The human cardiovascular system is a complex and extensive network that involves the heart, blood vessels, the circulating blood, and its cellular components. These components function in concert as interdependent systems to move nutrients, gases, and wastes to and from cells to keep all body systems functioning at optimum efficiency. Humans possess a closed cardiovascular system, as opposed to one that is opened; this means that the blood is confined to vessels and is distinct from the interstitial fluid. Closed systems offer the advantage of transporting circulatory fluids effectively at higher blood pressures, allowing humans and other vertebrates to meet high metabolic demands of cells, tissues, and organs (Badeer & Hicks, 1992).
The rhythmic beating of the heart is a ceaseless activity that pushes blood around the body. A chamber of the heart contracts when an electrical impulse moves across the sinoatrial node. This signal depolarizes the node and the depolarization spreads rapidly via the internodal pathway, through the Bundles of His and Purkinje fibers, causing the atria and ventricle to contract (Lange & Brooks, 1977). Heart action is generally thought to be regulated solely by autonomic nerves and humorally transmitted agents such as catecholamines (Lange & Brooks, 1977). Therefore, cardiac muscle is myogenic; its rhythmical contractions arise within the muscle tissue.
Resting heart rate is influenced by many variables, namely, cardiorespiratory fitness, the use of stimulants or depressants, and environmental factors, such climate and altitude. Caffeine is a well-known stimulant shown to cause increases in blood pressure and systemic vascular resistance under resting conditions (Daniels et al., 1998). It is an adenosine-receptor antagonist, and adenosine can cause vasodilation in several regional circulations (Daniels et al., 1998). As a result, blockade of adenosine receptors could cause cardiovascular and hormonal effects similar to those induced by caffeine. In order to understand the effects of caffeine and various other factors on the heart’s rhythmic cycle of contraction, the heart’s electrical impulses must be closely monitored. An electrocardiogram (ECG) displays the voltage between pairs of electrodes on different sides of the hearts, indicating the overall electrical activity of the heart during the cardiac cycle.
In light of these observations, the underlying purpose of this experiment is to investigate whether various stressors, such as temperature changes to the skin, physical exercise, and caffeine will have any direct effect on human cardiac physiology. Changes to volume pulse, heart rate, and peripheral circulation patterns in ECG recordings will be used to dictate whether any changes occurred to the heart’s rhythmic cycle of contraction. Since muscle contractions cause the release of adenosine, blockade of adenosine receptors might account for caffeine’s reported cardiovascular effects (Ballard et al., 1988); thus, it is predicted that the caffeine contained in coffee will induce a stimulatory effect on the cardiovascular system. Moreover, since vascular muscle tone is regulated via various vasoactive substances synthesized by vascular endothelial cells and released during physical exercise (Berry et al., 1997), it is predicted both hand and leg exercises will promote increased blood flow, which will, in turn, increase heart rate and pulse volumes by stimulating receptors lining the blood vessels. Finally, since warmer temperatures, as opposed to colder temperatures, tend to dilate cutaneous vascular beds and divert blood from skeletal muscles to skin (Kamijo et al., 2008), it is predicted that heat stress will augment the variables used to measure cardiac response, either through the release of local paracrine agents, such as nitric oxide or by the secretion of catecholamines, such as epinephrine, in response to warm-sensitive neurons (Ajisaka et al., 2003). In contrast, colder temperatures will induce the opposite effect in order to prevent the loss of bodily heat.