Comparative Analysis of the Effects of Exercise and Kapalbhati Pranayama on Heart Rate Variability and Electroencephalogram Activity: Unveiling Physiological and Cognitive Insights.

Physical activity and mindfulness techniques, such as exercise and Kapalbhati Pranayama, are known to have positive effects on health and well-being. However, limited research has directly compared their impact on physiological and psychological parameters. This study aimed to investigate and compare the effects of exercise and Kapalbhati Pranayama on Heart Rate Variability (HRV) and Electroencephalogram (EEG) activity, shedding light on their contributions to overall health and mental well-being. The study was conducted at All India Institute of Medical Sciences (AIIMS) in Bhopal, India, from 2018 to 2022. A prospective interventional design was employed over two months, involving 20 participants with normal BMI and no respiratory or cardiac conditions. Exclusion criteria included lung or cardiac diseases, smoking history, dyspnoea during physical activity, pedal edema, and high blood pressure. The Kapalbhati Pranayama intervention was supervised and limited to 5 minutes. HRV was assessed using the HRV Brain Tap Neuralchek Machine before, during, and after Kapalbhati. For exercise, a mild-intensity cycling protocol was performed on healthy volunteers aged 20 to 50. HRV was recorded before, during, and after exercise. The EEG analysis revealed notable changes in brain wave patterns. At baseline, participants exhibited higher levels of delta, theta, and alpha waves, indicating a state of relaxation and calmness. During exercise, there was a significant increase in beta waves and a decrease in delta, theta, and alpha waves, reflecting heightened brain activity and alertness. After Kapalbhati, beta wave levels remained elevated, while delta and theta wave suppression was more pronounced, suggesting a stimulating effect on the brain similar to exercise. The changes in beta and gamma EEG waves could be attributed to factors such as exercise intensity, duration, frequency, and the release of endorphins during both exercise and Kapalbhati. The HRV analysis demonstrated distinct responses to exercise and Kapalbhati. Exercise led to a significant reduction in HRV parameters, characterized by increased heart rate and decreased time-domain HRV measures, aligning with the typical sympathetic nervous system dominance during physical activity. In contrast, Kapalbhati's impact on HRV parameters was milder, with minor changes in heart rate and subtle alterations in time-domain HRV measures. The high LF/HF ratio during Kapalbhati suggested a potential stimulation of the sympathetic nervous system. More comprehensive research is required to confirm these findings and understand the long-term effects of Kapalbhati on HRV and cardiovascular health. This study contributes to the understanding of how exercise and Kapalbhati Pranayama affect both cognitive and cardiovascular aspects of health. It highlights that both interventions increase brain activity and alertness, but Kapalbhati may have a more potent effect. Exercise significantly reduces HRV parameters, indicating sympathetic nervous system dominance, while Kapalbhati has milder HRV effects. Further research with larger and more diverse populations is essential to confirm and expand on these findings, providing insights into optimizing cognitive function and cardiovascular health through tailored approaches of exercise and Kapalbhati Pranayama.

Light-emitting diode therapy reduces persistent inflammatory pain: Role of interleukin 10 and antioxidant enzymes.

BACKGROUND: During the last decades, the use of light-emitting diode therapy (LEDT) has increased significantly for the treatment of wound healing, analgesia and inflammatory processes. Nevertheless, scientific data on the mechanisms responsible for the therapeutic effect of LEDT are still insufficient. Thus, this study investigated the analgesic, anti-inflammatory and anti-oxidative effect of LEDT in the model of chronic inflammatory hyperalgesia. EXPERIMENTAL PROCEDURES: Mice injected with Complete Freund's Adjuvant (CFA) underwent behavioral, i.e. mechanical and hot hyperalgesia; determination of cytokine levels (tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß), IL-10), oxidative stress markers (protein carbonyls and thiobarbituric acid reactive species (TBARS)) and antioxidant enzymes (catalase (CAT) and superoxide dismutase (SOD)). Additionally, mice were pretreated with either naloxone or fucoidin and mechanical hyperalgesia was assessed. RESULTS: LEDT inhibited mechanical and thermal hyperalgesia induced by CFA injection. LEDT did not reduce paw edema, neither influenced the levels of TNF-α and IL1-ß; although it increased the levels of IL-10. LEDT significantly prevented TBARS increase in both acute and chronic phases post-CFA injection; whereas protein carbonyl levels were reduced only in the acute phase. LEDT induced an increase in both SOD and CAT activity, with effects observable in the acute but not in the chronic. And finally, pre-administration of naloxone or fucoidin prevented LEDT analgesic effect. CONCLUSIONS: These data contribute to the understanding of the neurobiological mechanisms involved in the therapeutic effect of LEDT as well as provides additional support for its use in the treatment of painful conditions of inflammatory etiology.

