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Cold water immersion after exercise: recent data and perspectives on “kaumatherapy”

2017; Wiley; Volume: 595; Issue: 9 Linguagem: Inglês

10.1113/jp274169

1469-7793

Thibaut Méline, Timothée Watier, Anthony M. J. Sanchez,

Sports Performance and Training

The Journal of PhysiologyVolume 595, Issue 9 p. 2783-2784 Journal ClubFree Access Cold water immersion after exercise: recent data and perspectives on “kaumatherapy” Thibaut Méline, Thibaut Méline University of Perpignan Via Domitia, Font-Romeu, France Centre de Ressources, d'Expertise et de Performance Sportives - Centre National d'Entraînement en Altitude, Font-Romeu, France Fédération Française des Sports de GlaceSearch for more papers by this authorTimothée Watier, Timothée Watier Laboratoire Européen Performance Santé Altitude, EA4604, University of Perpignan Via Domitia, Font-Romeu, FranceSearch for more papers by this authorAnthony MJ Sanchez, Corresponding Author Anthony MJ Sanchez anthony.sanchez@univ-perp.fr anthony.mj.sanchez@gmail.com orcid.org/0000-0003-3054-6349 Laboratoire Européen Performance Santé Altitude, EA4604, University of Perpignan Via Domitia, Font-Romeu, FranceEmail: anthony.sanchez@univ-perp.fr or anthony.mj.sanchez@gmail.comSearch for more papers by this author Thibaut Méline, Thibaut Méline University of Perpignan Via Domitia, Font-Romeu, France Centre de Ressources, d'Expertise et de Performance Sportives - Centre National d'Entraînement en Altitude, Font-Romeu, France Fédération Française des Sports de GlaceSearch for more papers by this authorTimothée Watier, Timothée Watier Laboratoire Européen Performance Santé Altitude, EA4604, University of Perpignan Via Domitia, Font-Romeu, FranceSearch for more papers by this authorAnthony MJ Sanchez, Corresponding Author Anthony MJ Sanchez anthony.sanchez@univ-perp.fr anthony.mj.sanchez@gmail.com orcid.org/0000-0003-3054-6349 Laboratoire Européen Performance Santé Altitude, EA4604, University of Perpignan Via Domitia, Font-Romeu, FranceEmail: anthony.sanchez@univ-perp.fr or anthony.mj.sanchez@gmail.comSearch for more papers by this author First published: 28 February 2017 https://doi.org/10.1113/JP274169Citations: 4 Linked articles: This Journal Club article highlights an article by Peake et al. To read this paper, visit https://doi.org/10.1113/JP272881. AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Physical exercise is a stress that induces substantial metabolic adaptations such as improvement of cell oxidative capacity. A single exercise bout may cause alterations in activity of intracellular systems and microscopic tears in the muscle tissue. Intense, unaccustomed or eccentric exercise is able to produce delayed onset muscle soreness (DOMS) and alter several markers of muscle damage. Exercise-induced metabolic overload and mechanical strain are well recognized to be the main factors generating muscle damage. An important symptom of muscle damage is disruption of the sarcolemma and extracellular matrix that may lead to increased blood level of several muscle proteins such as creatine kinase and myoglobin, and induce stiffness and swelling. Muscle damage can be promoted by both static and dynamic muscle actions, but eccentric actions result in greater muscle damage than concentric or isometric contractions. In the context of whole body exercises, greater muscle alteration is typically reported during running or cross-country skiing with higher mechanical stress on the muscles when compared with other activities such as cycling. In response to muscle damage, an inflammatory response appears and promotes a transfer of fluid and cells to eliminate cellular debris and damaged sarcomeric proteins from the muscles. Since exercise-induced muscle damage has a negative impact on performance and may extend recovery, different scenarios of recovery techniques have been investigated, including nutritional and physiological interventions. The latest interventions gather techniques such as massage, active recovery (ACT) and cryotherapy. Cryotherapy (from the Greek ‘cryo’ meaning cold) refers to a class of techniques that includes notably ice packs, whole-body cryotherapy for extreme cold air exposure, and cold water immersion (CWI) consisting of the submersion of parts of the body (typically the lower half) in cold water. The mechanism of cryotherapy intervention for post-exercise recovery is predominantly attributed to its vasoconstrictive effect and a decreased nerve conduction that may lead to a reduced perception of pain. In addition, a reduction of intramuscular temperature and metabolism may contribute to the limitation of inflammatory signalling and the resulting oedema. To date, the majority of studies have investigated the effects of cryotherapy interventions on recovery