Training response to 8 weeks of blood flow restricted training is not improved by preferentially altering tissue hypoxia or lactate accumulation when training to repetition failure.

Despite compelling muscular structure and function changes resulting from blood flow restricted (BFR) resistance training, mechanisms of action remain poorly characterized. Alterations in tissue O saturation (TSI%) and metabolites are potential drivers of observed changes, but their relationships with degree of occlusion pressure are unclear. We examined local TSI% and blood lactate (BL) concentration during BFR training to failure using different occlusion pressures on strength, hypertrophy, and muscular endurance over an 8-week training period. Twenty participants (11 males/9 females) trained 3/wk for 8 wk using high pressure (100% resting limb occlusion pressure, LOP; 20% one-repetition maximum (1RM)), moderate pressure (50% LOP, 20%1RM), or traditional resistance training (TRT; 70%1RM). Strength, size, and muscular endurance were measured pre/post training. TSI% and BL were quantified during a training session. Despite overall increases, no group preferentially increased strength, hypertrophy, or muscular endurance ( > 0.05). Neither TSI% nor BL concentration differed between groups ( > 0.05). Moderate pressure resulted in greater accumulated deoxygenation stress (TSI% × time) (-6352 ± 3081, -3939 ± 1835, -2532 ± 1349 au for moderate pressure, high pressure, and TRT,  = 0.018). We demonstrate that BFR training to task-failure elicits similar strength, hypertrophy, and muscular endurance changes to TRT. Further, varied occlusion pressure does not impact these outcomes or elicit changes in TSI% or BL concentrations. Training to task failure with low-load blood flow restriction elicits similar improvements to traditional resistance training, regardless of occlusion pressure. During blood flow restriction, altering occlusion pressure does not proportionally impact tissue O saturation nor blood lactate concentrations.