Peripheral and spinal activation of cannabinoid receptors by joint mobilization alleviates postoperative pain in mice.

The present study was undertaken to investigate the relative contribution of cannabinoid receptors (CBRs) subtypes and to analyze cannabimimetic mechanisms involved in the inhibition of anandamide (AEA) and 2-arachidonoyl glycerol degradation on the antihyperalgesic effect of ankle joint mobilization (AJM). Mice (25-35g) were subjected to plantar incision (PI) and 24h after surgery animals received the following treatments, AJM for 9min, AEA (10mg/kg, intraperitoneal [i.p.]), WIN 55,212-2 (1.5mg/kg, i.p.), URB937 (0.01-1mg/kg, i.p.; a fatty acid amide hydrolase [FAAH] inhibitor) or JZL184 (0.016-16mg/kg, i.p.; a monoacylglycerol lipase [MAGL] inhibitor). Withdrawal frequency to mechanical stimuli was assessed 24h after PI and at different time intervals after treatments. Receptor specificity was investigated using selective CB1R (AM281) and CB2R (AM630) antagonists. In addition, the effect of the FAAH and MAGL inhibitors on the antihyperalgesic action of AJM was investigated. AJM, AEA, WIN 55,212-2, URB937 and JZL184 decreased mechanical hyperalgesia induced by PI. The antihyperalgesic effect of AJM was reversed by pretreatment with AM281 given by intraperitoneal and intrathecal routes, but not intraplantarly. Additionally, intraperitoneal and intraplantar, but not intrathecal administration of AM630 blocked AJM-induced antihyperalgesia. Interestingly, in mice pretreated with FAAH or the MAGL inhibitor the antihyperalgesic effect of AJM was significantly longer. This article presents data addressing the CBR mechanisms underlying the antihyperalgesic activity of joint mobilization as well as of the endocannabinoid catabolic enzyme inhibitors in the mouse postoperative pain model. Joint mobilization and these enzymes offer potential targets to treat postoperative pain.

Light-emitting diode therapy induces analgesia and decreases spinal cord and sciatic nerve tumour necrosis factor-α levels after sciatic nerve crush in mice.

BACKGROUND: Neuropathic pain is severely debilitating and resistant to pharmacological approaches; therefore, the study of therapies to complement its treatment is especially relevant. In a case report study, light-emitting diode therapy (LEDT) has shown analgesic activity as well as reduced the expression of pro-inflammatory cytokines in a rabbit osteoarthritis model and in calcaneal tendinitis in rats. Although LEDT stimulated morphofunctional recovery after nerve injury in rats, its effect against neuropathic pain has not been tested. METHODS: To that purpose, mice under anaesthesia were subjected to the sciatic nerve crush (SNC) model. On the seventh post-operative day, after determining analgesic dose (energy density in joules), LEDT (950 nm, 80 mW/cm2, 2.5 J/cm2 ) was irradiated, daily for a period of 15 days, on the skin over the crush site. RESULTS: Compared with the SNC group, LEDT reduced mechanical hypersensitivity but not cold hypersensitivity which is induced by SNC, decreased spinal cord and sciatic nerve levels of tumour necrosis factor alpha (TNF-α) but did not alter interleukin (IL)-1ß and IL-10 levels, and finally, failed to accelerate motor functional recovery and morphological nerve regeneration. CONCLUSION: Taken together, these data provide first-hand evidence of LEDT effectiveness against neuropathic pain induced by SNC, with corresponding decrease of pro-inflammatory cytokine levels, both in the sciatic nerve and in the spinal cord, although at a small analgesic dose, LEDT failed to accelerate nerve regeneration.

