Thursday, December 27, 2018

Cold weather exercise - dangers, issues, strategy

As a cycling enthusiast and resident of Florida, winter is generally a great time to train.  The miserable summer heat and humidity are gone, which usually translates to an optimal environment to push exertional boundaries.  However, on occasion, the temperature drops below some sort of threshold where performance can dramatically drop.  Coupled with riding gear best suited to high temperature, minimal time to cold adapt, interesting hits to exercise metrics may occur.  In this post we will cover some basic concepts of cold induced physiology change as well as some of my personal observations with the Hexoskin and multiple muscle O2 sensor data.  In addition, some general health related concerns and cold temp compensation strategies will be outlined.

Cold induced exercise has many areas of physiologic effect that all lead to a decline in overall physical performance.  

Impairments occur along the entire neuromuscular chain from the muscle contraction apparatus, neurologic reflex arc as well as the cardiovascular system.
At the local level, upon cooling, muscular force may reduce through several biochemical pathways.  The end result is less maximum force.  In addition, shivering thermogenesis (involuntary muscle twitching) can lead to reduced efficiency of the contraction/relaxation cycle of a given muscle.  Shivering thermogenesis can also lead to depletion of glucose reserves, potentially causing early "bonking".  For example, if in warm/cool weather you are able to go 1 hour before carbohydrate replenishing, this time benchmark may be reduced depending on how cold you become.  Besides using carbohydrates, shivering can also use precious O2 reserves, thereby diverting this away from the intended exercise activity.

In terms of the cardiovascular system, some very dangerous changes can occur which could induce cardiac ischemia, arrhythmia and death.  

A prime mechanism for many of these issues is activation of the sympathetic nervous system resulting in elevation of resting heart rate, blood pressure, and peripheral vasoconstriction.  There can also be parasympathetic stimulation from the "diving reflex".  This dual confluence is felt to be a factor in the high risk of fatal arrhythmia in cold weather exercise.  In addition, if there is impairment of coronary vasodilatation from occlusive disease (plaque), the subject will be at higher risk of poor coronary perfusion leading to myocardial infarction when cardiac blood flow demand rises with intense exertion (from higher BP, HR, systemic vasoconstriction - see B below):

Apparently stoke volume is not markedly affected due to enhanced preload pressure from venous return.  As we will see below, VO2 peak and max heart rates can alter by variable degrees depending on the study, protocol, duration and temperature.  

Isolated effects on Muscle:
Both peak force, fatigue resistance and muscular efficiency (O2 consumption per unit of work) decline in low temp exercise according to a study using a frog muscle model.  

Fatigue resistance:

Force development:

Efficiency, O2 consumption:

The bottom line is that cold muscle loses significant advantageous exercise properties that can markedly effect performance.

VO2 max and heart rate during a ramp treadmill:
This study looked at VO2 max and heart rate during a treadmill ramp test.  They found a reduced VO2 max, shorter test duration and slight decline in peak HR at low temp.
In addition, at a submaximal exertion (50% VO2 max), the O2 consumption was higher at each step of cooler temps:
This is particularly concerning since much of a training/racing session will not be done at max output.  Given the higher degree of O2 usage at moderate power levels, one would expect a commensurate elevation of fuel usage.  However, although fuel use does increase, the proportion of carbohydrates burned seems to stay the same:
The SHIV group was subjected to cold and shivering conditions, the LOW vs MOD refer to either low or moderate exercise intensity.
  • The end result is that you may exhaust your carbohydrate reserves rapidly during exercise in the cold. 

Back to Heart rate:
Max heart rate in the cold is either about the same or less than neutral conditions.  But what about at submax power levels?  Here is a comparison at 50% VO2 max:

It appears that as the temperature drops, heart rate rises during steady state mid level power.  
However, there are other studies that do not show much in the way of heart rate change with temperature reduction:

Although HR did not really change, VO2 did rise with temp drop as many other publications have shown.

What about cold and wet conditions:
Adding the element of rain to the already cold air temperature places even more stress on an already marginal compensation process.  This was shown in the following study.
The subjects jogged at 70% VO2 max speed in 5 degree temps with and without rain.  Results showed a higher VO2, higher nor-epinephrine, higher lactate, higher ventilation rate in the rainy conditions:

VO2 (O2 consumption):

Lactate, Norepi levels:

Minute Ventilation: 

Therefore, if one is exercising in the cold and subsequently gets wet, an additional physiologic burden occurs that should be considered.  There appears to further effects on O2 consumption, stress hormone levels, lactate and ventilation rates.

Muscle metabolism:
Multiple sites of change can occur at the level of the muscle as noted above.  From a recent review:
As far as muscle O2 via NIRS, a recent paper looked at the effects of hypothermia with and without supplemental inspired O2.  They did find performance decreases with temp drop that were corrected by the subjects breathing a higher percent of oxygen.
I circled the cold exposed group who had lower power and longer time for completion than the control and hyperoxia group.

The fact that correction of the performance decline was possible with a higher O2 breathing mixture was a new and novel finding.  It does make one wonder if some of the effect of low temp on performance is related the change in the O2-Hb dissociation curve.  As an adaptation to exercise and muscle warming, hemoglobin affinity for O2 decreases, allowing more O2 offload to the active muscle.  Unfortunately, the reverse is also theoretically true, in cold conditions the Hb-O2 affinity rises, making tissue O2 offload decline.  Whether this is actually occurring in the athletes is unclear.  To make matters more complex, cold associated vasoconstriction may also play a role in tissue O2 extraction as well as absolute levels.

