Saturday, March 14, 2020

Intelligent training through the Pandemic

Although the news is full of opinion and advice on how to survive the new few months, I wanted to review some literature as well as personal recommendations on what we should be doing until the global coronavirus pandemic is under control and life is back to normal.  The strategy I would take would revolve around both the twin goals of maintaining fitness without compromising the immune system.  
I won't get into social distancing, but it is a no-brainer to avoid crowded gyms, training facilities or cycling classes.  Limited outdoor activity with a few people is possibly ok, especially if you are in a strong UV light environment. 

Before going over some recommendations from a recent publication, let's examine what we are trying to achieve.  Since races are cancelled, there is little reason to be at peak fitness at this time.  Letting go of that training goal is extremely important right now, since we will see shortly that many of the factors that suppress immunity are involved in reaching peak fitness.  That leaves us two options, letting things slide or trying to maintain at a reasonable level.  Either are reasonable, but the strategy of maintaining is most appealing to me.

The following data was obtained from a recent review of immune function and exercise.

Here are the factors involved:

Prolonged high intensity:
In athletes under heavy training both innate and acquired immunity are often observed to decrease transiently during the recovery period after prolonged heavy exertion (≥90 min); typically of the order 15–70%
Periods of overreaching and longer term maladaptation (coined ‘overtraining’),in particular, have been shown to decrease immunity
Empirical evidence,albeit in a small number of athletes, indicates that international athletes suffer fewer not greater URI episodes than national-level athletes and that URI incidence correlates negatively with training load,viz.‘the less sick the more the athlete can train’. However, there may be genetic and/or modifiable behavioural factors that account for why international athletes succumb to fewer URI’s than national-level  athletes during  high-volume training
In other words, we don't all ride (or have the physiology) like Lance (or Froome etc) - which we all realize.

Recent evidence lends some support for this notion by showing that gene polymorphisms for the high expression of pro-inflammatory cytokines predict URI in highly trained athletes 
The presence of a huge support staff of therapists, logistic personnel and planned nutrition for the pros, is also a mitigating factor to combat high intensity - which us amateurs do not have.

Sleep disruption or deficiency:
Chronic sleep disturbance and disruption to the normal circadian rhythm (e.g. shiftwork) are associated with inflammation and desynchronisation of rhythmic immune variables; likely contributing to increased risk of infection, cardiovascular disease and cancer in long-term shift workers
In other studies, those sleeping <6 h per night and those with sleep efficiency <92% the chance of developing a common cold after intra-nasal inoculation with rhinovirus increased∼4–5 times
Preliminary laboratory work shows increased muscular performance with∼2 hours additional sleep each night

As might be expected, research from the field of psycho-neuro-immunology indicates that chronic high stress impairs the immune response to challenge
So keep stress down:

The Environment:
Cold weather
A popular belief held by many athletes is that breathing cold, dry air and getting a‘chill’ through cooling of the skin cause the‘common cold’. Although controversial, some evidence shows that peripheral cooling of the nose and upper airways (and even the feet)can increase URI symptoms; indeed, peripheral cooling may inhibit immune cell trafficking and create a suitable local environment for viral replication(Johnson & Eccles,2005). In support of this contention, recent research provides the missing piece of the jig-saw by showing that the human rhinovirus, a common cold causing virus, replicates more robustly at cooler temperatures found in the nasal cavity (33–35°C) (Foxman, Storer, Vanaja, Levchenko, &Iwasaki,2016). The temperature-dependent rhino-virus amplification is largely a result of host cell anti-viral  restriction  mechanisms  operating  more effectively at 37°C than at 33°C (Foxman et al.,2016). This research may at last provide an explanation for  why  cold  ambient  conditions  often precede outbreaks of URIs such as the common cold(Mäkinen et al.,2009). With this in mind, wherever possible, athletes are recommended to take extra precautions to avoid breathing large volumes of cold, dry air when training and competing in the winter.
At the time of this writing, it is unclear if coronavirus behavior is related to cooler conditions or not.  

