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Abstract

Individuals born preterm have significantly impaired adaptability in maximal aerobic capacity (VO2 max) with exercise training. We have hypothesized that this impaired response is linked to immature mitochondrial development and maladaptation resulting from early birth. PURPOSE: This project is multifaceted with the overarching aim to measure mitochondrial respiration in peripheral blood mononuclear cells (PBMCs) and assess for potential mitochondrial genome variants and heteroplasmy that may explain poor adaptability in VO2 max with training. The purpose of this report is to confirm poor adaptability in VO2 max in preterm adults. METHODS: This is an ongoing project. Young adults aged 18-35 years who were born preterm (< 37 weeks gestational age) and term controls (≥ 37 weeks gestational age) are undergoing 16-weeks of aerobic exercise training program at 65-75% of HRmax. Exercise consists of walking or running and VO2 max is measured at four time points: before training, at 4 weeks, at 8 weeks, and after completing the 16-week training. RESULTS: Data presented here is from four female participants ( age25.5 ± 4.42) born prematurely that completed eight of the 16 weeks of training. At baseline, VO2 max was 26.1 ± 4.2 ml/kg/min (range = 10.61). No difference was found at 4 weeks (27.9 ± 4.7 ml/kg/min) or after 8 weeks (28 ± 7.0 ml/kg/min) of training (one-way ANOVA p=0.28, p = 0.90). As secondary measures, we did not find a change in BMI (p = 0.90) or resting heart rate (p = 0.51) over time. CONCLUSION: Our early interim analysis indicated that 8 weeks of moderate-intensity aerobic training are likely ineffective at increasing VO2 max in young women born preterm, which aligns with prior work. Further, the minimal increase in VO2 max we have observed thus far is still in the ‘below average’ category of recommendations set by the ACSM. Our continued work will assess mtDNA and mitochondrial respiration in PBMCs as molecular targets potentially linked to poor VO2 max trainability among this population.

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