The study did look at muscle O2 levels in the VL, cerebral O2:
There was a small but significant drop in TOI (muscle O2) in the VL as well as cerebral O2 in the low temp group.  The addition of inhaled O2 did correct both sites back to the normal range.
However, the authors did comment that measuring O2 at this site/depth of the muscle may not be totally representative of muscle O2 kinetics:

Lower ambient temperature leads to significant changes in both circulatory and local neuromuscular physiology that is generally detrimental to performance. The decline in power was corrected by a breathing a gas mixture higher in O2.  This also corrected the changes seen in muscle and cerebral O2.

My data:

This tracing was done on my typical 45 mile ride (1 hr modulating power warm up then 3 min max aerobic power/VO2 peak power interval, then returning home).  It was 39F degrees and I was not dressed warmly. In addition, it was the first real cold spell for the area so I was not cold adapted at all.

Here is my attempt at a 3 min MAP, VO2 max interval that should have been at 350 watts:
The power was barely above 300w for 45 seconds then I was unable to sustain even that.  Average power over the 5 minutes was 240w, less than my lactate threshold power (under normal circumstances).  I did not have a sensor on the legs.
The costal, biceps O2 declined minimally, which is expected since power was not very high.

Slightly higher ventilation rates were noted (usually about 140-150 for MLSS).

Heart rate:
Unfortunately the Hexoskin wasn't picking up heart rate well, but this is data from my Garmin Fenix 5 watch:
  • Baseline pre interval heart rate was higher.
  • Steady state interval HR was similar to normal temp sessions.
  • Ventilation rate was above what it would have been with normal temp.
  • Power was markedly down.  Either the muscles were unable to develop the intended force, neuromuscular coordination was disrupted, or by that time I had run low on carbohydrate stores (bonking). 
  • Mild changes only in non locomotor muscle O2 (costal, biceps) indicating minimal cardiac output redistribution. 
Another day:
A 3 hour ride in slight rain at 50F after several weeks of cold adaptation (with warmer clothing):

This time the 3 min power was in the usual range.  
The VL O2 desat was less than usual, but this appears due to a lower initial baseline.  The net drop in VL was about the same as in warmer conditions.
Costal O2 drop was similar to standard conditions.

Heart rate and ventilation:
  • Ventilation was in the same range as usual.
  • Heart rate was lower (generally near high 160s to 171).

Wingate 60 - max 1 min power:
The temp had warmed to about 54%

  • Peak and average power was slightly less than usual (505 vs 520w).
  • VL O2 desat was similar to the prior 3 min VO2 max interval, with baseline higher than the prior interval (temp rose several degrees by that time).
  • Baseline VL saturation continued to be lower in the cold (usually about 70% as opposed to 60% here.  However, other sessions in warmer weather have had baselines as low as 60%.
  • Costal O2 desat very similar to 3 min session.

Heart rate and ventilation:

  • Peak heart rate slightly lower than with normal temps (167 vs 171).
  • Peak ventilation about the same as normal and prior MAP interval.

During exertion, the change in percent desaturation was about the same as warmer conditions. The presence of the lower baseline VL saturation could be related to cold induced vasoconstriction or simply sensor placement variation.  Although cardiac output redistribution did not appear to be any more pronounced, it was noted in some of the above studies that overall VO2 (per unit of effort) was increased.  So it is likely that the lower baseline O2 saturation is related to multiple mechanisms.

In conclusion, potential mechanisms for these changes include:

Local factors
  • Decrease in peak strength.
  • Higher proportional O2 use (less efficient).
  • Diminished muscle endurance.
  • Increase usage of both fatty acids and carbohydrate per unit of power.
  • Slight decrease in muscle O2 of locomotor muscles.
  • Possible role of altered O2-Hb affinity, making O2 offload decrease.
 Systemic factors
  • Higher systemic vascular resistance via vasoconstriction.
  • Higher risk of arrhythmia, heart attack.
  • Higher heart rates at submax power.
  • Lower peak heart rate.
  • Lower VO2 peak/max.
  • Higher VO2 (usage of oxygen) at submax power.
  • Higher ventilation rates at submax power.

Final thoughts:
  • Depending on the degree of hypothermia, acclimation and occurrence of rain, the amount of performance impairment can vary widely.  At extreme conditions, it may not even be possible to sustain usual intensity levels.  Expectations of exercise power, endurance may need to be curtailed.
  • Strategies to compensate for activity in the cold include adequate clothing (including the legs), higher consumption of carbohydrates during the activity, adjustments to power/heart rate thresholds used to modulate training zones.   
  • Consideration of cardiac risk factors before embarking on cold weather exercise - age, family history, lipid levels, prior history of diabetes, vascular disease, arrhythmia, hypertension etc. 

A few days later the temp warmed up into the 70's.  I repeated the 3 min MAP interval.  The average power was 365, max HR 170, ventilation 230 indicating excellent return of VO2 peak.  Desaturations of the costal, VL, RF and calf were similar to the wet/cool weather conditions.  It seems that at least by my data, NIRS does not show major alteration in desaturation patterns in locomotor muscles.  

My guess is that there could be two opposing effects that cancel each other out: 
On one hand there should be relative vasoconstriction from sympathetic stimulation (leading to lower muscle O2 from decreasing flow) as well as low temperature shifting of the O2 dissociation curve (leading to higher overall muscle O2 from higher Hb-O2 affinity).

And finally - There does appear to be an inverse U shaped curve as far as overall performance - low at extreme cold, extreme heat, but optimal in the comfortable temperature range. 

Cold weather exercise part 2 - what sensor is best to rely on....

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