Key pointsr Cold water immersion is a popular strategy to recover from exercise. However, whether regular cold water immersion influences muscle adaptations to strength training is not well understood.r We compared the effects of cold water immersion and active recovery on changes in muscle mass and strength after 12 weeks of strength training. We also examined the effects of these two treatments on hypertrophy signalling pathways and satellite cell activity in skeletal muscle after acute strength exercise.r Cold water immersion attenuated long term gains in muscle mass and strength. It also blunted the activation of key proteins and satellite cells in skeletal muscle up to 2 days after strength exercise.r Individuals who use strength training to improve athletic performance, recover from injury or maintain their health should therefore reconsider whether to use cold water immersion as an adjuvant to their training.Abstract We investigated functional, morphological and molecular adaptations to strength training exercise and cold water immersion (CWI) through two separate studies. In one study, 21 physically active men strength trained for 12 weeks (2 days per week), with either 10 min of CWI or active recovery (ACT) after each training session. Strength and muscle mass increased more in the ACT group than in the CWI group (P < 0.05). Isokinetic work (19%), type II muscle fibre cross-sectional area (17%) and the number of myonuclei per fibre (26%) increased in the ACT group (all P < 0.05), but not the CWI group. In another study, nine active men performed a bout of single-leg strength exercises on separate days, followed by CWI or ACT. Muscle biopsies were collected before and 2, 24 and 48 h after exercise. The number of satellite cells expressing neural cell adhesion molecule (NCAM) (10−30%) and paired box protein (Pax7) (20−50%) increased 24-48 h after exercise with ACT. The number of NCAM + satellite cells increased 48 h after exercise with CWI. NCAM + -and Pax7 + -positive satellite cell numbers were greater after ACT than after CWI (P < 0.05). Phosphorylation of p70S6 kinase Thr421/Ser424 increased after exercise in both conditions but was greater after ACT (P < 0.05). These data suggest that CWI attenuates the acute changes in satellite cell numbers and activity of kinases that regulate muscle hypertrophy, which Abbreviations DAPI, 4 ,6-diamidino-2-phenylindole; ERK, extracellular regulated kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MRI, magnetic resonance imaging; mTOR, mammalian target of rapamycin; NCAM, neural cell adhesion molecule; Pax7, paired box protein 7; p70S6K, p70S6 kinase; RFD, rate of force development; RIPA, radioimmunoprecipitation assay; RM, repetition maximum; rpS6, ribosomal protein S6; Ser, serine; Thr, threonine; Tyr, tyrosine; 4E-BP1, (eukaryotic translation initiation factor) 4E-binding protein1.
-Resistance training (RT) has the capacity to increase skeletal muscle mass, which is due in part to transient increases in the rate of muscle protein synthesis during postexercise recovery. The role of ribosome biogenesis in supporting the increased muscle protein synthetic demands is not known. This study examined the effect of both a single acute bout of resistance exercise (RE) and a chronic RT program on the muscle ribosome biogenesis response. Fourteen healthy young men performed a single bout of RE both before and after 8 wk of chronic RT. Muscle cross-sectional area was increased by 6 Ϯ 4.5% in response to 8 wk of RT. Acute RE-induced activation of the ERK and mTOR pathways were similar before and after RT, as assessed by phosphorylation of ERK, MNK1, p70S6K, and S6 ribosomal protein 1 h postexercise. Phosphorylation of TIF-IA was also similarly elevated following both RE sessions. Cyclin D1 protein levels, which appeared to be regulated at the translational rather than transcriptional level, were acutely increased after RE. UBF was the only protein found to be highly phosphorylated at rest after 8 wk of training. Also, muscle levels of the rRNAs, including the precursor 45S and the mature transcripts (28S, 18S, and 5.8S), were increased in response to RT. We propose that ribosome biogenesis is an important yet overlooked event in RE-induced muscle hypertrophy that warrants further investigation. ribosomal RNA; cyclin D1; upstream binding protein; transcription initiation factor 1A
Myonuclei gained during exercise-induced skeletal muscle hypertrophy may be long-lasting and could facilitate future muscle adaptability after deconditioning, a concept colloquially termed “muscle memory.” The evidence for this is limited, mostly due to the lack of a murine exercise-training paradigm that is nonsurgical and reversible. To address this limitation, we developed a novel progressive weighted-wheel-running (PoWeR) model of murine exercise training to test whether myonuclei gained during exercise persist after detraining. We hypothesized that myonuclei acquired during training-induced hypertrophy would remain following loss of muscle mass with detraining. Singly housed female C57BL/6J mice performed 8 wk of PoWeR, while another group performed 8 wk of PoWeR followed by 12 wk of detraining. Age-matched sedentary cage-dwelling mice served as untrained controls. Eight weeks of PoWeR yielded significant plantaris muscle fiber hypertrophy, a shift to a more oxidative phenotype, and greater myonuclear density than untrained mice. After 12 wk of detraining, the plantaris muscle returned to an untrained phenotype with fewer myonuclei. A finding of fewer myonuclei simultaneously with plantaris deconditioning argues against a muscle memory mechanism mediated by elevated myonuclear density in primarily fast-twitch muscle. PoWeR is a novel, practical, and easy-to-deploy approach for eliciting robust hypertrophy in mice, and our findings can inform future research on the mechanisms underlying skeletal muscle adaptive potential and muscle memory.
Resistance training is the most effective method to increase muscle mass. It has also been shown to promote many health benefits. Although it is deemed safe and of clinical relevance for treating and preventing a vast number of diseases, a time-efficient and minimal dose of exercise has been the focus of a great number of research studies. Similarly, an inverted U-shaped relationship between training dose/volume and physiological response has been hypothesized to exist. However, the majority of available evidence supports a clear dose-response relationship between resistance training volume and physiological responses, such as muscle hypertrophy and health outcomes. Additionally, there is a paucity of data to support the inverted U-shaped response. Although it may indeed exist, it appears to be much more plastic than previously thought. The overarching principle argued herein is that volume is the most easily modifiable variable that has the most evidenced-based response with important repercussions, be these muscle hypertrophy or health-related outcomes.
Cold water immersion and active recovery are common post-exercise recovery treatments. However, little is known about whether these treatments influence inflammation and cellular stress in human skeletal muscle after exercise. We compared the effects of cold water immersion versus active recovery on inflammatory cells, pro-inflammatory cytokines, neurotrophins and heat shock proteins (HSPs) in skeletal muscle after intense resistance exercise. Nine active men performed unilateral lower-body resistance exercise on separate days, at least 1 week apart. On one day, they immersed their lower body in cold water (10°C) for 10 min after exercise. On the other day, they cycled at a low intensity for 10 min after exercise. Muscle biopsies were collected from the exercised leg before, 2, 24 and 48 h after exercise in both trials. Exercise increased intramuscular neutrophil and macrophage counts, MAC1 and CD163 mRNA expression (P < 0.05). Exercise also increased IL1β, TNF, IL6, CCL2, CCL4, CXCL2, IL8 and LIF mRNA expression (P < 0.05). As evidence of hyperalgesia, the expression of NGF and GDNF mRNA increased after exercise (P < 0.05). The cytosolic protein content of αB-crystallin and HSP70 decreased after exercise (P < 0.05). This response was accompanied by increases in the cytoskeletal protein content of αB-crystallin and the percentage of type II fibres stained for αB-crystallin. Changes in inflammatory cells, cytokines, neurotrophins and HSPs did not differ significantly between the recovery treatments. These findings indicate that cold water immersion is no more effective than active recovery for reducing inflammation or cellular stress in muscle after a bout of resistance exercise.
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