Ventilatory & VO2 Max Thresholds: Maximizing Training Stimulus For Optimal Adaptations

By Jonathan Davenport, CSCS, TSAC-F, CCC, CPT
A deeper look into understanding the physiology of ventilatory thresholds and VO2 max threshold.

When it comes to training, knowing your physiological thresholds can be a game-changer in terms of quantifying effort and optimizing your training load. VT1 (Ventilatory Threshold 1) and VT2 (Ventilatory Threshold 2) are two key thresholds that offer valuable insights into your body’s fuel utilization and can significantly impact your training outcomes. In this article, we will deconstruct these thresholds and explore their implications for your training.

To begin, it’s essential to understand that the human body utilizes a combination of fats and carbohydrates to generate energy, more specifically ATP (adenosine triphosphate), the molecule responsible for muscle contraction and energy production. However, the ratio of these fuel sources varies depending on the exercise intensity. Generally, at lower efforts, the body relies more on fats as the primary energy substrate, while higher-intensity training demand increased carbohydrate utilization.

Ventilatory Threshold 1

VT1, the first ventilatory threshold or aerobic threshold, represents the point at which your breathing pattern changes and becomes more pronounced. It indicates a shift from predominantly aerobic energy production to a combination of aerobic and anaerobic energy pathways. At VT1, your body’s primary fuel source is fat, and training around this threshold helps enhance fat metabolism and develop a strong aerobic base.

Identifying VT1 differs from person to person. Some individuals can maintain a jog or even a run, while others may reach this threshold with brisk walking. By training near VT1, your body receives a high stimulus for fat metabolism, leading to increased efficiency in utilizing oxygen and burning fat. Additionally, this type of training positively affects the development of slow-twitch (type I) muscle fibers and improves mitochondrial density and function.

Ventilatory Threshold 2

As your effort level increases beyond VT1, you enter the territory of VT2, also known as the second ventilatory threshold or lactate threshold. At VT2, the body’s reliance on carbohydrates as a fuel source intensifies. This transition occurs due to the recruitment of fast-twitch (type II) muscle fibers and increased CO2 production. It’s important to note that VT2 is not synonymous with the maximum lactate steady-state (MLSS), but rather marks the complete shift to carbohydrate fuel utilization.

Learn more: What is Maximum Lactate Steady-State?

Training at or near VT2 can be beneficial for lactate tolerance, particularly in preparation for races or events. However, prolonged training solely at VT2 can lead to increased fatigue and a decrease in mitochondrial density and respiration. Balancing training intensities and incorporating lower-intensity sessions near VT1 and higher-intensity sessions near VT2 is crucial for achieving optimal results.

VO2 Max

Beyond VT2 lies the point of VO2max, which represents the maximum amount of oxygen your body can utilize per minute per kilogram of body weight. Training efforts at or above VO2max improve mitochondrial respiration and fuel utilization at high loads. However, these sessions are highly intense and should be limited to 1-2 times per week, with longer recovery periods in both the short and long term.

Learn more: What is Mitochondrial Respiration?

Understanding your VT1 and VT2 thresholds allows you to gauge your body’s fuel utilization and make informed decisions about training intensities. By incorporating training sessions targeting each threshold, you can optimize energy systems, improve endurance, and enhance overall performance. It’s important to note that consulting with fitness professionals or sports scientists can provide personalized guidance and help tailor training plans based on individual thresholds and goals.

Summary

VT1 and VT2 thresholds are essential tools in training optimization. By delving into these physiological markers, athletes and fitness enthusiasts can leverage their knowledge to fine-tune training efforts, prevent overtraining, and maximize performance gains. Embrace the power of these thresholds and unlock your full potential in the pursuit of your fitness goals.

Sources

  1. Jeukendrup, Asker, and Andrew E. Wallis. “Maximal Fat Oxidation During Exercise in Trained Men.” ResearchGate, 2005, https://www.researchgate.net/profile/Asker_Jeukendrup/publication/9026407_Maximal_Fat_Oxidation_During_Exercise_in_Trained_Men/links/0fcfd50b07fb5af17b000000/Maximal-Fat-Oxidation-During-Exercise-in-Trained-Men.pdf.
  2. Astrup, Arne, et al. “Rate of digestion of foods and postprandial glycaemia in normal and diabetic subjects.” Acta medica Scandinavica, vol. 177, no. 2, 1965, pp. 153-156. ScienceDirect, https://www.sciencedirect.com/science/article/abs/pii/0002914964900128.
  3. Singh, Ritu, et al. “Autophagy regulates lipid metabolism.” NCBI Bookshelf, 2010, https://www.ncbi.nlm.nih.gov/books/NBK531494/.
  4. Hardie, D. Grahame. “AMP-activated protein kinase: a cellular energy sensor with a key role in metabolic disorders and in cancer.” Wiley Interdisciplinary Reviews: Systems Biology and Medicine, vol. 1, no. 1, 2009, pp. 161-173. Wiley Online Library, https://onlinelibrary.wiley.com/doi/full/10.1111/sms.13298.
  5. Dumke, Charles L., et al. “Effects of transcutaneous electrical nerve stimulation during exercise-induced muscle damage.” PubMed, 2017, https://pubmed.ncbi.nlm.nih.gov/28623613/.
  6. Preiss, Jack, et al. “Molecular biology of biotin-dependent carboxylations.” SpringerPlus, vol. 5, no. 1, 2016, p. 131. Springer, https://link.springer.com/article/10.1186/s40798-016-0060-1.
  7. Hirota, Naoki, et al. “Glutathione peroxidase 3 is a protective factor against acetaminophen-induced hepatotoxicity in vivo and in vitro.” Hindawi, 2014, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774727/.
  8. Zhang, Zhiwei, et al. “Alpha-Ketoglutarate: Physiological Functions and Applications.” PLOS ONE, vol. 11, no. 9, 2016, e0163389. PLOS, https://journals.plos.org/plosone/article/file?type=printable&id=10.1371/journal.pone.0163389.
  9. Uchida, Kenzo, et al. “Localization of 4-hydroxy-2-nonenal-modified proteins in kidney grafts with chronic rejection.” Hindawi, 2019, https://www.hindawi.com/journals/omcl/2019/7058350/.