through DOMS, blood plasma markers (including cytokines), performance parameters and the Borg scale (Hohenauer et al. 2015). However, the effects of cryotherapy on these variables are often unclear, the risk of bias is high and comparisons with others commonly used methods of recovery such as ACT are lacking. Importantly, the major limitation of the studies performed in humans is that they mostly used indirect blood markers. Even if data from animal studies suggest that cryotherapy may reduce inflammation in muscle injury, no study has examined whether CWI modulates local inflammation in skeletal muscle after resistance exercise in humans. In a recent study published in The Journal of Physiology, Peake and coworkers (2017) compared the effects of CWI versus ACT on skeletal muscle inflammatory and cellular stress responses after acute resistance exercises. For this purpose, nine male trained subjects performed a ∼45 min intense training session on two separate days with leg press, single-leg squats, knee extensions and walking lunge exercises. The training sessions were followed by either CWI in an inflatable bath at 10.3 ± 0.5°C for 10 min or 10 min of ACT on a cycle ergometer at low self-selected intensity. Blood samples were collected before, immediately after exercise, and immediately (i.e. 15 min), 30 min, 1, 2, 24 and 48 h after the recovery therapies. Muscles biopsies were taken before exercise and 2, 24 and 48 h after exercise. The authors investigated the activity of serum creatine kinase by spectrophotometric assay, plasma cytokine concentrations by ELISA, and the modulation of several skeletal muscle markers related to cell damage and inflammation by using RT-PCR, immunoblot analyses and immunohistochemistry. First, the authors found that the number of neutrophils (CD66b+) and macrophages (CD68+ and CD163 mRNA level), and MAC1 (marophage cell surface receptor) mRNA expression were increased in muscle at different time points over the 48 h period post-exercise, demonstrating an increase in skeletal muscle inflammatory response. However, when ACT and CWI were statistically compared, no significant difference was observed. Supporting these results, PCR analyses showed an upregulation of cytokine and chemokine mRNA expression (IL1β, IL6, IL8, TNF, CCL2, CCL4, CCL5, CXCL2, LIF), and neutrophil gene expression (NGF and GDNF) in skeletal muscle but without significant difference between ACT and CWI interventions. Concerning the heat shock proteins, considered as mediators of cellular stress, HSP70 mRNA expression was found higher than before exercise at 2 h after both trials in skeletal muscle. Importantly, immunoblot analysis of muscle homogenates revealed that the protein content of HSP70 in the cytosol fraction was lower than before exercise at 2 and 48 h after ACT, and only at 2 h after CWI. Concerning αB-crystallin, a marker of sarcomeric disruption, a decrease of its cytosolic protein content was observed at 2, 24 and 48 h post-exercise for both ACT and CWI. The authors argue that the diminution of HSP70 and αB-crystallin content after ACT or CWI suggests that heat shock proteins translocated from the cytosol to cytoskeletal structures after exercise, even if statistical analyses failed to show significant change in the protein content of HSP70 and αB-crystallin in the cytoskeletal fraction. Importantly, these responses did not differ significantly between ACT and CWI. Finally, the authors also investigated whether exercise and the recovery strategies may affect indirect muscle damage markers by measuring creatine kinase activity and interleukin concentration. Even if exercise moderately increased creatine kinase activity and plasma IL-6 content at different time points following exercise, especially from 2 h post-exercise for ACT, no statistical difference has been observed between ACT and CWI. Altogether, these important findings provide evidence that CWI does not help further than ACT in restricting inflammation and cellular stress responses in muscle following resistance exercise. Importantly, compared to ACT, regular application of CWI was shown by the same team to reduce gains in muscle strength and mass after 3 months of resistance training (Roberts et al. 2015). Such an application may result in a decrease in inflammation and cellular stress responses that appears necessary to induce cell adaptations. However, the findings by Peake et al. do not support the idea that a reduction in inflammation may be involved in the diminution of training adaptations since CWI and ACT do not promote different effects on inflammatory and cell stress markers. Nevertheless, another recent work from the same group demonstrated that regular CWI application leads to a suppression of ribosome biogenesis in skeletal muscle of athletes subjected to a resistance