Although respiratory sinus arrhythmia (RSA) is a commonly quantified physiological variable, the methods for quantification are not consistent. This manuscript questions the assumption that respiration frequency needs to be manipulated or monitored to generate an accurate measure of RSA amplitude. A review of recent papers is presented that contrast RSA amplitude with measures that use respiratory parameters to adjust RSA amplitude. In addition, data from two studies are presented to evaluate empirically both the relation between RSA amplitude and respiration frequency and the covariation between RSA frequency and respiration frequency. The literature review demonstrates similar findings between both classes of measures. The first study demonstrates, during spontaneous breathing without task demands, that there is no relation between respiration frequency and RSA amplitude and that respiration frequency can be accurately derived from the heart period spectrum (i.e., frequency of RSA). The second study demonstrates that respiration frequency is unaffected by atropine dose, a manipulation that systematically mediates the amplitude of RSA, and that the tight linkage between the RSA frequency and respiration frequency is unaffected by atropine. The research shows that the amplitude of RSA is not affected by respiration frequency under either baseline conditions or vagal manipulation via atropine injection. Respiration frequency is therefore unlikely to be a concern under these conditions. Research examining conditions that produce (causal) deviations from the intrinsic relation between respiratory parameters and the amplitude of RSA combined with appropriate statistical procedures for understanding these deviations are necessary.