Journal of Developmental Origins of Health and Disease

Original Article

Response to an aerobic training intervention in young adults depends on ponderal index at birth

T. D. Brutsaerta1 c1, K. H. Tamvadaa2, M. Kiyamua2, D. D. Whitea3 and T. B. Gagea2

a1 Departments of Exercise Science and Anthropology, Syracuse University, Syracuse, NY, USA

a2 Department of Anthropology, University at Albany, SUNY, Albany, NY, USA

a3 College of Nanoscale Science and Engineering, University at Albany, SUNY, Albany, NY, USA.


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 (VO2max), 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/cm3)-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 VO2max (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.

(Received October 10 2011)

(Revised January 30 2012)

(Accepted March 01 2012)

(Online publication April 04 2012)

Key words

  • fetal programing;
  • human performance;
  • intrauterine growth retardation;
  • metabolic;
  • muscle;
  • ponderal index


c1 Address for correspondence: Dr T. D. Brutsaert, Department of Exercise Science, Syracuse University, 820 Comstock Avenue, 201 Women's Building/Room 201, Syracuse, NY 13244-5040, USA. (Email