Cooling muscles following exercise

Cooling has a long history as an aid to muscle recovery after exercise. The humble ice pack applied to sore muscles has widespread community support and more recent innovations include whole body immersion in cold (10°C) water for 10–20 min or whole body cryotherapy in which the subject is exposed to liquid N₂ vapour at around −120°C for 2–3 min. Advocates maintain that cryotherapy reduces exercise‐induced muscle damage, improves recovery of muscle performance after exercise, speeds weight loss and rejuvenates the skin. Multiple retail outlets have emerged offering cryotherapy for these and other benefits and often boast lists of professional sport teams and elite athletes who endorse this approach.

In the above list of proposed benefits, reduction of exercise‐induced muscle damage or delayed onset muscle soreness (DOMS) has by far the best supporting evidence. A recent meta‐analysis (Honenauer et al. 2015) pooled data from 27 published studies and concluded that that cooling reduced subjective indicators of muscle damage such as DOMS for several days after exercise. On the other hand, objective measures of muscle damage such as plasma lactate, creatine kinase and inflammatory markers showed no consistent improvement with cooling.

A study in this issue of The Journal of Physiology (Cheng et al. 2017) investigates the second item on the above list of proposed benefits, namely whether cooling a muscle after exercise improves subsequent performance. On this topic the existing literature, both in isolated muscles and humans, is quite mixed. For instance, a recent meta‐analysis of human studies suggested that cooling muscles after exercise had no effect on recovery of strength but a small positive effect on the recovery of power (Leeder et al. 2012). The study by Cheng et al. first investigated human performance using an arm pedalling exercise. In a preliminary period the rate of fatigue in several brief periods of maximal exercise was measured, followed by a long (4 × 15 min) period of exhausting exercise. A 2 h recovery was allowed during which the upper arm was either heated by water perfused cuffs (muscle temperature 38°C), unmodified (33°C) or cooled (average temperature 20°C). Then the rate of fatigue during the brief periods of maximal exercise was remeasured as an indicator of recovery. In this particular exercise model, the recovery from exhausting exercise was accelerated by heating whereas cooling had no significant effect.

Cheng et al. then turned to an isolated mouse muscle approach and in a roughly equivalent model of exhausting exercise or fatigue, they again showed that heating improved recovery whereas cooling slowed recovery. Of course the power of the isolated mouse muscle is that mechanisms have been extensively investigated and it is well known that fatigue is associated with a decline of muscle glycogen and that if recovery of muscle glycogen is prevented (by removing extracellular glucose) then recovery after exercise is impaired. This suggested that the temperature dependence of recovery might be simply due to a temperature‐dependent resynthesis of glycogen and Cheng et al. confirmed this by showing that the rate of recovery correlated with the degree of recovery of muscle glycogen.

Fatigue and recovery in muscles are at least partly caused by parallel changes in Ca²⁺ release and the possibility that consumption of glycogen somehow impairs Ca²⁺ release has long been considered (for review see Allen et al. 2008). Recent studies have shown that glycogen stores close to the site of Ca²⁺ release seem to correlate best with the failure of Ca²⁺ release (Neilsen et al. 2014) and the hypothesis is that glycogen somehow maintains critical metabolic levels close to the Ca²⁺ release sites in muscle. Cheng et al. confirmed in the present study that changes in Ca²⁺ release correlate both with glycogen levels and with recovery from fatigue.

The strength of this study is the combination of human and animal studies both of which show that, in a defined model of muscle exercise, recovery is assisted by warming and impeded by cooling. In the animal model cogent evidence is provided that the mechanism involves the rate of recovery of glycogen which, as expected from basic chemistry, is accelerated by increases in temperature. Of course, the mechanism may be different in human muscle or masked by other temperature‐dependent factors, but we do now have a clear mechanistic basis for starting to understand one of the many effects of temperature on muscle performance. Advocates of cryotherapy will need to do more to convince rational observers that cooling muscles has a beneficial role in the recovery of performance after exercise.

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Competing interests

None declared.