DNA 101: Training lactate threshold? Know the genetic link

The playoffs are over and it’s officially off-season for hockey players. With only a few months to both recover and build a better foundation of strength, speed, and agility for next season, it’s crucial to come into the off-season with a solid plan.

Lactate threshold is one of the key aspects that many hockey players focus on in their training. Every athlete has been there – the end of a long sprint or shift and your legs are burning, so bad that you feel like you can’t go on. This is lactate threshold. Scientifically speaking, it’s when lactate, a byproduct of anaerobic (without oxygen, like during high-intensity exercise) energy production, is made more quickly than it can be removed from the bloodstream.

You can train your lactate threshold so that you can push harder before the pain of lactate and exhaustion sets in. But before you can develop a plan that maximizes the time you have to train and gives you the result you need, you should consider factors like your nutrition, injury risk, your personal goals, and DNA.

Are you the kind of athlete who struggles when it comes to training your lactate threshold – even though you may be doing all the ‘right’ things? Or maybe you’re lucky and you see great gains from only a few weeks of training.

The difference between you and your teammates can be partly explained by your DNA. Athletigen reports on the combined effect of two markers that have been associated with lactate threshold trainability through scientific research and can help to shed light on your own experience with your lactate threshold’s response to training.

DNA tells us that some people may have ‘high lactate threshold trainability’ while others may have ‘low lactate threshold trainability.’

When you understand your DNA and combine these insights with your experience, you may find that your approach to off-season training is drastically different. Armed with your genetics – and knowing your own body – it can be daunting to know where to start. We turned to expert in strength and conditioning for hockey players, Ryan Vigneau of RVXFactor, to find out what to consider when training your lactate threshold in the off-season.

“You have to be able to produce and sustain 95–98% of your max power,” said Vigneau. “Otherwise, you’re just turning over lactate and never training your systems to become more resistant to lactate.”

“The end of the season is probably the most optimal time for both high and low responders to train and optimize their lactate threshold, he said. “Through playing and training night in and night out, a low responder may be at the perfect conditioning level to train their lactate threshold. A high responder may take less time to reach their peak lactate threshold, so could prioritize other aspects of their training at the start of the off-season, while keeping lactate threshold in mind.”

“If an athlete is a low responder, it may take an exorbitant amount of time and exposure to go into the next season and see any benefit from lactate threshold training – especially if they take a few weeks off,” said Vigneau. “So while an athlete may have the muscular fitness in June with the hockey season in September in mind, that may still not be enough time to reach their goals. When I’m working with hockey athletes that have a low lactate threshold trainability, I might start their program in April and keep them going consistently until the new season in September.”

This intensity can be hard to maintain, and according to Vigneau, if you’re a low responder to lactate threshold training, even taking a few weeks off can be detrimental to your progress. But if you know that your body trains slower and you understand your DNA and other contributing factors, you can put together a year-long plan with milestones to help fight off overtraining and fatigue, and keep you motivated and moving towards your goals.

The exact recipe for success for low lactate trainability athletes is dependent on several factors.

As Vigneau pointed out, to train your lactate threshold, you need to be able to produce 95–98% of your max power and hold it there for several minutes. In order to produce enough power to effectively train your lactate threshold, you need to have a good baseline of fitness. Your genetics can contribute to your ability to produce power efforts – especially genes like ACTN3 that can tell you whether you’re more likely to be a power or endurance-oriented athlete.

But as many athletes know, when you’re striving to reach your limits – whether it’s in the gym or on the ice – you’re upping your chance of injury.

Certain genes may influence your risk of tendon or ligament injury, so Vigneau takes these into consideration when looking at an athlete’s overall off-season plan. Plyometrics and agility drills can be great tools to train an athlete’s power, but if you have an increased risk of tendon injury, either due to a previous injury or your COL5A1 gene, you want to be careful and ensure you leave enough time for rest and recovery.