training programme (Figueiredo et al. 2016). Consistent with this, the authors previously found that CWI attenuated and/or delayed the acute changes in satellite cell numbers and activity of a downstream target of the mechanistic target of rapamycin (mTOR) and extracellular signal-regulated kinase (ERK) pathways (i.e. p70S6K) that regulate muscle growth and hypertrophy (Roberts et al. 2015). Taken together, these results strongly suggest that the blunting of ribosome biogenesis may be one important factor that contributes to the impaired hypertrophic response with regular use of CWI after resistance training. Concerning endurance training, a recent work showed that CWI promotes the activation of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and vascular endothelial growth factor (VEGF) mRNA expression in human skeletal muscle after acute endurance exercise (Joo et al. 2016). However, even if these data suggest that post-exercise CWI may enhance the adaptive response to acute exercise at the transcriptional level, the authors did not find any additive effect on PGC-1α and VEGF protein expression. Thus, to the best of our knowledge, no data are actually able to demonstrate that CWI may enhance the adaptive response to acute endurance exercise. Further work is needed to highlight whether CWI may interfere with, or alternatively be of benefit to, cellular responses related to chronic endurance exercise. In addition, the use of opposite methods to cryotherapy, which should be called ‘kaumatherapy’ (from the Greek ‘kauma’ meaning heat), should be employed during chronic exercise in humans. Indeed, another work conducted in mice demonstrated that post-exercise whole body heat stress additively enhanced endurance training-induced mitochondrial adaptations (Tamura et al. 2014). In summary, the study by Peake and coworkers is the first to show that CWI is no more effective than ACT for minimizing the exercise-induced skeletal muscle inflammation, and neurotrophin and HSP production in humans. Thus, cryotherapy, especially CWI, does not appear to be a more efficient method than ACT for limiting muscle damage in response to resistance exercise. Since CWI also blunted the adaptive responses to chronic resistance exercise, the use of cryotherapy by athletes may be reconsidered, especially for resistance training. Furthermore, the use of cryotherapy during chronic endurance exercise warrants further investigations, and the same goes for the potential use of heat therapy or “kaumatherapy” during recovery, especially in humans. References Figueiredo VC, Roberts LA, Markworth JF, Barnett MPG, Coombes JS, Raastad T, Peake JM & Cameron-Smith D (2016). Impact of resistance exercise on ribosome biogenesis is acutely regulated by post-exercise recovery strategies. Physiol Rep 4, e12670. Hohenauer E, Taeymans J, Baeyens J-P, Clarys P & Clijsen R (2015). The effect of post-exercise cryotherapy on recovery characteristics: a systematic review and meta-analysis. PloS One 10, e0139028. Joo CH, Allan R, Drust B, Close GL, Jeong TS, Bartlett JD, Mawhinney C, Louhelainen J, Morton JP & Gregson W (2016). Passive and post-exercise cold-water immersion augments PGC-1α and VEGF expression in human skeletal muscle. Eur J Appl Physiol 116, 2315– 2326. Peake JM, Roberts LA, Figueiredo VC, Egner I, Krog S, Aas SN, Suzuki K, Markworth JF, Coombes JS, Cameron-Smith D & Raastad T (2017). The effects of cold water immersion and active recovery on inflammation and cell stress responses in human skeletal muscle after resistance exercise. J Physiol 595, 695– 711. Roberts LA, Raastad T, Markworth JF, Figueiredo VC, Egner IM, Shield A, Cameron-Smith D, Coombes JS & Peake JM (2015). Post-exercise cold water immersion attenuates acute anabolic signalling and long-term adaptations in muscle to strength training. J Physiol 593, 4285– 4301. Tamura Y, Matsunaga Y, Masuda H, Takahashi Y, Takahashi Y, Terada S, Hoshino D & Hatta H (2014). Postexercise whole body heat stress additively enhances endurance training-induced mitochondrial adaptations in mouse skeletal muscle. Am J Physiol Regul Integr Comp Physiol 307, R931– R943. Additional information Competing interests There is no conflict of interest, financial or otherwise to declare. Funding This study was supported by grant (16r03) from the French ‘Institut National du Sport, de l'Expertise et de la Performance’ (INSEP). Acknowledgements The authors thank the Fédération Française des Sports de Glace (FFSG), and the Centre de Ressources, d'Expertise et de Performance Sportives - Centre National d'Entraînement en Altitude (CREPS-CNEA) of Font-Romeu. The authors apologise for not citing all relevant articles due to reference limitations of the Journal Club format. Citing Literature Volume595, Issue91 May 2017Pages 2783-2784 ReferencesRelatedInformation