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P2 amplitude increased across sessions (p < 0.01) on passive as well as training blocks.
Post hoc tests revealed that left temporalis PPT was increased at 15, 30 and 50 min compared with BL within sessions (P < 0.023; Data not shown).
However, during months 2, 4, and 5, there were significant differences in intensity and TLRPE during hard sessions (p < 0.01) between female athletes and coaches.
There was no significant difference in the pain intensity at any time point between the MSG and placebo sessions (P > 0.333).
A post hoc test of the intervention × time interaction revealed that in the MSG sessions (P < 0.040) but not in placebo sessions (P > 0.900), sBP was elevated 15 and 30 min after intake (Figure 5). Figure 5 The time course of changes in mean (± SEM) systolic and diastolic blood pressure during monosodium glutamate (MSG) and placebo intervention.
Interestingly, OA patients had lower PPTs during both sessions (P < 0.001) and at all time points (P < 0.001) compared with arthralgia patients based on all diagnostic modalities except for CBCT (P > 0.324).
The post hoc test indicated that dBP was significantly elevated in the MSG sessions at 15 and 30 min after intake compared with placebo sessions (P < 0.043) (Figure 5).
There were no significant differences between the CS and MP groups regarding the intervals between the two TMS sessions (p = 0.87): 6.8 ± 1.7 days in MP and 6.3 ± 2.2 days in CS.
While there was great variability between mice within each recording session, and there was considerable variability for each mouse between sessions, the group average was not statistically different across sessions (p = 0.72, repeated measures ANOVA).
There was no significant difference in the number of treatment sessions (P = 0.164).
* significantly different from all other sessions (P < .01), † P value for main effect of test session.
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