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This is one of the contributions of activity monitoring.
Interestingly these right hemisphere functions reflected the contributions of activity in the high IoR but nonparanoid subgroups (Table 3, right).
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However, the results shown in Figures 1A and 1B, which are both derived from the same data as those shown in Figure 2, show there was no correlation between activity and EE in these animals, suggesting that while activity may be contributing to EE, the contribution of activity was not detectable independently of other variables that contribute to EE.
The importance of locomotor activity as a determinant of BP and HR in mice has been demonstrated in previous studies [26], [27], but our analysis is the first to assess the contribution of activity to circadian rhythms of cardiovascular physiology.
We then tested what signals might be important in interference by examining separately the contribution of activity in motor output pathways to, and sensory inputs from the plantar flexor muscles.
In most of these studies, factors that may confound the contribution of activity to EE were carefully controlled.
At 5°C there was no detectable contribution of activity to daily EE even after correcting for body weight.
We therefore consider the contribution of activity with stable phase relations (between channels) that are nonphase locked to the stimulus.
Regressing the %AEE for each mouse against activity gave a VAEE of 9.53% ± 1.1%, a figure similar to the contribution of activity to EE obtained from regression analysis.
In order to detect and attribute a contribution of activity to differences in EE between separate mice, we had to house animals at thermoneutrality (30°C).
However, when comparing across multiple mice, only 9.53% ± 1.1% of EE from activity appeared to be independent of other components involved in the thermogenic response, suggesting other metabolic processes may mask the contribution of activity to EE.
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