Low- and high-volume blood-flow restriction treadmill walking both improve maximal aerobic capacity independently of blood volume.

AIM: Assess the effect of low- and high-volume blood flow restriction training (BFR) on maximal aerobic capacity (VO2 max) and determine if alteration in VO2 max is mediated through changes in hemoglobin mass (Hbmass) and blood volume. METHODS: Participants' Hbmass (CO-rebreathe), single, and double-leg VO2 max and blood volume regulating hormonal responses (renin and copeptin) were measured before and after BFR training. Training consisted of treadmill walking either (1) twice-daily for 4week (CON and BFRHV ) or (2) twice-weekly for 6week (BFRLV ). Each session consisted of five intervals (3 min, 5% incline, 5 km/h, 100% of lowest occlusion pressure), with 1 min of standing rest between sets. RESULTS: VO2 max increased using both training exposures, in as quickly as 2-weeks (BFRLV baseline to 4week: +315 ± 241 mL (8.7%), p = 0.02; BFRHV baseline to 2week: +360 ± 261 mL (7.9%), p < 0.01), for the BFRLV and BFRHV groups, with no change in CON. Single- and double-leg VO2 max improved proportionately (single/double-leg VO2 max ratio: BFRLV 78 ± 4.9-78 ± 5.8%, BFRHV 79 ± 6.5-77 ± 6.5%), suggesting that the mechanism for increased VO2 max is not solely limited to central or peripheral adaptations. Hbmass remained unchanged across groups (CON: +10.2 ± 34 g, BFRLV : +6.6 ± 42 g, BFRHV : +3.2 ± 44 g; p = 0.9), despite a significant release of blood volume regulating hormones after initial BFR exposure (renin +20.8 ± 21.9 ng/L, p < 0.01; copeptin +22.0 ± 23.8 pmol/L, p < 0.01), which was blunted following BFRHV training (renin: +13.4 ± 12.4 ng/L, p = 0.09; copeptin: +1.9 ± 1.7 pmol/L, p = 0.98). CONCLUSION: BFR treadmill walking increases VO2 max irrespective of changes in Hbmass or blood volume despite a large release of blood volume regulating hormones in response to BFR treadmill walking.

Cellular and tissue expression of DAPIT, a phylogenetically conserved peptide.

DAPIT (Diabetes Associated Protein in Insulin-sensitive Tissues) is a small, phylogenetically conserved, 58 amino acid peptide that was previously shown to be down-regulated at mRNA level in insulin-sensitive tissues of type 1 diabetes rats. In this study we characterize a custom made antibody against DAPIT and confirm the mitochondrial presence of DAPIT on cellular level. We also show that DAPIT is localized in lysosomes of HUVEC and HEK 293T cells. In addition, we describe the histological expression of DAPIT in several tissues of rat and man and show that it is highly expressed especially in cells with high aerobic metabolism and epithelial cells related to active transport of nutrients and ions. We propose that DAPIT, in addition to indicated subunit of mitochondrial F-ATPase, is also a subunit of lysosomal V-ATPase suggesting that it is a common component in different proton pumps.