Hockey Conditioning: Understanding Fatigue

I hope you had a great holiday weekend with your families (even if you don’t celebrate the holiday!). Today is the day after Christmas, which means most of the people I know will be sleeping until around noon, then waking up and going shopping. I, on the other hand, was up at 5:30am to catch a plane to Minneapolis, MN. Several weeks ago, Reagan Carey, who is the Director of USA Hockey Women’s Ice Hockey Program, asked if I wanted to come serve on the Strength and Conditioning Staff for the US Women’s National Team winter camp, which I graciously accepted. I’ve helped out at two of these camps earlier in the year and the staff, both in terms of hockey and off-ice training, is outstanding. Great group of people with a ton of experience. There’s a lot to be learned when you spend a week surrounded by people like that! I fly back 12/31, right in time to take Emily out for dinner for New Year’s.

Hockey Conditioning
Hockey conditioning has come a long way in the last couple of decades. The norm has evolved from “play yourself into shape” to “endurance training on a bike” to “interval training using a combination of slideboards, shuttle runs, bike rides, and exercise circuits.” This is certainly a huge step in the right direction, but as with almost all things, the best practice typically involves a balance of several methodologies. Regarding conditioning, those that go high intensity intervals year-round are likely missing out on the powerful effects of aerobic training for hockey players. On the other hand, those that go steady-state aerobic training year-round are likely missing out on the powerful effects of a more strategic aerobic training progression AND the benefits of interval-based training. Progression and periodization are absolutely necessary for optimal results, especially as the athlete’s training age increases. In other words, the longer the athlete has trained, and the broader his/her base, the more focused his/her training needs to become to continue making progress.

In developing a hockey conditioning program, it’s important to understand what contributes to fatigue in the first place. This was a topic I covered in great detail in my book Ultimate Hockey Training.

The factors leading to performance decrements in a marathon-type event are different from those in repeat sprint performance events (as in most team sports), and as a result, training to improve performance (or minimize fatigue) must be specific to the mechanisms of fatigue. Last week, I read an excellent research review on this very topic from Girard et all., 2011.

The review identified the various mechanisms of fatigue that limit performance in “repeated sprint performance” (RSE), which they defined as short-duration sprints (<10s) interspersed with brief recovery periods (<60s). Below is a list of take-home points from the review that apply directly to conditioning for hockey:

  1. Fatigue develops immediately, following even a single sprint
  2. Performance on the initial sprint is directly related to the decrement in performance over subsequent sprints.
  3. In comparing performance decrements across five 6s cycling sprints repeated every 30s, those with low aerobic training fatigued more than those with moderate aerobic training.
  4. Previous fatiguing RSE, followed by a period of rest, accelerates the rate of fatigue during subsequent RSE.
  5. In monitoring field hockey players across three games within four days, the frequency of repeated sprints decreased across the three games.
  6. RSE results in an impairment of the Na+/K+ (sodium/potassium) pump, such that K+ ions accumulate outside of the cell, which impairs cell membrane excitability and force development. This will also cause a decrease in action potential amplitude and impulse conduction.
  7. M-waves (artificial muscle contractions secondary to an electrical stimulation of a motor nerve) experience a decrease in amplitude, but not duration following an RSE protocol (12 x 40m with 30s of recovery), which may indicate a decrease in action potential transmission across the synapse.
  8. Phosphocreatine (PCr) stores are reduced to 35-55% of resting levels following a single maximal 6 second sprint, and a full recovery can take more than 5 minutes. PCr loss is also greater in fast twitch fibers compared to slow twitch.
  9. Resynthesis of PCr is directly related to the recovery of power output int he first 10s of a 30s sprint
  10. Glycolysis contributions to ATP production decrease 8x from the first to last sprint in a 10 x 6s sprint protocol with 30s recovery periods.
  11. Oxidative phosphorylation contributes a mere 10% of the energy for a single short-duration sprint, but up to 40% as RSE protocols progress.
  12. Decreases in sprint performance are associated with decreases in blood pH (more acidic).
  13. Increased inorganic phosphate levels decreases calcium release from the sarcoplasmic reticulum and/or myofibrillar calcium sensitivity, which decreases cross-bridge formation and subsequent force production.
  14. 97% of the variance in total work performed during 10 cycle sprints with 30s of rest was explained by changes in quadriceps EMG, providing evidence of a decreased neural drive to the working muscle.
  15. The central nervous system (CNS) receives feedback from muscle spindles, Golgi tendon organs, free endings of group III and IV nerves, all of which are integrated into determining the level of descending neural drive to the working muscle. Reductions in central drive may serve to avoid peripheral fatigue beyond some threshold level.
  16. Progressive arterial O2 desaturation (less oxygen in the blood) is highly correlated to reductions in mechanical work, and O2 availability is also related to motor cortex excitability and neuromuscular activity in general.
  17. The relaxation rate of muscles decreases with fatigue, and so does the muscle firing rate to maintain an optimal tetanus in a changing metabolic environment.
  18. Fatigue results in an earlier activation of antagonistic muscles.
  19. Increases in core temperature beyond some threshold level results in decreased RSE performance, probably as a result of alterations in CNS function.

Take Home Points
I realize this can get a bit wordy. To be honest, I skipped over a lot of the really neat neuroscience stuff because it can get more confusing than we need for our purposes. The major take homes I want to leave with you are:

  1. Fatigue is multi-dimensional, incorporating neural, muscular, and metabolic relationships.
  2. Initial sprint performance is related to decreases in subsequent sprint performance, meaning the faster the first sprint, the greater the drop-off. This is likely the result of the athlete relying on more anaerobic systems during this first sprint, which results in a greater accumulation of metabolic “waste” and consequent more pronounced decrease in performance. From a more global perspective, this highlights the trade-off between max speed and max endurance and highlights the importance of finding the balance that is most appropriate for your position, within your sport, at your level (or the level you aspire to play at).
  3. With repeat sprint performance, there is an increase in aerobic contributions to energy. This highlights the importance of having a well-developed aerobic system, even for seemingly purely anaerobic sports.

Aerobic training isn’t all bad!

Check back in a couple days to find out how to use all this information to effectively train for improved repeat sprint performance!

To your success,

Kevin Neeld

P.S. Don’t forget to check out Ultimate Hockey Training, which covers year-round hockey conditioning principles in detail and provides a ton of implementable training progressions!

Girard, O., Mendez-Villanueva, A., & Bishop, D. (2011). Repeated-Sprint Ability – Part 1: Factors Contributing to Fatigue. Sports Medicine, 41(8), 673-694.

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