One emerging trend from the literature is that immunity and host defence are typically decreased in studies where athletes complete live-high train-high or live-high train-low altitude training methods but not in studies  involving  intermittent  hypoxic  training 
 Long distance travel:
Studies are required to determine whether the increase in URI symptoms with long-haul travel is due to hypoxia-induced immune alterations, increased exposure to pathogens in the aircraft cabin, or some other mechanism. It is quite conceivable that the increase in psychological stress, anxiety and travel fatigue associated with long-haul travel to training camps and competitions may increase URI. For example, athletes may experience anxiety related to fear of flying, flight delays and baggage issues; they may also experience travel fatigue related to sleep loss and jet lag. 

Diet and Carbohydrate use:
Despite much interest and fervour amongst exercise immunologists, promising early findings demonstrating the benefits of carbohydrate sports drinks to blunt in-vitro immune impairment with heavy exercise have not been realised in studies assessing clinically relevant in-vivo immunity

Paradoxically,  nutritional  strategies  currently adopted by endurance athletes, including training-low- and sleeping-low-carbohydrate (Marquet et al.,2016), may benefit training adaptations and performance at the expense of immunity 

Vitamin D is a familiar topic in my field of endocrinologyAlthough having your Vit D level in a "normal range" is quite desirable, the evidence on immune function is very complex and often contradictory.  My recommendation is to keep the Vit D level between 40-80 ng/ml, and don't go by a blanket supplement dose - there are huge differences in personal requirements - get levels if possible.

And the final recs:
My final comments:
  • Take advantage of polarized training - 90% or more of your time spent in zone 1, otherwise brief HIT/SIT above VT2/MLSS.  Do not spend much, if any time in zone 2 or at MLSS.  Since we are aiming to maintain fitness with no impact on immunity, there is little advantage to going above this type of program.  If you have a low artifact HRV recording, consider following DFA a1 and make sure it is above .7 for the bulk of your training.  It is a marker of neuro cardiovascular stress, values of .5 and below correspond to a stress response.
  • Do not restrict carbs during any day that you train in zone 3.  Doing an hour of zone 1 while fasting seems fine, but could lead to exaggerated stress hormone elevation in zone 3.
  • Get extra sleep.  If you can't, do not train in zone 3.
  • Hand hygiene and the other advice will be helpful as well.
  • Do not do group indoors exercise class!!!

Tuesday, March 3, 2020

A just published article on DFA a1 and Zone 1 demarcation

Over the past year, several posts have been presented looking at the relationship of certain HRV parameters and the first ventilatory threshold.  I decided to take a closer look at the usage of DFA a1 as a zone 1 marker for exercise prescription and write up it up as a case report .  As part of the investigation, incremental exercise ramps were done with and without beta blocker therapy.  The use of beta blockade allows us to change the stroke volume x heart rate proportions, without affecting the end result, the cardiac output.  One of my questions was whether absolute heart rate was the prime driver of DFA a1 change or was it cycling power/VO2.
The investigation used many of the devices discussed over the past years including muscle O2 as an index of A-V O2 extraction, Hexoskin for artifact free HRV recording as well as ventilation rates. 
Here is the link to full text and the abstract is below:

The introduction and discussion will be instructive from the viewpoint of the various pitfalls of LT1/VT1 determination for zone 1 limitation.  The use of beta blockade was quite interesting to explore.  For any of the readers out there who are athletes on beta blocker therapy, this should reassure you that no major impairment of endurance performance should occur.

In addition to the data presented in the above paper, I would like to add another piece of the puzzle.  Although I did 10 minute intervals in the published study, looking for stability of the DFA a1, longer cycling sessions near VT1 were not done. To address what happens with prolonged cycling just below VT1 for about 80 minutes of constant power cycling was done.

Below is a trace of DFA a1 over about 80 minutes, recorded with the Hexoskin (no artifacts), with DFA a1 readings every 7 minutes or so (raw data to the left).  The power was fixed at 8 watts below VT1 by the Elite Suito trainer.

  • What this is showing is that as long as power is below VT1 (by 8w - clamped by the trainer), DFA a1 stays above .6 (orange).  Even though there is some minimal cardiac drift in heart rate past the 40 minute mark (blue), DFA a1 remains quite stable at .6 to .7.  
  • For my purposes, this is comforting to see.  Power just below my VT1 does not lead to demonstrable suppression of DFA a1 despite continuous effort for long duration.  Since the goal is to spend large amounts of time in zone 1, undue neuro-vascular stress is undesirable.
  • Further testing with slightly higher power would also be interesting, looking for progressive decline, for example at 10 watts above VT1.  

Heart rate variability during dynamic exercise