel construction of new sarcomeres are the two ways that cardiomyocytes proliferate.¹⁵ This will result in a higher contractile force for each cell. This homogenous remodeling type causes the myocardium's myocyte count to rise.¹⁶

Physiological remodeling is the term used to describe this hypertrophic reaction brought on by exercise. The concentric and eccentric cardiac hypertrophies are shown in Figures 1 and 2.¹⁴
 

 

 

Cardiac Morphology

In the past, echocardiography was a non-invasive technique for identifying cardiac conditions.¹⁷ Not only are ultrasonic cardiographic techniques advised for the examination of very sick patients, but they also help us answer some of the unresolved issues in sports physiology. The cardiac output values, internal heart volume, cardiac wall thickness, and left ventricle muscle mass may all be determined with the use of additional metrics. While other procedures often need multiple exams, this straightforward procedure allows for the rapid and painless acquisition of a wealth of information regarding circulation.^18,19 In the study, cardiac morphological parameters included left ventricular end-diastolic and systolic diameters (LVESD and LVEDV), left ventricular posterior wall thickness (LVPW), interventricular septum thickness (IVS), left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), and left ventricular muscle mass (LVM).

Dynamic and Static Training in Sports

Adaptive changes in cardiac structure and function are stimulated by engaging in intense physical exercise regularly. Ethnicity, sex, genetics (underlying genome), and epigenetic factors such as sporting discipline and duration of exercise exposure, are just a few of the variables that affect this process, also known as exercise induce cardiac remodeling (EICR), which varies significantly across athletic populations and individual athletes.²⁰

According to Levine et al,20 both static and dynamic exercise physiology are involved in some capacity in all types of intense physical activity including competitive athletics. In terms of skeletal muscle activity patterns and the resulting modifications to heart structure and function, the phrases static and dynamic are used. Brief, powerful skeletal muscular contractions that may be measured as an approximate proportion of the maximum voluntary contraction for the implicated muscle groups are indicative of static activity. during periods of comparatively pure static/strength exercises, as powerlifting, weightlifting and throwing competitions in field events. In the face of increasing left ventricular afterload, the cardiovascular system's major function during brief periods of static activity is to sustain cardiac output. All of the elements that go into total myocardial wall stress (or tension) following systolic ejection are collectively referred to as afterload.²¹ On the other hand, dynamic and endurance exercises necessitate higher levels of oxidative metabolism because they include the repeated, frequently rhythmic contraction and relaxation of skeletal muscle groups. Thus, oxygen uptake (VO2) may be measured to determine the degree of dynamic exercise. To combat the stress, the heart experiences a significant preload during endurance activities. According to Norton,²¹ the word "preload" refers to all of the variables that affect the passive ventricular wall stress (or tension) at the end of diastole.

Concentric Cardiac Hypertrophy

Exercise plays a crucial role in promoting overall metabolic wellness, as supported by various studies conducted by Boule et al, Helmrich et al, Lawlor and Hopker, and Chalder et al.^22-25 Furthermore, exercise has been found to have a positive impact on mental health, as evidenced by research conducted by Egan and Zierath.²⁶ It is also important to note that exercise aids in the development and preservation of musculoskeletal function, as highlighted by the work of Paffenbarger et al, Blair et al, Myers, and Holme and Anderssen.^27-30 Moreover, exercise has been shown to increase lifespan, as established by the studies conducted by Wei, Liu, and Rosenzweig, Platt et al.^31,32 These beneficial effects of exercise are primarily attributed to the improved function and health of cardiovascular tissues, as well as the increased resistance of the heart to injury.

The adaptation of cardiovascular tissues to exercise is driven by the periodic metabolic stress induced by regular physical activity. However, it is important to recognize that different types, intensities, and durations of exercise can result in varying levels of metabolic stress and may promote different types of tissue remodeling, as indicated by Fulghum and Hill.³³ One specific type of exercise that leads to haemodynamic alteration is resistance training, which is associated with an elevation in blood pressure and pressure overload in the heart. This repeated overload on the cardiac muscle causes an increase in the number of sarcomeres, actin, and myosin,³⁴ increasing cardiomyocyte cell width and left ventricular wall thickness without reducing the internal cavity size during diastole. This phenomenon is known as concentric left ventricular hypertrophy, as explained by Pluim et al, Dorn, and Longhurst.^35-37

The increase in wall thickness observed in cases of pressure overload is primarily due to an increase in cardiomyocyte cross-sectional area, as suggested by Grossman.³⁸ In terms of cardiovascular response, resistance training is characterized by intermittent increases in blood pressure during exercise, as demonstrated by MacDougall et al³⁹ and MacDougall et al.⁴⁰ Various studies have shown that resistance training leads to an increase in left ventricular internal cavity dimension, ventricular septal wall thickness (IVS), posterior wall thickness (LVPW), relative wall thickness (RWT), and left ventricular muscle mass (LVM), as evidenced by the research conducted by Fagard and Pluim et al.³⁵ It is widely believed in the fields of sports cardiology and exercise physiology that serious resistance training for sports results in cardiac hypertrophy, specifically concentric hypertrophy characterized by an increase in left ventricular mass and wall thickness with minimal changes in internal cavity dimension. However, other studies have shown that resistance training does not exceed normal clinical limits for IVS, LVPW, LVM, and RWT, as indicated by Haykowsky et al, Haykowsky et al.^41-44 This pattern of concentric hypertrophy is identified by an increased left ventricular mass index and relative wall thickness.