Glycogen synthase kinase 3-specific inhibitor AR-A014418 decreases neuropathic pain in mice: evidence for the mechanisms of action.

The present study examined the antihyperalgesic effect of a specific inhibitor of Glycogen Synthase Kinase 3 (GSK3), AR-A014418, on the partial ligation of the sciatic nerve (PSNL), a neuropathic pain model in mice and investigated some mechanisms of action. AR-A014418 (0.01-1 mg/kg) administered by intraperitoneal route (i.p.) inhibited mechanical hyperalgesia. This action started 30 min after i.p. administration and remained significant up to 2 h. When administered daily for 5 days, AR-A014418 (0.3 mg/kg, i.p.) significantly reduced the mechanical hyperalgesia caused by PSNL. Intraperitoneal (i.p.) treatment with AR-A014418 (0.3 mg/kg) also significantly inhibited cold hyperalgesia induced by PSNL. Pre-administration of PCPA (100 mg/kg, i.p., inhibitor of serotonin synthesis) and AMPT (100 mg/kg, i.p., inhibitor of tyrosine hydroxylase), but not l-arginine (600 mg/kg, i.p., a nitric oxide precursor), significantly reduced the mechanical hyperalgesia elicited by AR-A014418. Furthermore, the administration of AR-A014418 significantly prevented the increase of TNF-α (inhibition of 76±8%) and IL-1ß (inhibition of 62±10%), but did not alter lumbar spinal cord IL1-ra and IL-10 levels. Finally, intraperitoneal administration of AR-A014418 did not affect locomotor activity in the open-field test. Taken together, these results provide experimental evidence indicating that AR-A014418 produces marked antihyperalgesic effects in neuropathic pain in mice, possibly due to mechanisms that reduce proinflammatory cytokines, as well as increases in serotonergic and catecholaminergic pathways. The present study suggests that GSK3 may be a novel pharmacological target for the treatment of neuropathic pain and AR-A014418 might be a potential molecule of interest for chronic pain relief.

Manual acupuncture inhibits mechanical hypersensitivity induced by spinal nerve ligation in rats.

Manual acupuncture (MA) has presented analgesic activity against neuropathic pain in patients and animal models, yet a series of questions remain: Is MA effectiveness dependent of acupoint selection or combination? Is it equally efficient when treatment starts on the initial (acute) or sub-chronic phase of spinal nerve ligation (SNL)-induced neuropathy? Is MA effect related to the release of endogenous opioids? Does MA produce similar effects to gabapentin? To answer these questions rats submitted to the L5/L6 SNL injury were treated with unilateral MA (ST36 (Zusanli), SP6 (Sanyingjiao) or ST36+SP6 acupoint stimulation); or with gabapentin (30 mg/kg i.p., used as positive control). Both acupoints have been demonstrated to present analgesic activity and are used in clinical practice and basic science research. In addition, we investigated the influence of naloxone (1 mg/kg i.p., a nonselective opioid receptor antagonist) on MA treatment and also the effect of unilateral ST36+SP6 MA treatment beginning acutely (5 days) or sub-chronically (14 days) after SNL. Our results demonstrate that single or combined unilateral stimulation was able to reduce mechanical hypersensitivity with treatment beginning in both acute and sub-chronic phases of SNL-induced neuropathy; MA effect was blocked by naloxone, and finally; SP6+ST36 MA presented similar effect to gabapentin (30 mg/kg). In conclusion, our results demonstrate, for the first time, that unilateral MA (ST36, SP6 or ST36+SP6) reduces hypersensitivity induced by the SNL with effect dependent of the opioid system and comparable with the one obtained with gabapentin (used as positive control).