Purpose <p>Heart rate recovery (HRR) indicates post-exercise autonomic regulation and serves as a marker of cardiorespiratory fitness and mortality risk. Autonomic and metabolic recovery are both integral to post-exercise homeostasis, yet how HRR relates to metabolic recovery remains unclear.</p> Methods <p>To address this gap, we analyzed data from a randomized crossover trial in 17 healthy, physically active young men, each performing 30&#xa0;min of both moderate- and vigorous-intensity ergometer cycling. Plasma samples collected before exercise and at multiple recovery time points were analyzed using UPLC–MS/MS–based untargeted metabolomics, covering more than 1000 metabolites. HRR was calculated using a monoexponential decay model, and associations were examined using linear mixed models.</p> Results <p>Individuals with faster HRR exhibited significantly lower post-exercise levels across a range of lipid metabolites, particularly acylcarnitines. These associations were stronger for HRR than VO₂peak and were statistically significant only in the later recovery period (90–180&#xa0;min post-exercise), exclusively following vigorous-intensity exercise. Our findings suggest that HRR reflects post-exercise lipid metabolism under conditions of high metabolic demand. The observed metabolite patterns are indicative of differences in β-oxidation, lipid accumulation, reliance on ω-oxidation, and mitochondrial turnover, and are consistent with more efficient post-exercise lipid metabolism.</p> Conclusion <p>HRR may provide a simple marker of metabolic or cardiorespiratory fitness and could be relevant for monitoring exercise responses and assessing cardiometabolic health. However, confirmation in larger and more diverse cohorts is required.</p> Clinical trials register <p>The trial was registered on October 5, 2017, at the German Clinical Trials Register under the registration number DRKS00009743 (Universal Trial Number of WHO: U1111-1200–2530).</p> Graphical abstract <p></p>

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Heart rate recovery as a marker of post-exercise lipid metabolism following moderate- and vigorous-intensity exercise

  • Dirk Weber,
  • Paola G. Ferrario,
  • Achim Bub

摘要

Purpose

Heart rate recovery (HRR) indicates post-exercise autonomic regulation and serves as a marker of cardiorespiratory fitness and mortality risk. Autonomic and metabolic recovery are both integral to post-exercise homeostasis, yet how HRR relates to metabolic recovery remains unclear.

Methods

To address this gap, we analyzed data from a randomized crossover trial in 17 healthy, physically active young men, each performing 30 min of both moderate- and vigorous-intensity ergometer cycling. Plasma samples collected before exercise and at multiple recovery time points were analyzed using UPLC–MS/MS–based untargeted metabolomics, covering more than 1000 metabolites. HRR was calculated using a monoexponential decay model, and associations were examined using linear mixed models.

Results

Individuals with faster HRR exhibited significantly lower post-exercise levels across a range of lipid metabolites, particularly acylcarnitines. These associations were stronger for HRR than VO₂peak and were statistically significant only in the later recovery period (90–180 min post-exercise), exclusively following vigorous-intensity exercise. Our findings suggest that HRR reflects post-exercise lipid metabolism under conditions of high metabolic demand. The observed metabolite patterns are indicative of differences in β-oxidation, lipid accumulation, reliance on ω-oxidation, and mitochondrial turnover, and are consistent with more efficient post-exercise lipid metabolism.

Conclusion

HRR may provide a simple marker of metabolic or cardiorespiratory fitness and could be relevant for monitoring exercise responses and assessing cardiometabolic health. However, confirmation in larger and more diverse cohorts is required.

Clinical trials register

The trial was registered on October 5, 2017, at the German Clinical Trials Register under the registration number DRKS00009743 (Universal Trial Number of WHO: U1111-1200–2530).

Graphical abstract