Circadian rhythm disruption (i.e., arrhythmicity) in motor activity is an abnormal behavioral pattern. In rats, it can be caused by the lesion of the hypothalamic suprachiasmatic nucleus (SCN) and by prolonged exposure to constant light (LL). We carried out a comparative study of these arrhythmic phenotypes to assess the role of the SCN in the regulation of the motor output beyond circadian rhythmicity. Motor activity series were studied in rats that had become arrhythmic as a result of 1) LL exposure at 2 light intensities: 300 lux (LL(300)) and 1.3 lux (LL(1.3)), and 2) SCN lesion (SCNx). The Fourier spectra, the fractal Hurst coefficient (H) from the autocorrelation function, and the beta slope from the power spectral density were calculated in data sections at baseline, when the rats were still rhythmic, and later at stages with undetectable circadian rhythms. In the LL(300) group, high power content was detected at frequencies of 8 to 4 h (i.e., ultradian). Lower power content for these harmonics was found in the LL(1.3) group, whereas no dominant harmonics appeared in the SCNx group. Independently of the manifestation of circadian rhythm, H values were higher and more sustained in time in rats exposed to LL( 300) but gradually decreased in rats exposed to LL(1.3). Fractal correlation was found in control DD group but was absent in the SCNx group. We conclude that scale-invariant regulation of the motor pattern by SCN activity is dependent on light intensity but independent of the circadian rhythm output. Adjusting the light intensity by modifying the coupling degree between the population of oscillations could affect the dynamics of each individual oscillator in the SCN, making it less predictable.