The control mechanisms and implications of heart rate variability (HRV) under the sympathetic (SNS) and parasympathetic nervous system (PNS) modulation remain poorly understood. Here, we establish the HR model/HRV responder using a nonlinear process derived from Newton\'s second law in stochastic self-restoring systems through dynamic analysis of physiological properties. We conduct model validation by testing, predictions, simulations, and sensitivity and time-scale analysis. We confirm that the outputs of the HRV responder can be accepted as the real data-generating process. Empirical studies show that the dynamic control mechanism of heart rate is a stable fixed point, rather than a strange attractor or transitions between a fixed point and a limit cycle; HR slope (amplitude) may depend on the ratio of cardiac disturbance or metabolic demand mean (standard deviation) to myocardial electrical resistance (PNS-SNS activity). For example, when metabolic demands remain unchanged, HR amplitude depends on PNS to SNS activity; when autonomic activity remains unchanged, HR amplitude during resting reflects basal metabolism. HR parameter alterations suggest that age-related decreased HRV, ultrareduced HRV in heart failure, and ultraelevated HRV in ST segment alterations refer to age-related decreased basal metabolism, impaired myocardial metabolism, and SNS hyperactivity triggered by myocardial ischemia, respectively.