“We really try to maximize rest and recovery if the athlete has a greater risk of tendon injury,” said Vigneau. If this sounds like you, coach Vigneau suggests taking on a very regimented foam rolling program, try PNF stretching (a type of stretching where resistance is applied), and limit change of direction drills – or spread it out so that it’s not as high-impact.

If you’re lucky enough to be a high responder to lactate threshold training, you can leave a six to eight week window to prepare for competition and prioritize other aspects of your training in the meantime.

So, how are you going to maximize your off-season to come back as a fitter player next year? And why should you incorporate genetics into the mix? It’s simple, says Vigneau. “Using genetics helps us to know how to optimize each of your body’s systems in a way that allows you to continuously feel good – not just from a physical standpoint, but mental, too.”  

If you already know your strengths and weaknesses, you can understand how to train to optimize them – and you’ll get much more satisfaction knowing you’re on the right track.


What does your DNA say about you? Find out at athletigen.com


References:

  • Stefan, N., Thamer, C., Staiger, H., Machicao, F., Machann, J., Schick, F., Häring, H.- U. (2007). Genetic variations in PPARD and PPARGC1A determine mitochondrial function and change in aerobic physical fitness and insulin sensitivity during lifestyle intervention. The Journal of Clinical Endocrinology and Metabolism, 92(5), 1827–1833.
  • Friedman, E. A. (2010). Evolving pandemic diabetic nephropathy. Rambam Maimonides Medical Journal, 1(1), e0005.
  • Garatachea, N., Santiago, C., Yvert, T., Verde-Rello, Z., Fiuza-Luces, C., Santos-Lozano, A., Lucia, A. (2015). Genetic variants in the PPARD-PPARGC1A-NRFTFAM mitochondriogenesis pathway are neither associated with muscle characteristics nor physical performance in elderly. [Variaciones genéticas en la vía de la mitocondriogénesis PPARD-PPARGC1A-NRF-TFAM no están asociadas ni con características musculares ni con rendimiento físico en personas mayores]. RICYDE. Revista Internacional de Ciencias Del Deporte, 11(41), 196–208.
  • Gielen, M., Westerterp-Plantenga, M. S., Bouwman, F. G., Joosen, A. M. C. P., Vlietinck, R., Derom, C., Westerterp, K. R. (2014). Heritability and genetic etiology of habitual physical activity: a twin study with objective measures. Genes & Nutrition, 9(4).
  • Maciejewska-Karlowska, A., Hanson, E. D., Sawczuk, M., Cieszczyk, P., & Eynon, N. (2014). Genomic haplotype within the Peroxisome Proliferator-Activated Receptor Delta (PPARD) gene is associated with elite athletic status: PPARD haplotype and elite athletic status. Scandinavian Journal of Medicine & Science in Sports, 24(3), e148–e155.
  • Ordelheide, A.-M., Heni, M., Gommer, N., Gasse, L., Haas, C., Guirguis, A., Staiger, H. (2011). The myocyte expression of adiponectin receptors and PPARδ is highly coordinated and reflects lipid metabolism of the human donors. Experimental Diabetes Research, 2011, 692536.
  • San-Millán, J. L., & Escobar-Morreale, H. F. (2010). The role of genetic variation in peroxisome proliferator-activated receptors in the polycystic ovary syndrome (PCOS): an original case-control study followed by systematic review and metaanalysis of existing evidence. Clinical Endocrinology, 72(3), 383–392.
  • Santiago, C., Garatachea, N., Yvert, T., Rodríguez-Romo, G., Santos-Lozano, A., FiuzaLuces, C., & Lucia, A. (2013). Mitochondriogenesis genes and extreme longevity. Rejuvenation Research, 16(1), 67–73.
  • Thamer, C., Machann, J., Stefan, N., Schäfer, S. A., Machicao, F., Staiger, H., … Haring, H.-U. (2008). Variations in PPARD determine the change in body composition during lifestyle intervention: a whole-body magnetic resonance study. The Journal of Clinical Endocrinology and Metabolism, 93(4), 1497–1500.

join the Discussion

%d bloggers like this: