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Abstract
Cooling has a long history as an aid to muscle recovery after exercise. This article is protected by copyright. All rights reserved
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Key points:
We investigated whether intramuscular temperature affects the acute recovery of exercise performance following fatigue-induced by endurance exercise. Mean power output was better preserved during an all-out arm-cycling exercise following a 2 h recovery period in which the upper arms were warmed to an intramuscular temperature of ̴ 38°C than when they were cooled to as low as 15°C, which suggested that recovery of exercise performance in humans is dependent on muscle temperature. Mechanisms underlying the temperature-dependent effect on recovery were studied in intact single mouse muscle fibres where we found that recovery of submaximal force and restoration of fatigue resistance was worsened by cooling (16-26°C) and improved by heating (36°C). Isolated whole mouse muscle experiments confirmed that cooling impaired muscle glycogen resynthesis. We conclude that skeletal muscle recovery from fatigue-induced by endurance exercise is impaired by cooling and improved by heating, due to changes in glycogen resynthesis rate.
Abstract:
Manipulation of muscle temperature is believed to improve post-exercise recovery, with cooling being especially popular among athletes. However, it is unclear whether such temperature manipulations actually have positive effects. Accordingly, we studied the effect of muscle temperature on the acute recovery of force and fatigue resistance after endurance exercise. One hour of moderate-intensity arm cycling exercise in humans was followed by 2 h recovery in which the upper arms were either heated to 38°C, not treated (33°C), or cooled to ∼15°C. Fatigue resistance after the recovery period was assessed by performing 3 × 5 min sessions of all-out arm cycling at physiological temperature for all conditions (i.e. not heated or cooled). Power output during the all-out exercise was better maintained when muscles were heated during recovery, whereas cooling had the opposite effect. Mechanisms underlying the temperature-dependent effect on recovery were tested in mouse intact single muscle fibres, which were exposed to ∼12 min of glycogen-depleting fatiguing stimulation (350 ms tetani given at 10 s interval until force decreased to 30% of the starting force). Fibres were subsequently exposed to the same fatiguing stimulation protocol after 1-2 h of recovery at 16-36°C. Recovery of submaximal force (30 Hz), the tetanic myoplasmic free [Ca2+ ] (measured with the fluorescent indicator indo-1), and fatigue resistance were all impaired by cooling (16-26°C) and improved by heating (36°C). In addition, glycogen resynthesis was faster at 36°C than 26°C in whole flexor digitorum brevis muscles. We conclude that recovery from exhaustive endurance exercise is accelerated by raising and slowed by lowering muscle temperature.
The aim of this review and meta-analysis was to critically determine the possible effects of different cooling applications, compared to non-cooling, passive post-exercise strategies, on recovery characteristics after various, exhaustive exercise protocols up to 96 hours (hrs). A total of n = 36 articles were processed in this study. To establish the research question, the PICO-model, according to the PRISMA guidelines was used. The Cochrane’s risk of bias tool, which was used for the quality assessment, demonstrated a high risk of performance bias and detection bias. Meta-analyses of subjective characteristics, such as delayed-onset muscle soreness (DOMS) and ratings of perceived exertion (RPE) and objective characteristics like blood plasma markers and blood plasma cytokines, were performed. Pooled data from 27 articles revealed, that cooling and especially cold water immersions affected the symptoms of DOMS significantly, compared to the control conditions after 24 hrs recovery, with a standardized mean difference (Hedges’ g) of -0.75 with a 95% confidence interval (CI) of -1.20 to -0.30. This effect remained significant after 48 hrs (Hedges’ g: -0.73, 95% CI: -1.20 to -0.26) and 96 hrs (Hedges’ g: -0.71, 95% CI: -1.10 to -0.33). A significant difference in lowering the symptoms of RPE could only be observed after 24 hrs of recovery, favouring cooling compared to the control conditions (Hedges’ g: -0.95, 95% CI: -1.89 to -0.00). There was no evidence, that cooling affects any objective recovery variable in a significant way during a 96 hrs recovery period.
Keywords: Exercise, Recovery, Cryotherapy, Cold, Systematic Review, Meta-Analysis
Elite-level athletic training and competition is accompanied by the recovery of a series of physiological stressors. The physiological stress will vary considerably depending upon the specific exercise type, duration and intensity and also on the athletes' familiarisation to the exercise insult. It is well documented that when the exercise stress incorporates a novel eccentric component or the exercise is of considerable intensity or duration,1 athletes will likely experience numerous signs and symptoms of fatigue and cellular disturbance that have the potential to reduce performance.
