Table 1.

FPC was not affected by modulators of adenosine receptor, protein kinase C modulators and by ROS scavengers

Fatigue conditions		Tetanic force (%)		Unstimulated force (%)
FAT1	FAT2	FAT1	FAT2	FAT1	FAT2
A. Control	Gli	58.9 ± 0.6	63.4 ± 0.8	0.05 ± 0.33	0.40 ± 0.60
B. 10 μm Gli	—	40.2 ± 4.2§	—	17.0 ± 1.5§	—
C. 1 μm R-PIA	Gli	—	−35.1 ± 11.3*	—	24.67 ± 10.44*
1 μm Chel	Gli	−5.2 ± 11.7	−8.3 ± 5.7	2.06 ± 3.69	0.86 ± 2.16
1 mm 2-MPG	Gli	0.6 ± 4.3	−0.8 ± 4.2	0.61 ± 4.25	0.77 ± 4.14
10 mm NAC	Gli	1.1 ± 4.0	−0.7 ± 10.0	1.59 ± 1.24	0.21 ± 0.75
10 mm Tiron	Gli	−1.6 ± 9.2	−4.0 ± 5.7	0.35 ± 0.84	−0.27 ± 1.13

Fatigue protocols, using paired muscles, were as in Fig. 9, apart from (a) 5-HD during FAT1 was replaced by the modulators shown in the table and (b) in the case of R-PIA, FAT1 was not elicited but the muscle was exposed to R-PIA for 1 h and removed 30 min prior to FAT2. In A and B, tetanic force and unstimulated force at 30 s during the fatigue bout are expressed as a percentage of the pre-FAT1 force. In C, for each paired FDB, the percentage tetanic force and unstimulated force at 30 s during FAT1 of protocol Fig. 9Ab was subtracted from the values during FAT1 of protocol Fig. 9Aa. The same calculations were done for FAT2. So, a difference close to zero signifies that the modulators had no effect during FAT1 or FAT2. In the case of FAT2 it also means that FPC was observed.

^§Significantly different from FAT1-Con.

^*Significant differences between paired muscles, ANOVA and LSD P < 0.05. Chel, chelerythrine; 2-MPG, N-(2-mercaptopropionyl)glycine; NAC, N-acetyl-l-cysteine.