Bodybuilder, You're Missing Gains: Why Endurance Matters More Than You Think?

Introduction

The pursuit of maximal muscle hypertrophy and minimal body fat often leads bodybuilders and physique athletes to prioritize resistance training while neglecting aerobic conditioning. This stems from a long-held belief that endurance exercise interferes with muscle growth. However, a growing body of evidence suggests that a moderate level of aerobic fitness, far from hindering gains, actually enhances them by optimizing mitochondrial function and metabolic efficiency. This article will synthesize current scientific literature to demonstrate how strategic incorporation of endurance training can improve body composition outcomes in resistance-trained individuals.

Mitochondrial Adaptations: Endurance vs. Resistance Training

Skeletal muscle mitochondria are highly adaptable organelles, responding differently to endurance and resistance training stimuli.

• Endurance Training: Endurance training promotes mitochondrial biogenesis – an increase in both the number and size of mitochondria (Bishop et al., 2019; Hawley et al., 2018). This is driven by upregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), a master regulator of mitochondrial biogenesis,  along with increased expression of transcription factors like nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM) (Ruiz et al., 2021). The result is enhanced oxidative capacity, allowing for more efficient ATP production from fatty acids (Porter et al., 2015). Studies show a 40-50% increase in mitochondrial volume density with consistent endurance training (Bishop et al., 2019).   

• Resistance Training: Resistance training, while not significantly increasing overall mitochondrial content in type II fibers, induces mitochondrial fission (Hawley et al., 2018). This process creates smaller, more dispersed mitochondria, likely to facilitate ATP supply to the contractile apparatus during high-force muscle actions. Importantly, resistance training improves mitochondrial quality control through mitophagy (selective removal of damaged mitochondria) and autophagy (general cellular recycling) (Hawley et al., 2018).

• Substrate Utilization: These adaptations lead to distinct substrate preferences. Endurance-trained muscle prioritizes fat oxidation due to increased carnitine palmitoyltransferase 1 (CPT-1) activity and enhanced β-oxidation flux (Bishop et al., 2019). Resistance-trained muscle, while still capable of fat oxidation, maintains a higher reliance on glycolysis to support rapid ATP turnover during high-intensity contractions (Hawley et al., 2018).

Fat Oxidation: Mitochondrial Efficiency as a Metabolic Regulator

Increased mitochondrial density and function, primarily driven by aerobic training, directly impact both resting and exercise-induced fat oxidation.

• Resting Metabolic Rate (RMR): Studies demonstrate a strong positive correlation between mitochondrial density and resting fat oxidation rates. A 10% increase in mitochondrial density is associated with a 6.2% elevation in resting fat oxidation (p < 0.01) (Porter et al., 2015). This is attributed to several factors:

  • Improved electron transport chain coupling efficiency, reducing proton leak and favoring fatty acid oxidation.
  • Increased expression of uncoupling protein 3 (UCP3) in aerobically trained muscle, promoting nutrient futile cycling and elevating energy expenditure.
  • Enhanced inhibition of acetyl-CoA carboxylase (ACC), reducing malonyl-CoA levels and facilitating fatty acid transport into the mitochondria.

• Exercise-Induced Fat Oxidation: During submaximal exercise (e.g., 50-65% of VO2max), individuals with higher mitochondrial density exhibit greater reliance on intramuscular triglycerides (IMTGs), a lower respiratory exchange ratio (RER), and faster palmitate oxidation rates during recovery (Hawley et al., 2018). This contributes to a prolonged "afterburn" effect, or excess post-exercise oxygen consumption (EPOC).

Muscle Hypertrophy: Reconciling Aerobic and Resistance Training Adaptations

The "interference effect" – the notion that endurance training hinders muscle growth – is a central concern for bodybuilders. The proposed mechanism involves AMPK-mediated suppression of the mammalian target of rapamycin complex 1 (mTORC1), a key regulator of muscle protein synthesis (MPS).

• AMPK-mTOR Crosstalk: Acute endurance exercise activates AMP-activated protein kinase (AMPK), which can transiently inhibit mTORC1 phosphorylation (Hawley et al., 2018). However, this suppression is time-limited (typically 3-8 hours) and can be mitigated by consuming leucine-rich meals soon after aerobic exercise (Kerksick et al., 2017).

• Longitudinal Studies: Meta-analyses of concurrent training (combining resistance and endurance training) show mixed results. In untrained individuals, concurrent training may lead to slightly lower hypertrophy compared to resistance training alone (Wilson et al., 2015). However, in trained athletes, including bodybuilders, moderate endurance training (e.g., 2-3 sessions per week) does not significantly impair muscle growth and may even improve lean mass retention during caloric restriction (Wilson et al., 2015). This suggests that experienced lifters develop adaptations that minimize interference.

Training Intensity and Volume: Cardiovascular Determinants of Resistance Performance

Improved aerobic capacity, often measured as VO2max, directly benefits resistance training performance.

• Neuromuscular Efficiency: A higher VO2max (≥50 mL/kg/min) allows resistance-trained individuals to sustain higher training volumes (total weight lifted) at a given intensity (e.g., 70% of 1-repetition maximum [1RM]), reduce inter-set rest periods without compromising force output, and maintain bar velocity during high-repetition sets (Hawley et al., 2018).

