. Author manuscript; available in PMC: 2013 Aug 1.

Published in final edited form as: Eur J Appl Physiol. 2011 Dec 20;112(8):3045–3052. doi: 10.1007/s00421-011-2279-3

Table 3.

Monocyte TNFα (pg·mL⁻¹) production for PL and VitD groups at baseline and following the 12 weeks of resistance training.

	Placebo (n = 13)		Vitamin D (n = 10)

	Baseline	12 weeks	Baseline	12 weeks
1 ng/mL LPS	441.1 ± 247.8	750.8 ± 436.8	603.1 ± 453.1	730.5 ± 544.0
1 ng/mL LPS+PMB	1.6 ± 1.5	2.3 ± 1.2	1.4 ± 1.5	1.9 ± 0.9
25 μg/mL LPS	939.4 ± 412.0	1255.1 ± 482.6	1029.5 ± 604.6	1276.1 ± 738.3
25 μg/mL LPS+PMB	275.3 ± 104.9	398.5 ± 155.9^a	265.2 ± 99.9	343.2 ± 129.5
No LPS	1.6 ± 0.9	0.6 ± 0.5^a	1.5 ± 0.6	0.6 ± 0.5^a

Whole blood was treated as follows in five 2 ml wells: 1) 1 ng/ml lipopolysaccharide (LPS); 2) 1 ng/ml LPS and 100 μg/ml polymixin B (PMB); 3) 25 μg/ml LPS; 4) 25 μg/ml LPS and 100 μg/ml PMB; and 5) 0 μg/ml LPS. PMB interferes with LPS-stimulated tumor necrosis factor alpha (TNFα) production by binding to LPS and thus, preventing its interaction with the monocyte cell-surface. Plates were incubated for 24 hours. Values are means ± SD.

Significant difference from baseline (P<0.05). No differences were detected between groups (P>0.05).