Aerobic exercise with blood flow restriction causes local and systemic hypoalgesia and increases circulating opioid and endocannabinoid levels

Abstract

Aim: This study examined the effect of aerobic exercise with and without blood flow restriction on exercise-induced hypoalgesia and endogenous opioid and endocannabinoid systems. Methodology: In a randomised crossover design, pain-free individuals performed 20 min of cycling in four experimental trials: 1) Low intensity aerobic exercise (LI-AE) at 40% V̇O2max; 2) LI-AE with low pressure BFR (BFR40); 3) LI-AE with high pressure BFR (BFR80); and 4) High intensity aerobic exercise (HI-AE) 70% V̇O2max. Pressure pain thresholds (PPT) were assessed before and 5 min post-exercise. Circulating concentrations of beta-endorphin and 2-arachidonoylglycerol were assessed before and 10 min post-exercise. Results: In the exercising legs, post-exercise PPTs were increased following BFR40 and BFR80 compared to LI-AE (23-32% vs 1-2%, respectively). Post-exercise PPTs were comparable to HI-AE (17-20%) with BFR40 and greater with BFR80 (30-32%). Both BFR80 and HI-AE triggered comparable systemic hypoalgesia in remote areas of the body (26-28% vs 19-21%). Post-exercise circulating beta-endorphin concentration was increased following BFR40 (11%) and HI-AE (14%, with the greatest change observed following BFR80 (29%). Post-exercise circulating 2-arachidonoylglycerol concentration was increased following BFR40 (22%) and BFR80 (20%), with the greatest change observed following HI-AE (57%). Conclusion: Addition of BFR to LI-AE can trigger both local and systemic hypoalgesia that is not observed follow LI-AE alone and activate endogenous opioid and endocannabinoid systems of pain inhibition. Compared to HI-AE, local and systemic hypoalgesia following LI-AE with high pressure BFR is greater and comparable, respectively. LI-AE with BFR may help pain management in load compromised individuals.

Potential physiological responses contributing to the ergogenic effects of acute ischemic preconditioning during exercise: A narrative review

“…IPC-induced hypoalgesia may be governed by endogenous substances that have antinociceptive effects on pain pathways. Metabolic mediators including adenosine, bradykinin, opioids, and endocannabinoids–all of which are involved in pain signalling during exercise ( Sgherza et al, 2002 ; Murase et al, 2010 ; Aguiar et al, 2020 ; Hughes and Patterson, 2020 ; Hughes et al, 2021 )—have been purported to contribute to the protective response to RIPC ( Lee et al, 1996 ; Tomai et al, 1999 ; Cohen et al, 2000 ; Schoemaker and van Heijningen, 2000 ; Dickson et al, 2002 ; Patel et al, 2002 ; Hajrasouliha et al, 2008 ). Furthermore, the endogenous release of some of these autacoids is thought to modulate the stimulation and signalling of group III/IV afferents ( Amann et al, 2009 , Amann et al, 2011 ; Bouffard et al, 2021 ).…”

“…Indeed, activation of opioid and endocannabinoid receptors in the central and peripheral sites of the pain pathway such as the spine and peripheral nerves can modulate ascending and descending pain signalling ( Sgherza et al, 2002 ; Hughes and Patterson, 2020 ; Hughes et al, 2021 ). Specifically, plasma concentrations of an opioid neuropeptide known as beta-endorphin (BE) and the endocannabinoid endogenous ligand agonist 2-arachidonoylglycerol (2-AG) have recently been shown to be elevated following BFR exercise in humans ( Hughes and Patterson, 2020 ; Hughes et al, 2021 ). Although there is a distinction between BFR and IPC, the similarities between these techniques involves overlapping mechanisms ( Jessee et al, 2018 ; Patterson et al, 2019 ), which may implicate the involvement of these substances in the IPC response.…”

Exercise‐induced hypoalgesia with end‐stage knee osteoarthritis during different blood flow restriction levels: Sham‐controlled crossover study

“…Research models have identified several possible mechanisms to explain EIH, like conditioned pain modulation, recruitment of high threshold motor units, a link between baroreceptors and pain pathways, and ischemic and metabolite‐induced pain, which are thought to trigger descending inhibitory pathways 10,16 . Recently, first evidence for the underlying mechanisms of EIH with BFR resistance training hint at the endogenous opioid and endocannabinoid systems and conditioned pain modulation associated with the augmented physiological stress of BFR training 10,37 …”

Blood Flow Restriction Training for Tendinopathy Rehabilitation: A Potential Alternative to Traditional Heavy-Load Resistance Training

“…Whilst traditional resistance training utilises heavy training loads of 70% or more of 1 repetition maximum (1-RM), low intensity BFRT typically uses loads in the range of 20-40% of 1RM, which may be more tolerable for patients not able to tolerate high muscle-tendon training loads, while still preventing muscle atrophy and promoting hypertrophy [11,133,134]. Additionally, BFRT has been shown to cause exercise-induced hypoalgesia through endogenous opioid and endocannabinoid mechanisms, so could therefore be a useful pain management tool in early musculoskeletal rehabilitation, particularly in the presence of an acute pain response [135][136][137][138].…”