• Circulatory Adaptations: Concurrent aerobic training enhances capillary density in type II muscle fibers, improves muscle reoxygenation rates, and increases stroke volume, even during Valsalva maneuvers (Bishop et al., 2019). These adaptations reduce peripheral fatigue, allowing for more frequent and productive resistance training sessions.

Recovery: Mitochondrial Mediators of Post-Exercise Regeneration

Aerobic fitness plays a crucial role in post-exercise recovery.

• Lactate Clearance: Higher mitochondrial density facilitates lactate clearance through both intracellular conversion to pyruvate (which then enters the Krebs cycle) and increased Cori cycle activity (lactate conversion to glucose in the liver) (Bishop et al., 2019).

• Glycogen Resynthesis: Aerobic training upregulates glucose transporter type 4 (GLUT4) expression in fast-twitch muscle fibers, accelerating post-workout glycogen replenishment (Hawley et al., 2018).

Practical Applications: Optimizing Concurrent Training

Based on the evidence, here are recommendations for incorporating aerobic training into a bodybuilding program:

Counterarguments and Limitations

• Excessive Volume: High volumes of endurance training (>5 hours/week) can indeed reduce muscle fiber size, particularly in power athletes (Hawley et al., 2018).
• Nutrient Partitioning: Chronic, high-intensity cardio can elevate cortisol levels, potentially promoting muscle protein breakdown (although this is more likely with prolonged, intense endurance exercise) (Kerksick et al., 2017).
• Genetic Variability: Individuals with certain genetic variations (e.g., ApoE ε4 allele) may be more susceptible to interference effects (Smith et al., 2020).

Research Gaps:

• Long-term studies (>2 years) on the effects of concurrent training in elite bodybuilders are needed.
• Sex-specific responses in female physique athletes require further investigation.
• The influence of mitochondrial haplogroups on training adaptation warrants more research (Ruiz et al., 2021).

Insufficient Aerobic Endurance: Consequences for Body Composition

Neglecting aerobic fitness can hinder both fat loss and muscle growth:

• Fat Loss Impairments: Lower mitochondrial density is associated with reduced 24-hour fat oxidation rates, impaired adipokine signaling (e.g., leptin resistance), and a diminished EPOC response to resistance training (Porter et al., 2015).

• Hypertrophy Limitations: Poor cardiovascular fitness can lead to longer inter-set recovery needs, slower muscle glycogen resynthesis, and increased systemic inflammation, all of which can impair muscle growth (Hawley et al., 2018).

Net Effect Analysis

For resistance-trained athletes, optimizing aerobic capacity to a VO2max range of 45-55 mL/kg/min appears to provide the most favorable balance:

• Enhanced Fat Loss: Increased daily fat oxidation and improved body fat reduction during caloric restriction.
• Improved Hypertrophy: Increased training density tolerance, faster recovery, and enhanced nutrient partitioning.
• Synergistic Effects: The combination of resistance and moderate aerobic training can lead to superior body composition outcomes compared to either modality alone.

The "tipping point" where aerobic training becomes detrimental appears to be around >6 hours/week of high-intensity endurance work (Hawley et al., 2018).

Conclusion

Bodybuilders and physique athletes can benefit significantly from incorporating moderate aerobic training into their routines. The key is to view aerobic fitness not as a threat to muscle growth, but as a support system that enhances training capacity, recovery, and metabolic efficiency. By strategically programming endurance work, focusing on moderate intensity and volume, athletes can optimize mitochondrial function and achieve superior body composition results. A polarized approach, emphasizing resistance training with a smaller proportion of low-intensity cardio, is recommended.

References

Bishop, D. J., Granata, C., & Eynon, N. (2019). Can we optimise the exercise training prescription to maximise improvements in mitochondria function and content? Biochimica et Biophysica Acta (BBA) - General Subjects,  1863(9), 1279-1288.   

Hawley, J. A., Lundby, C., Cotter, J. D., & Burke, L. M. (2018). Maximizing cellular adaptation to endurance exercise in skeletal muscle. Cell Metabolism, 27(5), 962-976.    

Kerksick, C. M., Wilborn, C. D., Roberts, M. D., Smith-Ryan, A., Kleiner, S. M., Jäger, R., ... & Kreider, R. B. (2017). ISSN exercise & sport nutrition review update: Research & recommendations. Journal of the International Society of Sports Nutrition,  14(1), 1-35.   

Porter, C., Reidy, P. T., Bhattarai, N., Sidossis, L. S., & Rasmussen, B. B. (2015). Resistance exercise training alters mitochondrial function in human skeletal  muscle. Medicine and Science in Sports and Exercise, 47(9), 1922-1931.    

Ruiz, J. R., Fan, B., & Lucia, A. (2021). Mitochondrial DNA and physical performance: A brief update. Current Opinion in Clinical Nutrition & Metabolic Care, 24(6), 498-502.

Smith, C. E., Arnett, D. K., Tsai, M. Y., Borecki, I. B., Krauss, R. M., Ordovas, J. M., ... & Lai, C. Q. (2020). The APOE polymorphism, cardio, and strength training. Medicine & Science in Sports & Exercise, 52(7), 1538-1547.

Wilson, J. M., Marin, P. J., Rhea, M. R., Wilson, S. M., Loenneke, J. P., & Anderson, J. C. (2012). Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises.  Journal of Strength and Conditioning Research, 26(8), 2293-2307.