Discussion

The efficacy of CWI has not been clearly established despite the large volume of research, therefore this systematic review of literature has provided insight into the potential benefits conferred by such interventions that allow practitioners to make an informed decision on their efficacy and application. The main findings of this study were as follows: (1) CWI alleviated symptoms of DOMS at 24, 48, 72 and 96 h post exercise and was effective at 24 and 48 h following high intensity exercise. (2) CWI had a small but significant effect in reducing efflux of CK post exercise. (3) CWI had no effect on recovery of muscle strength but was effective in improving recovery of muscle power.

One proposed mechanism of CWI is a cold-induced reduction in muscle blood flow and tissue temperature causing decreased inflammation induced via strenuous exercise. Gregson et al10 recently showed reduced femoral artery blood flow (>40%) and muscle temperature (2–4°C) following 10 min of immersion in 8°C and 22°C water. The proposed reduction in inflammation is associated with a reduction of the sensation of pain caused by reducing the osmotic pressure of exudate, which pressurises nociceptors, signalling pain via type IV afferent fibres.14 24,–,26 Cold-induced vasoconstriction is thought to reduce permeability of cellular, lymphatic and capillary vessels, which reduces fluid diffusion into the interstitial space, which is the suggested mechanism of reduced inflammation following muscle-damaging exercise.27 The reduction in muscle tissue temperature following CWI is another proposed mechanism of CWI and may reduce metabolic enzymatic activity and limit secondary hypoxic damage to uninjured cells.28 Myrer et al29 indicated that the amount of adipose over the area of cold treatment significantly affects rate of intramuscular cooling and therefore should be taken into account when administering CWI protocols to athletes of varying body composition. It is currently unknown whether the major mechanism of CWI is reduced blood flow or whether tissue temperature needs to be reduced concomitantly.

The present findings show that CWI appears to be an effective analgesic, lasting up to 96 h post exercise. The overall Hedges' G of 0.53 (figure 3) suggests that 69% of the population will likely experience lower DOMS using CWI30; however, this does not indicate the magnitude of DOMS reduction. For comparative purposes, DOMS scores from visual analogue scales were standardised and compared retrospectively between control and CWI groups.12 13 15 16 31,–,36 The results showed CWI reduced perception of soreness on average by 16%. Whether this outweighs the logistical inconvenience of CWI remains the decision of the applied practitioner. Interestingly, at 24 and 48 h post exercise, CWI appears to have more effective analgesic properties following high-intensity exercise than eccentric biased exercise (table 2). Further mechanistic work is needed to understand the physiological effects of CWI following different exercise types to elucidate whether this is a true physiological effect or simply reflects the placebo effect.

Given the perceptual nature of DOMS assessments, it is plausible that the placebo effect phenomenon may have an impact on the efficacy of CWI as recovery strategy.37 Given the rapidly increasing popularity of water immersion recovery strategies, despite a lack of evidence to support their use, it is quite possible that participants believed and expected a positive outcome from CWI, thereby influencing the measure of DOMS. Unfortunately, due to the nature of water immersion, it is not possible to provide a true placebo condition within such experimental trials. Figure 2 indicates this by the high risk of bias in the blinding category. Whether the placebo effect contaminates these results or whether in fact it is an important aspect of any recovery strategy remains to be elucidated and warrants further consideration in future research. Studies which incorporate objective methods of inflammation and swelling, as well as subjective markers of perception of soreness, will contribute to understanding of the role of the placebo effect in CWI research.

Cold water immersion was not effective at improving recovery of muscle strength post exercise. The effect of eccentric exercise on muscle strength has been extensively reviewed and is proposed to relate to disrupted sarcomeres in myofibrils and damage to the excitation-contraction coupling system.38,–,40 Following the primary phase of muscle damage, a disruption in calcium homeostasis in the cytosol leads to a cascade of events following the exercise that further damages the cell partly via oxidative mechanisms.9 It would appear CWI is not able to alleviate this secondary damage and muscle strength loss; however, there is little evidence investigating the potential mechanism of CWI reducing post-exercise oxidative stress.

