"Cardiorespiratory and metabolic consequences of detraining in endurance athletes" [Article Review]
- Whistle Performance
- Feb 2
- 4 min read
This detailed review analyzes the systematic review titled "Cardiorespiratory and metabolic consequences of detraining in endurance athletes," published in Frontiers in Physiology (2024). The authors, Barbieri et al., synthesized data from 41 studies to examine how stopping or reducing training affects the physiological and anatomical adaptations of endurance athletes.
1. Objective and Context
The review was prompted largely by the COVID-19 pandemic, which forced many athletes into sudden inactivity due to confinement measures. The primary objective was to investigate the effects of detraining on cardiorespiratory, metabolic, hormonal, and muscular parameters, as well as performance changes over time. The authors utilized PRISMA guidelines to select studies focusing specifically on endurance athletes (e.g., runners, cyclists, swimmers) with at least two years of experience or high VO2max levels.
2. Classification of Detraining
The review categorizes detraining based on the duration of inactivity:
• Short-term detraining: Cessation or reduction of training lasting less than or equal to 4 weeks.
• Long-term detraining: Inactivity extending beyond 4 weeks.
3. Cardiorespiratory Consequences
The cardiovascular system undergoes rapid regression upon training cessation.
• VO2max Decline: This is the most significant marker of detraining. A total stop leads to a rapid decrease in VO2max, with studies showing a roughly 7% decline after just 12 days and up to 20% after two months. The initial decline (first 2–4 weeks) is primarily caused by reduced blood and plasma volume, while long-term decline is attributed to a reduction in the arterial-venous oxygen difference.
• Blood Volume and Heart Rate: A 2–4 week cessation can reduce blood volume by 9% and plasma volume by 12%. To compensate for this lower volume and reduced stroke volume, the body increases heart rate; maximal heart rate rises by 2–9 beats per minute in the short term, and resting heart rate may increase by roughly 7 beats per minute after one year.
• Cardiac Remodeling: Long-term endurance training enlarges the heart, but these adaptations are reversible. While left ventricular (LV) dimensions do not change significantly in the first 10 days, significant reductions in LV mass and wall thickness occur after longer periods (e.g., 8 weeks or more).
• Blood Pressure: Mean blood pressure can increase by 7% during submaximal exercise after short-term cessation, due to increased total peripheral resistance.
4. Metabolic and Hormonal Adaptations
Detraining shifts the body’s metabolic preference away from fat oxidation toward carbohydrate reliance.
• Substrate Utilization: The Respiratory Exchange Ratio (RER) increases, indicating a higher dependence on carbohydrates and a compromised lipid metabolism. Resting triglyceride levels may increase, and the body’s ability to transport glucose declines due to a reduction in the GLUT4 protein (a glucose transporter).
• Lactate Threshold: Performance is impaired by a rapid decline in the lactate threshold. Blood lactate concentrations rise significantly during submaximal exercise; for instance, one study noted a fourfold increase in lactate concentration in rowers after 5 weeks of cessation.
• Body Composition: Interestingly, body weight and composition generally remain unchanged during short-term detraining (<4 weeks). However, significant weight gain and increases in body fat are observed when inactivity exceeds 4 weeks.
• Insulin Sensitivity: Short-term detraining causes a rapid decrease in insulin sensitivity, although levels of cortisol, glucagon, and growth hormone typically remain unchanged in the short term.
5. Muscular Changes
Muscle tissue loses its oxidative efficiency quickly.
• Enzymatic Activity: There is a marked decline in mitochondrial enzymes necessary for aerobic energy production. Citrate synthase activity, a key marker of mitochondrial density, can drop by 28.6% after just 10 days of inactivity and up to 40% after 56 days.
• Fiber Type: While data is somewhat conflicting, there is evidence of a shift from Type IIa (oxidative-fast) to Type IIx (glycolytic-fast) fibers, with Type IIx fibers increasing from 5% to 19% in one long-term study.
• Capillarization: Results vary, but muscle capillary density generally decreases or reverts to untrained levels after 2–3 weeks of inactivity.
6. Mitigation and Return to Fitness
The review discusses strategies to minimize losses and how to rebuild fitness.
• Partial Reduction Strategy: To prevent drastic physiological losses, the authors suggest a "partial reduction" rather than a total stop. Maintaining VO2max is possible for up to 4 weeks if athletes continue with reduced volume but include at least one moderate-to-high intensity session per week. Conversely, relying solely on low-intensity training during a reduction period is less effective at preserving adaptations.
• Re-training: High-Intensity Interval Training (HIIT) is highlighted as an efficient method for returning to fitness. Low-volume, high-intensity sessions can rapidly stimulate mitochondrial biogenesis and skeletal muscle adaptations necessary to reverse detraining effects.
• Age Factors: Effects differ by age; younger athletes tend to lose VO2max faster, while older "master" athletes may retain some structural adaptations longer but lose maximal power output more significantly.
Conclusion
The article concludes that detraining is a systemic regression where physiological capabilities gained through endurance training are reversed. The data indicates that even short interruptions (<4 weeks) significantly impair VO2max, insulin sensitivity, and oxidative enzyme activity, while structural cardiac changes and weight gain are more characteristic of long-term inactivity. The authors emphasize the need for further research into optimal "tapering" or reduction protocols to help coaches manage transition periods without severe performance loss
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