UNLABELLED: Previous research attempts to identify an oxidative stress response to acute resistance exercise have yielded mixed results. Inconsistencies in the current literature base probably reflect study-to-study variance in resistance exercise protocols; where high volume and short recovery elicit the most identifiable oxidative stress response. PURPOSE: This study examined the effect of resistance exercise intensity on blood oxidative stress. METHODS: To elicit a blood oxidative stress, 10 subjects undertook two different back squat protocols: 1) a hypertrophy protocol of four sets, 10 repetitions with 90 s of rest at 75% one-repetition max (1RM); and 2) a strength protocol of 11 sets, three repetitions with 5 min of rest at 90% 1RM. The resistance exercise protocols were standardized for total volume and completed in a randomized crossover fashion with 1 wk between trials. Blood drawn before (PRE), immediately following exercise (IP), and 60 min following exercise (60POST) was analyzed for markers of oxidative stress and damage. RESULTS: In response to both hypertrophy and strength exercise protein carbonyls were significantly elevated IP and 60POST while plasma lipid hydroperoxides were not. Following the hypertrophy protocol, trolox equivalent antioxidant capacity was elevated IP while urate lower than baseline. At the 60POST time point plasma ferric reducing ability of plasma was elevated following the hypertrophy protocol. Based on protein carbonyl data, a similar oxidative stress was incurred following both hypertrophy and strength protocols. CONCLUSION: Normalization for time of blood draw following the two protocols indicates that the magnitude of blood oxidative protein damage was identical between the protocols. These findings demonstrate that both resistance exercise protocols elicited a blood oxidative stress in a time-dependent fashion.
RCT Entities:
UNLABELLED: Previous research attempts to identify an oxidative stress response to acute resistance exercise have yielded mixed results. Inconsistencies in the current literature base probably reflect study-to-study variance in resistance exercise protocols; where high volume and short recovery elicit the most identifiable oxidative stress response. PURPOSE: This study examined the effect of resistance exercise intensity on blood oxidative stress. METHODS: To elicit a blood oxidative stress, 10 subjects undertook two different back squat protocols: 1) a hypertrophy protocol of four sets, 10 repetitions with 90 s of rest at 75% one-repetition max (1RM); and 2) a strength protocol of 11 sets, three repetitions with 5 min of rest at 90% 1RM. The resistance exercise protocols were standardized for total volume and completed in a randomized crossover fashion with 1 wk between trials. Blood drawn before (PRE), immediately following exercise (IP), and 60 min following exercise (60POST) was analyzed for markers of oxidative stress and damage. RESULTS: In response to both hypertrophy and strength exercise protein carbonyls were significantly elevated IP and 60POST while plasma lipid hydroperoxides were not. Following the hypertrophy protocol, trolox equivalent antioxidant capacity was elevated IP while urate lower than baseline. At the 60POST time point plasma ferric reducing ability of plasma was elevated following the hypertrophy protocol. Based on protein carbonyl data, a similar oxidative stress was incurred following both hypertrophy and strength protocols. CONCLUSION: Normalization for time of blood draw following the two protocols indicates that the magnitude of blood oxidative protein damage was identical between the protocols. These findings demonstrate that both resistance exercise protocols elicited a blood oxidative stress in a time-dependent fashion.
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