Don’t Hibernate Over Winter. Its not worth it!

Don’t Hibernate Over Winter. Its not worth it!

 Injury or illness often necessitates a period of prolonged inactivity or bed rest. In the absence of the stimulation afforded by physical activity, metabolic homeostasis is compromised, and a rapid deterioration in functional capacity can occur. This same response will occur to long, frequent spells away from the gym. Commonly, in today’s society appearance is afforded greater importance than health. Hence, once we wrap our bodies in long pants, jumpers, coats and scarfs many ignore the consequences of physical inactivity. The object of this article is to provide you with some simple (research based) home truths on the consequences of inactivity and at least arm you with the ammunition to either fire yourself up, your training partner, a family member or friend over the winter months.

So if we examine some of the more extreme examples of immobilisation/inactivity, what may we expect to occur to the muscle we have worked so hard to improve and maintain over the summer months? Here are a few examples:

  • There is a significant decrease in muscle fibre cross-sectional area with inactivity.1
  • Increase in fatty infiltration into the muscle results from inactivity.2
  • 17-weeks of bed rest amounted to a loss of 18% in muscle volume.3
  • 30 days of bed rest amounted to a loss of 11% in muscle cross-sectional area.4
  • 4-weeks of immobilisation in a cast resulted in a loss of 21% in muscle cross-sectional area.5
  • With 28-days of bed rest there was a 6% loss of lean muscle mass from the legs, which is consistent with an approximately 4kg loss of whole-body lean muscle mass.6
  • 6.4kg (23%) loss of whole-body lean muscle mass over a 25-d period after blunt trauma injury.7

As you can see it does not take much to remove that precious muscle we work so hard to maintain and the bed rest model is widely employed to mimic inactivity. When individuals are confined to bed due to illness or injury there is some other interesting changes that occur to add to the muscle atrophy. There is also an increase in blood cortisol levels (catabolic to muscle) and muscle protein catabolism is accelerated.8,9

Marked decreases in the protein content of skeletal muscle in the early stages of disuse is one of the most significant adaptations of this tissue to reduced tension, resulting from fibre shrinking and weakening.10 Disuse induced skeletal muscle atrophy is accompanied by whole-body negative nitrogen balance. 11 It’s generally considered that disuse induced skeletal muscle wasting or atrophy is chiefly determined by the downregulation of protein synthesis.

So how can we prevent muscle atrophy? Motion is the most important element for preventing muscle loss: however tensionless or unloaded contractions have no substantial effect on protein turnover and therefore do not differ significantly from absolute inactivity. Muscle tension is fundamental. It’s interesting to note that tension of unloaded muscles by stretching has been proven beneficial for preventing atrophy and increasing rates of protein synthesis.12 As the majority of us shine our backsides on a seat for the best part of 8 hours a day we are not helping matters by giving the gym a miss.

So what’s the message here? Many of us for any number of reasons may have had a layoff from training particularly over winter. Just keep in mind that winter is probably the most important time of year to maintain your training stimulus. A layoff off of a few weeks to more than a month will set your training back, your muscle mass and strength will decrease and the journey back is never pleasant. Continuing your training load through winter will keep you on track and in control of your body composition.

DR JARROD D. MEERKIN PhD  AEP ESSAF

References

  1. Hikida et al. 1989
  2. Josa et al. 1990
  3. LeBlanc et al. 1992
  4. Berry et al. 1993
  5. Veldhuizen et al. 1993
  6. Paddon-Jones et al. 2006
  7. Monk et al. 1996
  8. Wolfe et al. 1989
  9. Hart et al. 2000
  10. Tomason et al. 1987
  11. Leonard et al. 1983
  12. Falempin et al. 1998
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