Introduction: From rest to exercise the human body’s cardiovascular and respiratory systems must integrate and adapt to changing conditions—especially during incremental increases in submaximal exercise to maximal exercise. The coordination of cardiovascular and respiratory systems coalesce to form what is known as the cardiorespiratory system (Lotric & Stefanovska, 2000). Within muscle cells there are extremely limited stores for anaerobic energy; thus, a well-coordinated cardiovascular and respiratory system must be maintained to permit the utilization of aerobic energy pathways during exercise (Poole & Jones, 2012). In short, the aforementioned systems during resting and exercise conditions influence one another with the common goal of
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Detected changes in arterial gas content (CO2 & O2) and subsequent rises in ventilation are modulated by central command mechanism in the hypothalamus (Eldridge, 1994). There are several respiratory feedback mechanisms responsible for communicating with central command—namely—central chemoreceptors due to arterial pressures of CO2 (PCO2), or peripheral chemoreceptor carotid bodies as the result of changes in pH due fluctuating arterial pressures of O2 (PO2) and PCO2 in arterial blood (Eldridge, 1994). Additionally, non-respiratory mechanisms are responsible for the relay of information to central command such as feedback from thermal mechanisms, pulmonary stretch receptors and receptors in exercising muscle (Eldridge, F. L. (1994). VE during the onset of exercise can be broken up into three phases (See Figure 1). Phase I—stimulated by central command—shows the initial increase in ventilation (Eldridge, F. L. (1994). During phase II, central command helps maintain stimulation along with feedback from exercising muscle tissue (Eldridge, F. L. (1994). Lastly, phase III occurs once all of the aforementioned modulating factors reach steady state (Eldridge, F. L. (1994). As an exercising individual moves from steady state or submaximal exercise towards maximal effort, ventilatory variables further fluctuate as a result of loss of homeostasis and inability to maintain oxygen supply to exercising muscle. Progressive increases in exercise intensity and their subsequent increases in minute ventilation are portrayed in Figure 2. The first increase in VE is identified as ventilatory threshold 1 (VT1) results from rising CO2 levels; whereas, ventilatory threshold 2 (VT2) is the result of the linear breakaway of ventilation during high intensity exercise and its accumulating byproducts (Lucía, Hoyos, Pérez &
Detected changes in arterial gas content (CO2 & O2) and subsequent rises in ventilation are modulated by central command mechanism in the hypothalamus (Eldridge, 1994). There are several respiratory feedback mechanisms responsible for communicating with central command—namely—central chemoreceptors due to arterial pressures of CO2 (PCO2), or peripheral chemoreceptor carotid bodies as the result of changes in pH due fluctuating arterial pressures of O2 (PO2) and PCO2 in arterial blood (Eldridge, 1994). Additionally, non-respiratory mechanisms are responsible for the relay of information to central command such as feedback from thermal mechanisms, pulmonary stretch receptors and receptors in exercising muscle (Eldridge, F. L. (1994). VE during the onset of exercise can be broken up into three phases (See Figure 1). Phase I—stimulated by central command—shows the initial increase in ventilation (Eldridge, F. L. (1994). During phase II, central command helps maintain stimulation along with feedback from exercising muscle tissue (Eldridge, F. L. (1994). Lastly, phase III occurs once all of the aforementioned modulating factors reach steady state (Eldridge, F. L. (1994). As an exercising individual moves from steady state or submaximal exercise towards maximal effort, ventilatory variables further fluctuate as a result of loss of homeostasis and inability to maintain oxygen supply to exercising muscle. Progressive increases in exercise intensity and their subsequent increases in minute ventilation are portrayed in Figure 2. The first increase in VE is identified as ventilatory threshold 1 (VT1) results from rising CO2 levels; whereas, ventilatory threshold 2 (VT2) is the result of the linear breakaway of ventilation during high intensity exercise and its accumulating byproducts (Lucía, Hoyos, Pérez &