Cold-water immersion and other forms of cryotherapy: physiological changes potentially affecting recovery from high-intensity exercise

Abstract

High-intensity exercise is associated with mechanical and/or metabolic stresses that lead to reduced performance capacity of skeletal muscle, soreness and inflammation. Cold-water immersion and other forms of cryotherapy are commonly used following a high-intensity bout of exercise to speed recovery. Cryotherapy in its various forms has been used in this capacity for a number of years; however, the mechanisms underlying its recovery effects post-exercise remain elusive. The fundamental change induced by cold therapy is a reduction in tissue temperature, which subsequently exerts local effects on blood flow, cell swelling and metabolism and neural conductance velocity. Systemically, cold therapy causes core temperature reduction and cardiovascular and endocrine changes. A major hindrance to defining guidelines for best practice for the use of the various forms of cryotherapy is an incongruity between mechanistic studies investigating these physiological changes induced by cold and applied studies investigating the functional effects of cold for recovery from high-intensity exercise. When possible, studies investigating the functional recovery effects of cold therapy for recovery from exercise should concomitantly measure intramuscular temperature and relevant temperature-dependent physiological changes induced by this type of recovery strategy. This review will discuss the acute physiological changes induced by various cryotherapy modalities that may affect recovery in the hours to days (<5 days) that follow high-intensity exercise.

Figures

Figure 1

Exercise-induced cell signalling. High intensity or high duration exercise induces metabolic stress and increases reactive oxygen species (ROS) production at the mitochondria of skeletal muscle, which contributes to lipid peroxidation and structural cell damage, as well as alters the redox status of the cell. Several transcription factors (TFs), such as nuclear factor kappa B (NFκB), Map Kinase (MapK), activator protein-1 (AP-1), heat shock factor protein-1 (HSF-1), and peroxisome proliferator-activated receptor-γ coactivator (PCG)-1α, are redox sensitive; thus, their function may be altered by the change in redox status. Some of these TFs are involved in muscle adaptation pathways, while others are involved in the production and secretion of cell signalling molecules such as interleukin-6 (IL-6) and interleukin-8 (IL-8). These cytokines are involved in the trafficking of leukocytes, which are attracted to the cell to clear away damaged tissue, but they may also contribute to ROS production at the muscle cell, contributing to structural damage and propagating the positive feedback pattern of the inflammatory response. Similarly, mechanical stress, such as that induced by high force contraction or highly eccentric exercise, may directly cause structural damage, initiating a similar positive feedback mechanism, but attracting leukocytes, which produce ROS and compound structural damage incurred. Lastly, high temperatures induced by exercise may increase the production of ROS from NADPH oxidase (NOX), contributing to the structural damage, change in redox status, nuclear signalling and positive feedback signalling associated with the other forms of exercise stress.

Figure 2

Relative pattern of temperature change in different tissue layers during exercise, cooling and post-cooling period. Data are averaged from studies measuring changes in tissue temperatures using various forms of cryotherapy [4,9,43,45-48,54,55]. Skin temperature (green, Tsk) increases during exercise, decreases exponentially through cryotherapy, reaching nadir earliest, and increases exponentially through post-cooling period. Core temperature (blue dashed, Tc-general) changes induced by cryotherapy applied to large mass increases during exercise, and decreases during cryotherapy (rate dependent on thermal gradient and peripheral blood flow). Core temperature cools slower than other tissues and does not begin to return to baseline until 1 h post-cooling. Core temperature (blue solid, Tc-local) changes induced by cryotherapy applied to a small mass is minor during cryotherapy and modest throughout post-cooling period as blood cooled at periphery is returned to core. Superficial intramuscular temperature (red, Tm@1) increases during exercise, declines linearly during cryotherapy, and increases linearly to baseline within 1 h. Deeper intramuscular temperature (yellow, Tm@3) increases during exercise decreases linearly during cryotherapy at a lower rate than Tm@1, continues to cool through the post-cooling phase as heat is transferred to warmer superficial tissues, returning to baseline later than 1 h.