The only positive effect of improving recovery of muscle function was in tests of muscle power. The effect of CWI acting specifically to recovery of muscle power and not muscle strength is an interesting finding with no obvious explanation, so the following proposed mechanisms are speculative. Inter-individual differences in muscle strength are predominated by muscle cross-sectional area,41 whereas muscle power involves an intricate interaction of muscle cross-sectional area and excitation-relaxation kinetics.42 It is unknown whether CWI may specifically affect different characteristics of the force–velocity relationship of skeletal muscle. An alternative explanation is that type 2 fibres are preferentially damaged following eccentric exercise and are the predominant fibre type in high-velocity muscle contractions involving elevated power production.24 It could be speculated CWI is associated with a heightened recovery of type 2 fibres. Following strenuous exercise such as various field sports, preferential recovery of power over strength may have implications for periodising training in subsequent days. Whether CWI has specificity to recover muscle power over strength requires further research.

Following high-intensity exercise, CWI was more effective at alleviating DOMS at 24 and 48 h than following eccentric exercise (table 2). While there are physiological differences between high-intensity exercise and eccentric exercise, it is difficult to explain the mechanisms of action as to why CWI may be more efficacious following high-intensity exercise than eccentric exercise. It was also clear that although markers of physiological stress and recovery may appear to be similar following different exercise modes, the underlying aetiology of the stress is likely to be different between the two exercise modes. Bimodal contributions to reduced performance potential following strenuous exercise are speculated to be (1) an initial mechanical and/or metabolic muscle injury that transpires during the exercise and (2) a secondary phase subsequent to the exercise that involves a disruption in intracellular homeostasis followed by an inflammatory response.9 It is suggested the contributions of the mechanical and metabolic stress that contribute to this first phase of physiological disturbance vary considerably between eccentric and high-intensity exercise types. Furthermore, identification and analysis of indices thought to be implicated in various causes of physiological stress, such as oxidative stress, substrate depletion, hyperthermia, stress hormones and cytokines, as well as the common markers of recovery will help contribute to understanding the recovery process and provide greater rationale for the inclusion of interventions.

Vaile et al36 43 have consistently found positive effects from CWI on recovery of muscle power. One lucid difference of these studies is the contribution of hydrostatic pressure by immersing to the neck. The physiological responses to hydrostatic pressure have been extensively reviewed.27 During thermoneutral water immersions to the neck, there is a displacement of fluid and gas from higher pressure areas at the ankle to low pressure areas at the water surface. This ‘squeezing’ effect induces alterations in fluid within the intracellular, interstitial and intravascular spaces. Water immersion causes increases in central blood volume44 due to fluid shifts from interstitial to intravascular space.27 This is one proposed mechanism of hydrostatic pressure to reduce oedema caused by strenuous exercise. Research has not yet focused on controlling water temperature and assessing the effect of different hydrostatic pressures. This could help ascertain the contribution of hydrostatic pressure to the efficacy of water immersions.

Intramuscular proteins have been extensively used as biochemical markers of muscle damage. Figure 4 indicates that although there was a statistically significant reduction (p = 0.022) in the efflux of CK post exercise, the Hedges' g of 0.221 showed this was a very small effect. This agrees with recommendations from Warren et al19 not to use intramuscular proteins as markers of muscle damage as they do not accurately reflect functional loss resulting from strenuous exercise. Blood levels of intramuscular proteins represent a balance not only between rate of release but also between rate of removal. Consequently, measurement of CK is likely to be sensitive to changes in blood flow, which may explain the high variability of this measure. Clarkson et al45 showed that following eccentric exercise, variations in participant genotypes that code for myofibrillar proteins influence the phenotypic response to muscle damage response in the form of CK and functional loss of strength. This is a potential reason for diverse inter-individual CK responses to strenuous exercise, despite similar participant characteristics (age, sex, athletic status).

A rationale for utilising CWI is to reduce the post-exercise inflammatory response, with the aim of minimising the reduction of muscle function and increase in DOMS associated with strenuous exercise. It has, however, been suggested that the inflammatory response is critical for optimal repair of damaged tissue.28 Although the mechanisms of training adaptation are not fully understood, it may be detrimental to reduce the commonly accepted damage-repair-adaptation model by diminishing the inflammatory response; however, there is a lack of evidence to support this.32 46 This raises the question of whether frequent or habitual use of strategies designed to reduce inflammatory responses can be detrimental for elite athlete adaptation to training.