PurposeWe tested the hypothesis that both post-exercise and passive cold water immersion (CWI) increases PGC-1α and VEGF mRNA expression in human skeletal muscle.Method Study 1 Nine males completed an intermittent running protocol (8 × 3-min bouts at 90 % , interspersed with 3-min active recovery (1.5-min at 25 % and 1.5-min at 50 % ) before undergoing CWI (10 min at 8 °C) or seated rest (CONT) in a counterbalanced, randomised manner. Study 2 Ten males underwent an identical CWI protocol under passive conditions.Results Study 1 PGC-1α mRNA increased in CONT (~3.4-fold; P < 0.001) and CWI (~5.9-fold; P < 0.001) at 3 h post-exercise with a greater increase observed in CWI (P < 0.001). VEGFtotal mRNA increased after CWI only (~2.4-fold) compared with CONT (~1.1-fold) at 3 h post-exercise (P < 0.01). Study 2 Following CWI, PGC-1α mRNA expression was significantly increased ~1.3-fold (P = 0.001) and 1.4-fold (P = 0.0004) at 3 and 6 h, respectively. Similarly, VEGF165 mRNA was significantly increased in CWI ~1.9-fold (P = 0.03) and 2.2-fold (P = 0.009) at 3 and 6 h post-immersion.ConclusionsData confirm post-exercise CWI augments the acute exercise-induced expression of PGC-1α mRNA in human skeletal muscle compared to exercise per se. Additionally CWI per se mediates the activation of PGC-1α and VEGF mRNA expression in human skeletal muscle. Cold water may therefore enhance the adaptive response to acute exercise.

Postexercise CWI does not attenuate muscle glycogen resynthesis rates during short-term recovery even when CHO availability is considered suboptimal. Athletes who regularly incorporate CWI as a recovery strategy to alleviate symptoms of exercise-induced muscle damage should therefore not be concerned with potential negative effects of the associated reductions in muscle blood flow on the restoration of muscle glycogen stores.

Mechanisms mediating postexercise cold-induced increases in PGC-1α gene expression in human skeletal muscle are yet to be fully elucidated but may involve local cooling effects on AMPK and p38 MAPK-related signaling and/or increased systemic β-adrenergic stimulation. Therefore, we aimed to examine whether postexercise cold water immersion enhancement of PGC-1α mRNA is mediated through local or systemic mechanisms. Ten subjects completed acute cycling (8 × 5 min at ~80% peak power output) followed by seated-rest (CON) or single-leg cold water immersion (CWI; 10 min, 8°C). Muscle biopsies were obtained preexercise, postexercise, and 3 h postexercise from a single limb in the CON condition but from both limbs in CWI [thereby providing tissue from a CWI and nonimmersed limb (NOT)]. Muscle temperature decreased up to 2 h postexercise following CWI (-5°C) in the immersed limb, with lesser changes observed in CON and NOT (-3°C, < 0.05). No differences between limbs were observed in p38 MAPK phosphorylation at any time point ( < 0.05), whereas a significant interaction effect was present for AMPK phosphorylation ( = 0.031). Exercise (CON) increased gene expression of PGC-1α 3 h postexercise (~5-fold, < 0.001). CWI augmented PGC-1α expression above CON in both the immersed (CWI; ~9-fold, = 0.003) and NOT limbs (~12-fold, = 0.001). Plasma normetanephrine concentration was higher in CWI vs. CON immediately postimmersion (860 vs. 665 pmol/l, = 0.034). We report for the first time that local cooling of the immersed limb evokes transcriptional control of PGC-1α in the nonimmersed limb, suggesting increased systemic β-adrenergic activation of AMPK may mediate, in part, postexercise cold induction of PGC-1α mRNA. We report for the first time that postexercise cold water immersion of one limb also enhances PGC-1α expression in a contralateral, nonimmersed limb. We suggest that increased systemic β-adrenergic stimulation, and not localized cooling per se, exerts regulatory effects on local signaling cascades, thereby modulating PGC-1α expression. Therefore, these data have important implications for research designs that adopt contralateral, nonimmersed limbs as a control condition while also increasing our understanding of the potential mechanisms underpinning cold-mediated PGC-1α responses.

Glucose restriction (GR) impairs muscle cell differentiation and evokes myotube atrophy. Resveratrol treatment in skeletal muscle cells improves inflammatory-induced reductions in skeletal muscle cell differentiation. We therefore hypothesised that resveratrol treatment would improve muscle cell differentiation and myotube hypertrophy in differentiating C2C12 myoblasts and mature myotubes during GR. Glucose restriction at 0.6 g/L (3.3 mM) blocked differentiation and myotube hypertrophy versus high-glucose (4.5 g/L or 25 mM) differentiation media (DM) conditions universally used for myoblast culture. Resveratrol (10 µM) treatment increased SIRT1 phosphorylation in DM conditions, yet did not improve differentiation when administered to differentiating myoblasts in GR conditions. Resveratrol did evoke increases in hypertrophy of mature myotubes under DM conditions with corresponding elevated Igf-I and Myhc7 gene expression, coding for the ‘slow’ type I MYHC protein isoform. Inhibition of SIRT1 via EX-527 administration (100 nM) also reduced myotube diameter and area in DM conditions and resulted in lower gene expression of Myhc 1, 2 and 4 coding for ‘intermediate’ and ‘faster’ IIx, IIa and IIb protein isoforms, respectively. Resveratrol treatment did not appear to modulate phosphorylation of energy-sensing protein AMPK or protein translation initiator P70S6K. Importantly, in mature myotubes, resveratrol treatment was able to ameliorate reduced myotube growth in GR conditions over an acute 24-h period, but not over 48–72 h. Overall, resveratrol evoked myotube hypertrophy in DM conditions while favouring ‘slower’ Myhc gene expression and acutely ameliorated impaired myotube growth observed during glucose restriction.