Physiological stress induced by intense exercise is associated with energy substrate depletion, hyperthermia, mechanical muscle damage, oxidative stress, inflammation and nervous system fatigue. The resulting symptoms manifest as reduced performance potential, likely due to increased muscle soreness and decreased muscle function,2 disturbed muscle position sense and reaction time3 as well as increased stiffness and swelling that can last for several days.4 The aetiology of reduced performance potential will vary depending upon the exact physiological stress being recovered from. For example, eccentric exercise is associated with a large mechanical stress and relatively low metabolic cost,5 whereas intermittent sprint exercise may involve both a large mechanical stress and a heightened metabolic cost.6 It is possible that the underlying time course of recovery between different exercise stressors is different, and this consequently may influence how recovery strategies could be implemented. For the purpose of this review, exercise will be subdivided into two categories: ‘eccentric exercise’ that refers to the stress caused from exercise incorporating high mechanical stress (eg, eccentric contractions) and ‘high-intensity exercise’ that refers to stress caused from exercise with a high metabolic cost as well as some elements of eccentric muscle contractions (eg, repeat sprint sports).
Given the potential for physiological stress to compromise training and/or competition performance, there has been …
Key points
Muscle glycogen (the storage form of glucose) is consumed during muscle work and the depletion of glycogen is thought to be a main contributor to muscle fatigue.
In this study, we used a novel approach to first measure fatigue‐induced reductions in force and tetanic Ca ²⁺ in isolated single mouse muscle fibres following repeated contractions and subsequently quantify the subcellular distribution of glycogen in the same fibre. Using this approach, we investigated whether the decreased tetanic Ca ²⁺ induced by repeated contractions was associated with glycogen depletion in certain subcellular regions.
The results show a positive correlation between depletion of glycogen located within the myofibrils and low tetanic Ca ²⁺ after repetitive stimulation.
We conclude that subcellular glycogen depletion has a central role in the decrease in tetanic Ca ²⁺ that occurs during repetitive contractions.
Abstract
In skeletal muscle fibres, glycogen has been shown to be stored at different subcellular locations: (i) between the myofibrils (intermyofibrillar); (ii) within the myofibrils (intramyofibrillar); and (iii) subsarcolemmal. Of these, intramyofibrillar glycogen has been implied as a critical regulator of sarcoplasmic reticulum Ca ²⁺ release. The aim of the present study was to test directly how the decrease in cytoplasmic free Ca ²⁺ ([Ca ²⁺ ] i ) during repeated tetanic contractions relates to the subcellular glycogen distribution. Single fibres of mouse flexor digitorum brevis muscles were fatigued with 70 Hz, 350 ms tetani given at 2 s (high‐intensity fatigue, HIF) or 10 s (low‐intensity fatigue, LIF) intervals, while force and [Ca ²⁺ ] i were measured. Stimulation continued until force decreased to 30% of its initial value. Fibres were then prepared for analyses of subcellular glycogen distribution by transmission electron microscopy. At fatigue, tetanic [Ca ²⁺ ] i was reduced to 70 ± 4% and 54 ± 4% of the initial in HIF ( P < 0.01, n = 9) and LIF ( P < 0.01, n = 5) fibres, respectively. At fatigue, the mean inter‐ and intramyofibrillar glycogen content was 60–75% lower than in rested control fibres ( P < 0.05), whereas subsarcolemmal glycogen was similar to control. Individual fibres showed a good correlation between the fatigue‐induced decrease in tetanic [Ca ²⁺ ] i and the reduction in intermyofibrillar ( P = 0.051) and intramyofibrillar ( P = 0.0008) glycogen. In conclusion, the fatigue‐induced decrease in tetanic [Ca ²⁺ ] i , and hence force, is accompanied by major reductions in inter‐ and intramyofibrillar glycogen. The stronger correlation between decreased tetanic [Ca ²⁺ ] i and reduced intramyofibrillar glycogen implies that sarcoplasmic reticulum Ca ²⁺ release critically depends on energy supply from the intramyofibrillar glycogen pool.
Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+ release by various mechanisms, and the effects of reactive oxygen species. Many different activities lead to fatigue, and an important challenge is to identify the various mechanisms that contribute under different circumstances. Most of the mechanistic studies of fatigue are on isolated animal tissues, and another major challenge is to use the knowledge generated in these studies to identify the mechanisms of fatigue in intact animals and particularly in human diseases.