Chronic methamphetamine use increases apoptosis, leading to heart failure and sudden cardiac death. Previous studies have shown the importance of high-intensity interval training (HIIT) in reducing indices of cardiac tissue apoptosis in different patients, but in the field of sports science, the molecular mechanisms of apoptosis in methamphetamine-dependent rats are still unclear. The present article aimed to investigate the changes in cardiac apoptosis markers in methamphetamine-dependent rats in response to HIIT. Left ventricular tissue was used to evaluate caspase-3, melusin, FAK, and IQGAP1 gene expression. Rats were divided into four groups: sham, methamphetamine (METH), METH-control, and METH-HIIT. METH was injected for 21 days and then the METH-HIIT group performed HIIT for 8 weeks at 5 sessions per week. The METH groups showed increased caspase-3 gene expression and decreased melusin, FAK, and IQGAP1 when compared to the sham group. METH-HIIT showed decreased caspase-3 and increased melusin and FAK gene expression compared with the METH and METH-control groups. The IQGAP1 gene was higher in METH-HIIT when compared with METH, while no difference was observed between METH-HIIT and METH-control. Twenty-one days of METH exposure increased apoptosis markers in rat cardiac tissue; however, HIIT might have a protective effect, as shown by the apoptosis markers.

We aimed to evaluate the effects of seven weeks of aerobic exercise training and piperine on paraquat-induced lung damage. Forty-eight male Wistar rats (230 g, six-eight weeks old) were randomly divided into six groups (n = 8): sham, paraquat (5 mg/kg three times a week; intraperitoneally), paraquat + piperine (10 mg/kg/day; orally), paraquat + aerobic exercise training, paraquat + piperine + aerobic exercise training; and paraquat + vitamin E (20 mg/kg/day; orally) as a positive control. Rats were sacrificed on day 50, and both lung tissues were isolated to measure oxidative (MDA), anti-oxidative (GSH), inflammatory (TNF-α), anti-inflammatory (IL-10) markers, and histological evaluations (hematoxylin-eosin staining). The results of the present study revealed that paraquat significantly decreased body weight, GSH, GSH/MDA ratio, IL-10, and IL-10/TNF-α ratio while increasing MDA, TNF-α, and histopathological damage in lung tissue (P < 0.01 to 0.001). In contrast, treatment with all four interventions meaningfully diminished oxidative, inflammatory markers, and histopathological damage while propagating body weight, anti-oxidative and anti-inflammatory markers following the paraquat-induced lung damage (P < 0.05 to P < 0.001). Interestingly, piperine and piperine + exercise training possessed stronger protective effects against paraquat-induced lung damage than exercise training alone (P < 0.01 to 0.001). Treatment with piperine, exercise training, piperine + exercise training, and vitamin E significantly ameliorated paraquat-induced lung damage. Interestingly, the piperine and piperine + exercise training had more protective effects than other groups. Therefore, piperine and the combination of piperine and exercise training may be valuable candidates for preventing lung injuries.

Mitochondrial fission and fusion both contribute to maintaining mitochondrial function and optimizing bioenergetic capacity. The aim of this study was to compare the effect of aerobic and resistance training on mitochondrial fission and fusion markers in skeletal and cardiac muscles of Wistar rats. 24 male Wistar rats were randomly divided into four groups of moderate-intensity interval training (MIIT), high-intensity interval training (HIIT), resistance training (RT) and control (CON). The MIIT and HIIT groups performed treadmill exercises with an intensity of 60–65% and 80–85% of the maximum speed, respectively, while the RT group performed resistance training with an intensity of 30–60% of the rat’s body weight for 8 weeks. The soleus (SOL), extensor digitorum longus (EDL) and left ventricular tissues were used to evaluate markers of mitochondrial fission and fusion PGC-1α (fusion/fission), Opa-1 (fusion), Fis-1 (fission), Drp-1 (fission), Mfn-1 and Mfn-2 (fusion) genes expression. In all three tissues, a significant increase in some mitochondrial fusion markers was observed after 8 weeks of training (p = < 0.0001–0.0452). Furthermore, a significant decrease in cardiac mitochondrial fission markers was observed in all three groups (p = < 0.0001–0.0156). This reduction in some markers was evident in the SOL tissue of the HIIT group (p < 0.0001 for Drp-1 and p = 0.0007 for Fis-1) and in the EDL tissue of the RT group (p = 0.0005 for Fis-1 and p = 0.0012 for Drp-1). The mitochondrial fission/fusion markers in the heart (p = 0.0007–0.0449) and SOL (p = 0.0050–0.0258) tissues of the HIIT group had more changes than the RT group, while the mitochondrial fission markers in the EDL tissue of the RT group had a lower level than the HIIT (p = 0.0087 for Drp-1) and MIIT (p = 0.0130 for Fis-1 and p = 0.0010 for Drp-1) groups. Our study demonstrated that HIIT, through better regulation of mitochondrial fusion and fission than RT, improves mitochondrial dynamics in cardiac and SOL tissues.