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Response to an aerobic training intervention in young adults depends on ponderal index at birth
T D Brutsaert1, K H Tamvada2, M Kiyamu2
11 Departments of Exercise Science and Anthropology, Syracuse University, Syracuse, NY, USA.
Insights
Individuals with poor fetal growth (low ponderal index) exhibit lower exercise lactate levels, suggesting metabolic adaptations. These findings highlight potential long-term physiological differences related to intrauterine growth restriction.
Area of Science:
- Exercise Physiology
- Developmental Biology
- Metabolic Health
Background:
- Poor fetal growth is linked to altered adult body composition and reduced muscle function.
- Limited research exists on the impact of poor fetal growth on exercise capacity and metabolic responses.
- Intrauterine growth restriction may induce lasting physiological changes affecting adult health.
Purpose of the Study:
- To examine the association between poor fetal growth (low ponderal index) and maximal oxygen consumption (VO2max).
- To investigate differences in exercise lactate levels between individuals with high and low ponderal indices.
- To assess the impact of aerobic training on VO2max and lactate response in relation to fetal growth patterns.
Main Methods:
- Thirty-six college students were divided into high ponderal index (HIGHPI) and low ponderal index (LOWPI) groups, matched for key characteristics.
- Participants underwent an 8-week aerobic training program.
- Maximal oxygen consumption (VO2max) and blood lactate levels during exercise were measured before and after training.
Main Results:
- No significant differences in VO2max or training-induced changes were observed between HIGHPI and LOWPI groups.
- LOWPI individuals exhibited significantly lower pre-training lactate levels at equivalent relative workloads.
- LOWPI individuals showed smaller reductions in lactate at fixed absolute workloads post-training, independent of fitness changes.
Conclusions:
- Poor fetal growth, indicated by a low ponderal index, is associated with altered lactate metabolism during exercise in young adults.
- These metabolic differences may stem from intrauterine growth restriction-induced reprogramming or changes in muscle morphology.
- Further research is needed to elucidate the specific mechanisms linking fetal growth to adult exercise metabolism.
Abstract:
Poor fetal growth is associated with later-life changes in adult body composition and decrements in muscle strength and morphology. Few studies have investigated the association of poor fetal growth with whole-body exercise. The purpose of this study was to investigate the association of poor fetal growth with the maximal oxygen consumption (VO(2)max), lactate levels during exercise and the response to aerobic training. Thirty-six college-aged men and women (aged 20.8 ± 0.3 years), born to term (37-42 weeks gestation), were recruited to participate in an 8-week training program. Participants comprised two groups, high ponderal index (HIGHPI) and low ponderal index (LOWPI) (n = 18/group), identified as falling above and below the 10th percentile of the ponderal index (g/cm(3))-for-gestational age distribution, respectively. The HIGHPI and LOWPI were matched pair-wise on age, sex, body mass index and pre-study physical activity patterns. The LOWPI and HIGHPI did not differ significantly before training, after training or with a change (Δ) in training VO(2)max (l/min or ml/min kg/fat-free mass (FFM)). However, LOWPI had significantly lower pre-training lactate levels at similar levels of relative work output (P = 0.016), and significantly smaller decreases in lactate at a fixed level of absolute work after training (P = 0.044). These differences were independent of pre-training aerobic fitness, the change in fitness with training, diet and fuel substrate choice. The lower lactate of untrained LOWPI subjects during exercise could reflect metabolic reprograming due to intrauterine growth restriction, or could be secondary to muscle morphological and/or fiber-type distribution changes that also associate with poor fetal growth.
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