Objectives We investigated whether high responsiveness or low responsiveness to exercise training aggregates in the same individuals across seven cardiometabolic traits.
Methods A total of 564 adults (29.2% black, 53.7% female) from the HERITAGE family study completed a 20-week endurance training programme (at 55%–75% of participants’ maximal oxygen uptake (VO2max)) with VO2max, per cent body fat, visceral adipose tissue, fasting levels of insulin, high-density lipoprotein cholesterol, small low-density lipoprotein particles and inflammatory marker GlycA measured before and after training. For each exercise response trait, we created ethnicity-specific, sex-specific and generation-specific quintiles. High responses were defined as those within the 20th percentile representing the favourable end of the response trait distribution, low responses were defined as the 20th percentile from the least favourable end, and the remaining were labelled as average responses.
Results Only one individual had universally high or low responses for all seven cardiometabolic traits. Almost half (49%) of the cohort had at least one high response and one low response across the seven traits. About 24% had at least one high response but no low responses, 24% had one or more low responses but no high responses, and 2.5% had average responses across all traits.
Conclusions Interindividual variation in exercise responses was evident in all the traits we investigated, and responsiveness did not aggregate consistently in the same individuals. While adherence to an exercise prescription is known to produce health benefits, targeted risk factors may not improve.
- exercise training
- exercise physiology
Data availability statement
Data are available on reasonable request of the corresponding author.
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Contributors JLB and MS analysed data and prepared the manuscript with important intellectual input from JR-R, RG, JR and CB. CB, JS, DCR and AL designed and conducted the study including participant recruitment and data collection. All authors reviewed and approved the final manuscript.
Funding The HERITAGE Family Study was supported by grants from the NIH/NHLBI: HL-45670, HL-47323, HL-47317, HL-47327, HL-47321. MS is supported by NIH/NHLBI R01HL146462.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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