Cold water immersion or LED therapy after training sessions: effects on exercise-induced muscle damage and performance in rats.

Cryotherapy and phototherapy have been suggested as recovery methods due to their anti-inflammatory effects. They may also induce mitochondrial biogenesis, thus favoring endurance training adaptation. The aim of this study was to evaluate the anti-inflammatory and ergogenic effects of phototherapy or cold water immersion (CWI) applied daily after exercise in rats. Thirty-five rats were divided into five groups: control (CO), non-exercised (CE), passive recovery (PR), cold water immersion (CWI), and LED therapy (LED). The CO and CE groups were not submitted to training; however, the CE were submitted to an exhaustion test after the training period. Low-intensity swimming training (21 sessions, 45 min) was performed followed by passive recovery (PR), CWI (10 °C, 5 min), or infrared irradiation (940 nm, 4 J/cm2). Forty-eight hours after the final training session, the CE, PR, CWI, and LED animals were submitted to an exhaustion test. The animals were euthanized 24 h later and submitted to hematological, creatine kinase (CK), and C-reactive protein (PCR) analysis. Gastrocnemius and soleus muscles were submitted to histological analysis. No differences in blood cell counts, CK, and PCR were detected between groups. The CE group presented an increased number of areas with necrosis in the gastrocnemius and soleus muscles. The PR group presented the highest frequency of areas with edema and inflammation followed by CWI and LED groups. None of the recovery methods improved the performance in the exhaustion test. Successive applications of recovery methods do not improve exercise performance, but downmodulate the inflammation and prevent muscle necrosis.

Post-exercise cold water immersion does not alter high intensity interval training-induced exercise performance and Hsp72 responses, but enhances mitochondrial markers.

This study aims to evaluate the effect of regular post-exercise cold water immersion (CWI) on intramuscular markers of cellular stress response and signaling molecules related to mitochondria biogenesis and exercise performance after 4 weeks of high intensity interval training (HIIT). Seventeen healthy subjects were allocated into two groups: control (CON, n = 9) or CWI (n = 8). Each HIIT session consisted of 8-12 cycling exercise stimuli (90-110 % of peak power) for 60 s followed by 75 s of active recovery three times per week, for 4 weeks (12 HIIT sessions). After each HIIT session, the CWI had their lower limbs immersed in cold water (10 °C) for 15 min and the CON recovered at room temperature. Exercise performance was evaluated before and after HIIT by a 15-km cycling time trial. Vastus lateralis biopsies were obtained pre and 72 h post training. Samples were analyzed for heat shock protein 72 kDa (Hsp72), adenosine monophosphate-activated protein kinase (AMPK), and phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) assessed by western blot. In addition, the mRNA expression of heat shock factor-1 (HSF-1), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), nuclear respiratory factor 1 and 2 (NRF1 and 2), mitochondrial transcription factor A (Tfam), calcium calmodulin-dependent protein kinase 2 (CaMK2) and enzymes citrate synthase (CS), carnitine palmitoyltransferase I (CPT1), and pyruvate dehydrogenase kinase (PDK4) were assessed by real-time PCR. Time to complete the 15-km cycling time trial was reduced with training (p < 0.001), but was not different between groups (p = 0.33). The Hsp72 (p = 0.01), p38 MAPK, and AMPK (p = 0.04) contents increased with training, but were not different between groups (p > 0.05). No differences were observed with training or condition for mRNA expression of PGC-1α (p = 0.31), CPT1 (p = 0.14), CS (p = 0.44), and NRF-2 (p = 0.82). However, HFS-1 (p = 0.007), PDK4 (p = 0.03), and Tfam (p = 0.03) mRNA were higher in CWI. NRF-1 decrease in both groups after training (p = 0.006). CaMK2 decreased with HIIT (p = 0.003) but it was not affected by CWI (p = 0.99). Cold water immersion does not alter HIIT-induced Hsp72, AMPK, p38 MAPK, and exercise performance but was able to increase some markers of cellular stress response and signaling molecules related to mitochondria biogenesis.

LED therapy or cryotherapy between exercise intervals in Wistar rats: anti-inflammatory and ergogenic effects.

The aim of this study was to test, between two bouts of exercise, the effects of light-emitting diode (LED) therapy and cryotherapy regarding muscle damage, inflammation, and performance. Male Wistar rats were allocated in four groups: control, passive recovery (PR), cryotherapy (Cryo), and LED therapy. The animals were submitted to 45 min of swimming exercise followed by 25 min of recovery and then a second bout of either 45 min of exercise (muscle damage analysis) or time to exhaustion (performance). During the rest intervals, the rats were kept in passive rest (PR), submitted to cold water immersion (10 min, 10 °C) or LED therapy (940 nm, 4 J/cm(2)) of the gastrocnemius muscle. Blood samples were collected to analyze creatine kinase activity (CK), C-reactive protein (CRP), and leukocyte counts. The soleus muscles were evaluated histologically. Time to exhaustion was recorded during the second bout of exercise. After a second bout of 45 min, the results demonstrated leukocytosis in the PR and Cryo groups. Neutrophil counts were increased in all test groups. CK levels were increased in the Cryo group. CRP was increased in PR animals. The PR group presented a high frequency of necrosis, but the LED group had fewer necrotic areas. Edema formation was prevented, and fewer areas of inflammatory cells were observed in the LED group. The time to exhaustion was greater in both the LED and Cryo groups, without differences in CK levels. CRP was decreased in LED animals. We conclude that LED therapy and cryotherapy can improve performance, although LED therapy is more efficient in preventing muscle damage and local and systemic inflammation.

Effects of chronic caffeine intake and low-intensity exercise on skeletal muscle of Wistar rats.

Caffeine can affect muscle cell physiology and the inflammatory response during exercise. The purpose of this study was to analyse muscle damage markers and inflammatory cell infiltration into the soleus muscle of sedentary and exercised animals submitted to chronic caffeine intake. Thirty-two male Wistar rats were divided into the following four groups (n = 8 per group): sedentary control (SCO); sedentary + caffeine (SCAF); trained control (TCO); and trained + caffeine (TCAF). The animals were housed in individual cages and received tap water or caffeine (1 mg ml(-1)); they were maintained at rest or submitted to swimming for up to 40 min day(-1) with a 4% load, five times per week for 30 days. Blood samples were collected for analysis of serum lactate, creatine kinase and calcium. The right soleus muscle and the epididymal fat depot were weighed, and the muscle was submitted to histological analysis. Training and caffeine did not change body or muscle weight, food and liquid intake or serum calcium levels among groups. Decreased fat tissue (P < 0.05) was observed in the SCAF (4.05 ± 1.03 g), TCO (4.14 ± 0.78 g) and TCAF groups (4.02 ± 1.02 g) compared with the SCO group (5.31 ± 1.06 g). Serum creatine kinase activity was significantly reduced in the SCAF (787.3 ± 230.3 U l(-1)), TCO (775.3 ± 232.3 U l(-1)) and TCAF groups (379.5 ± 110.5 U l(-1)) compared with the SCO group (1610.2 ± 276.5 U l(-1)). Few damaged muscle fibres (P < 0.05) were found in SCAF (16.7 ± 12.8%) and TCAF groups (17.3 ± 11.7%) compared with the SCO group (53.6 ± 13.9%). The SCAF group presented fewer fields with inflammatory cells (7.6 ± 8.7 fields) compared with the SCO group (123 ± 146 fields). The results suggest that the chronic intake of caffeine, as well as chronic low-intensity exercise, decreased muscle damage and inflammatory infiltration into skeletal muscle.