BACKGROUND: We have previously shown that 7d of New Zealand Blackcurrant (NZBC) supplementation reduces the gastrointestinal barrier permeability response that normally accompanies exertional heat stress.
PURPOSE: To determine the effect of NZBC supplementation on inflammatory capacity and apoptotic drive in peripheral blood mononuclear cells (PBMC) collected before and after exertional heat stress.
METHODS: Twelve men (Age: 28 ± 6 years, Stature: 1.81 ± 0.07 m, Mass: 80.5 ± 9.8 kg, VO2max: 56 ± 6 mL-1kg-1.min-1) ingested 2 capsules of CurraNZ™ (210 mg anthocyanin day-1) or a visually matched placebo (microcrystalline cellulose) for 7d prior to a 1h treadmill run (65% VO2max) in hot ambient conditions (34°C / 40% RH). PBMC were isolated from EDTA plasma samples that were collected before (Pre), after (Post), 1h after (1-Post) and 4h after (4-Post) exercise. Inflammatory capacity was calculated as the ratio between phosphorylated and total
NF-κB content in cell lysates. Apoptotic drive was calculated as the ratio between BAX and BCL-2 in cell lysates. Caspase 9 was measured to provide additional confirmation. Western blot data were analysed with two-way (Condition x Time) RM-ANOVA with Duncan post-hocs.
RESULTS: The p-NF-κB:NF-κB ratio was reduced following 7d NZBC supplementation (-46%, p=0.03). Post hoc analysis indicated p-NF-κB:NF-κB content at 4-Post had fallen below values at Post (-24%, p=0.02) and 1-Post (-60%, p=0.04). The BAX:BCL-2 ratio was increased following 7d NZBC supplementation (+106%, p<0.01). Post hoc analysis indicated the BAX:BCL-2 ratio increased from Pre to Post exercise (+119%, p=0.01) in NZBC and remained elevated (above Pre) at 1-Post (+77%, p=0.04 ) and 4-Post (+59%, p=0.04). Caspase 9 content also increased following 7d NZBC supplementation (p <0.05). Post hoc analysis indicated elevated Caspase 9 content at PRE in NZBC (+86%, p<0.01), with differences between conditions being resolved by 4-Post exercise (p=0.94).
CONCLUSIONS: Study data suggest 7d NZBC supplementation may reduce inflammatory capacity and increase apoptotic drive in PBMC. This might call nascent leukocytes into circulation to ensure maintenance of the putative inflammatory response that accompanies exertional heat stress. However, the exact physiologic relevance of these changes remains to be determined.