Number 26, 2005
Cardiovascular effects of exercise

Cardiac adaptation to exercise

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Harm Kuipers
Faculty of Health Sciences, Maastricht University, Maastricht, The Netherlands
Correspondence: Dr Harm Kuipers, Faculty of Health Sciences, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands. E-mail: harm.kuipers@bw.unimaas.nl

Introduction
Regular physical exercise induces changes in the body that are a physiological adaptation to increased loads. In general, these adaptations are favorable and enable the individual to increase physical performance capacity. Adaptations to training also include the structure and function of the cardiovascular system, in addition to its functional control (Figure 1 [1]). Strength training induces changes to pressure loads, whereas endurance training requires volume loads and elicits an increased maximal cardiac output, by increasing stroke volume [2]. Compared with the maximal cardiac output in non athletic adults of approximately 25L/min, that of elite athletes can reach values of up to 30–35L/min [2].

Autonomic control with training
Adaptations to regular exercise also include the autonomic control of cardiovascular function [4,5]. Regular training causes adjustments in the autonomic nervous system that may change the physiological response of the heart and blood vessels to exercise, and increase its functional capacity (Figure 2). The speed of depolarization and conduction velocity of myocardial cells determine heart rhythm, which can be changed by different input from the autonomic fibers [4,7]. Increased sympathetic activity leads to increased heart rate and increased contractility, whereas increased parasympathetic input retards heart rate and decreases contractility [4,7]. Endurance-trained individuals are characterized by an increased parasympathetic tone at rest, which is reflected in bradycardia and compensatory increased stroke volume [8] (Figure 3). Because of an increased parasympathetic tone and slow pulse rate in the resting state in well-trained athletes, the baroreflex may not always adequately counteract the blood pressure changes associated with sudden changes in posture [10]. Because of this, endurance-trained athletes may be more susceptible than untrained individuals to orthostatic hypotension with sudden changes in posture [10]. A profession that is associated with sudden changes in static pressure from sudden changes in G-forces is that of fighter pilot. Although the author is not aware of relevant published data, it is possible that fighter pilots who are endurance trained and have a pronounced bradycardia may have a less adequate baroreflex and a lower G-force tolerance than non trained individuals. In that case, special attention should be given to teaching strategies for coping with high G-forces in flight [11].

Doping in sport and the heart
In sports in which muscle strength and muscle mass are determining factors for success, it has been shown that the use of androgenic anabolic steroids can enhance sport performance [12]. In spite of the positive effects on performance, the use of such drugs may have serious adverse effects that also involve the cardiovascular system. The abuse of androgenic anabolic steroids has been associated with an increased risk for serious cardiovascular events such as myocardial infarction, cerebrovascular accidents, acute heart failure, and thromboembolism [12]. It has been demonstrated that the use of androgenic anabolic steroids can unfavorably affect some risk factors for cardiovascular disease, especially the serum lipid profile. In athletes, administration of high doses of these drugs may lead to decreased concentrations of high-density lipoprotein cholesterol [13]. However, the effects of androgenic anabolic steroid abuse are reversible and, after administration is stopped, serum lipids return to pre-drug concentrations [13].
There is some indication from cross-sectional echocardiography and from animal studies that abuse of androgenic anabolic steroids may change cardiac structure and function. Some investigators reported larger ventricular mass and interventricular septal thickness in association with the use of the drugs. Others could not confirm these changes [12]. One prospective study reported echocardiographic changes during use of androgenic anabolic steroids [14], whereas other studies failed to show any significant change to ventricular parameters [12]. Thus, at present, it remains to be established whether the use of androgenic anabolic steroids by athletes does affect cardiac structure and function.
Another drug that is abused, especially in endurance sports, is erythropoietin. It has been shown that the administration of erythropoietin increases hemoglobin mass and oxygen transport capacity, and hence endurance performance [15]. However, with an increase in hemoglobin mass, blood viscosity increases, which may lead to hypertension and thromboembolic events [16]. It is rumored that some athletes use aspirin to prevent thromboembolism. Although never proven, it has been suggested that the sudden death of some young athletes in the late 1980s and early 1990s was associated with the use of erythropoietin. Some large international sport bodies have introduced regular blood testing in athletes in order to monitor their hematological profile and detect and prevent possible manipulation [14].
A drug that was frequently abused in the sport of cycling during the 1960s was amphetamine. In contrast to popular belief, amphetamine is not a strong performance enhancer in high-intensity events; nevertheless, its use is widespread [85]. However, amphetamines may be cardiotoxic and may cause acute infarction and sudden death [18]. In addition, heat dissipation during exercise is impaired, which may lead to hyperthermia and cardiac failure [18]. After some deaths occurred in athletes during competition, the International Olympic Committee put a ban on the use of these drugs. Although no evidence is available, it cannot be ruled out that regular use of amphetamines or other performance-enhancing drugs may cause structural, functional, and possibly irreversible changes to the heart. ?

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REFERENCES

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