Over the past decade, significant research has focussed on optimising the recovery of elite athletes. The premise behind such a theory is that sub-optimal recovery often leads to fatigue, reducing the quality of subsequent training sessions and/or competitive performances, whilst potentially hindering adaptive processes. There is now a plethora of research focussing on the impact of one such recovery strategy, cold-water immersion (CWI), and the benefits it may provide post-exercise.Proposed mechanisms of action are hypothesised to be a combined result of reduced perception of pain via decreased nerve conduction velocity alongside temperature and pressure induced changes in blood flow and reduced skeletal muscle temperature. As such, cold temperatures may facilitate enhanced recovery from exercise by reducing intramuscular temperature and metabolism, thereby limiting hypoxic stress and the generation of reactive oxygen species (ROS).

In the last decade, cold water immersion (CWI) has emerged as one of the most popular post-exercise recovery strategies utilized amongst athletes during training and competition. Following earlier research on the effects of CWI on the recovery of exercise performance and associated mechanisms, the recent focus has been on how CWI might influence adaptations to exercise. This line of enquiry stems from classical work demonstrating improved endurance and mitochondrial development in rodents exposed to repeated cold exposures. Moreover, there was strong rationale that CWI might enhance adaptations to exercise, given the discovery, and central role of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) in both cold- and exercise-induced oxidative adaptations. Research on adaptations to post-exercise CWI have generally indicated a mode-dependant effect, where resistance training adaptations were diminished, whilst aerobic exercise performance seems unaffected but demonstrates premise for enhancement. However, the general suitability of CWI as a recovery modality has been the focus of considerable debate, primarily given the dampening effect on hypertrophy gains. In this mini-review, we highlight the key mechanisms surrounding CWI and endurance exercise adaptations, reiterating the potential for CWI to enhance endurance performance, with support from classical and contemporary works. This review also discusses the implications and insights (with regards to endurance and strength adaptations) gathered from recent studies examining the longer-term effects of CWI on training performance and recovery. Lastly, a periodized approach to recovery is proposed, where the use of CWI may be incorporated during competition or intensified training, whilst strategically avoiding periods following training focused on improving muscle strength or hypertrophy.

Forty-seven patients, 29 with chronic inflammatory bowel disease (IBD) and 18 with presumed irritable bowel syndrome, including one with uncomplicated diverticular disease, were studied with simultaneous technetium-99m hexamethylpropylene amine oxime and indium-111 oxine labelled leucocyte scans performed at 1, 3 and 24 h. Twenty-seven patients with IBD had active disease as judged by clinical and laboratory criteria and all of these had positive scans with both agents. No false positive studies were obtained. The 1-h 99mTc-HMPAO WBC scans showed the same distribution to disease as the 3-h 111-In WBC scans, with no difference in intensity (P < 0.92); they showed more extensive disease (P < 0.02) and more intense uptake (P < 0.001) than did the 1-h 111-In scans. The 3-h 99mTc-HMPAO WBC scans showed more extensive disease (P < 0.002), with greater intensity (P < 0.0005), than did the 3-h 111In WBC scans. Physiological bowel activity on 3-h 99mTc-HMPAO WBC scans was present in 12 patients but was faint and did not interfere with assessment of disease extent and activity. It is concluded that in terms of isotope availability, radiation dosimetry and image quality, 99mTc-HMPAO is the agent of choice in detecting active IBD, with localization of disease possible at 1-h after re-injection and optimal resolution and definition of disease extent at 3 h. A negative scan reliably excludes active disease.

We assessed the effects of post‐exercise cold‐water immersion (CWI) in modulating PGC‐1α mRNA expression in response to exercise commenced with low muscle glycogen availability. In a randomized repeated‐measures design, nine recreationally active males completed an acute two‐legged high‐intensity cycling protocol (8 × 5 min at 82.5% peak power output) followed by 10 min of two‐legged post‐exercise CWI (8°C) or control conditions (CON). During each trial, one limb commenced exercise with low (LOW: <300 mmol·kg −1 dw) or very low (VLOW: <150 mmol·kg −1 dw) pre‐exercise glycogen concentration, achieved via completion of a one‐legged glycogen depletion protocol undertaken the evening prior. Exercise increased ( P < 0.05) PGC‐1α mRNA at 3 h post‐exercise. Very low muscle glycogen attenuated the increase in PGC‐1α mRNA expression compared with the LOW limbs in both the control (CON VLOW ~3.6‐fold vs. CON LOW ~5.6‐fold: P = 0.023, ES 1.22 Large) and CWI conditions (CWI VLOW ~2.4‐fold vs. CWI LOW ~8.0 fold: P = 0.019, ES 1.43 Large). Furthermore, PGC‐1α mRNA expression in the CWI‐LOW trial was not significantly different to the CON LOW limb ( P = 0.281, ES 0.67 Moderate). Data demonstrate that the previously reported effects of post‐exercise CWI on PGC‐1α mRNA expression (as regulated systemically via β‐adrenergic mediated cell signaling) are offset in those conditions in which local stressors (i.e., high‐intensity exercise and low muscle glycogen availability) have already sufficiently activated the AMPK‐PGC‐1α signaling axis. Additionally, data suggest that commencing exercise with very low muscle glycogen availability attenuates PGC‐1α signaling.