Whether serious resistance training (RT) promotes LV hypertrophy probably depends on multiple variables. The disparity between studies on whether RT increases LV mass could be partly caused by the performance during exercise. A brief ventricular mass (VM) may minimize the acute increase in LV transmural pressure and wall stress. It seems possible that in younger resistance-trained athletes, increased LV mass may occur with short-term training whereas individuals who initiate an RT programme later in life may require a longer training period to induce LV hypertrophy. The percentage change of left ventricular dimension and wall stress is shown in the Figure 3.⁴⁵

 

Eccentric Cardiac Hypertrophy

The hemodynamic alterations associated with cardiac outputs in long-duration, dynamic activities are caused by an increase in heart rate and stroke volume. The skeletal muscle pump's enhanced efficiency and the reduced peripheral vascular resistance are the main causes of the increased venous return to the heart. Heart overload resulting from ventricular volume during isotonic exercise therefore causes the development of eccentric left ventricular hypertrophy.^36,46 The eccentric hypertrophy induced by aerobic or endurance training is predominantly characterized by the addition of sarcomeres in series, which leads to an increase in myocyte cell length and consequently increases the cardiac mass with increased chamber volume.³⁴

For performing isotonic types of exercises for a prolonged period the following cardiological changes occur. Left ventricular end-diastolic diameter (LVEDD), left ventricular posterior wall thickness (LVPW), and Inter ventricular septum thickness (IVS) is significantly higher for endurance sports performers, which results in significantly higher left ventricular muscle mass (LVM) in contrast to the sedentary individuals. During long-distance running, the heart has to adapt to both a volume and a pressure load, whereby the endurance-trained heart shows an increase in both left ventricular internal diameter and left ventricular wall thickness.^4,5,47-65

Sports Specific Cardiac Remodeling

During exercise, the heart is subjected to intermittent hemodynamic stresses of pressure overload, volume overload, or both. To normalize such stress and to meet the systemic demand for an increased blood supply, the heart undergoes morphological adaptation to recurrent exercise by increasing its mass, primarily through an increase in ventricular chamber wall thickness. The nature and types of chronic exercises are more responsible for putting stress on the myocardium, which facilitates different types of cardiac remodeling. Table 1 represents the cardiac morphological features of long-term endurance, strength and combined training male athletes from the age group of 18-40 years.³⁵

ETA = Endurance-Trained Athletes, CESTA= Combined Endurance and Strength-Trained Athletes, STA= Strength-Trained Athletes, C= Control subject, LVEDD= Left Ventricular End Diastolic Diameter, LVESD= Left ventricular End Systolic Diameter, IVST= Interventricular Septum Thickness, LVM= Left Ventricular Muscle Mass, LVEF= Left Ventricular Ejection Fraction, LVFS= Left Ventricular Fractional Shortening.  

Table 1 indicates that all the left ventricular variables are changes of male subjects depending upon the type of training i.e. aerobic, anaerobic and a combination of aerobic and anaerobic which indicates that cardiac remodeling following training is not identical, it is much related to the nature of training. Table 2 represents the comparison of cardiological variables between different track and field male athletes.

LVEDD= Left Ventricular End Diastolic Diameter, IVST= Interventricular Septum Thickness, LVM= Left Ventricular Muscle Mass and LVEF= Left Ventricular Ejection Fraction. 

Table 2 indicates that the average value of echocardiographic findings of 14 male throwers (58.6 ± 14.2 years), 40 endurance runners (60.8 ± 10.5 years) and 47 sprinters (57.5 ± 12.6 years)⁶⁵ and the changes of these variables are mainly due to the training effect. Sports-specific training may helpful for the left ventricular remodeling of athletes and the type of remodeling (concentric, eccentric or combination) may be differ depending upon the sports-specific types of training.^66-74

Conclusion

The present review-based research discussed the concept of left ventricular remodeling and its significance in different sports and games. Different track and field athlete's physiological requirement is different in parity with the nature of activity and sports-specific physical demands. Prolonged participation in sports of specific types results in left ventricular hypertrophy and thus the capacity to deal with larger stress is increased. Left ventricular hypertrophy may be concentric, eccentric or combination and this is a prerequisite for better sporting performance. At the time of athlete training the concept of sports cardiology should be given proper weightage.

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