Cannabidiol and Sports Performance: a Narrative Review of Relevant Evidence and Recommendations for Future Research Open Access This article is licensed under a Creative Commons Attribution 4.0 CBD is available in in a dizzying array of shapes and styles: lotions, tinctures, capsules, baked goods, coffee—it’s even in pet food.
Cannabidiol and Sports Performance: a Narrative Review of Relevant Evidence and Recommendations for Future Research
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Cannabidiol (CBD) is a non-intoxicating cannabinoid derived from Cannabis sativa. CBD initially drew scientific interest due to its anticonvulsant properties but increasing evidence of other therapeutic effects has attracted the attention of additional clinical and non-clinical populations, including athletes. Unlike the intoxicating cannabinoid, Δ 9 -tetrahydrocannabinol (Δ 9 -THC), CBD is no longer prohibited by the World Anti-Doping Agency and appears to be safe and well-tolerated in humans. It has also become readily available in many countries with the introduction of over-the-counter “nutraceutical” products. The aim of this narrative review was to explore various physiological and psychological effects of CBD that may be relevant to the sport and/or exercise context and to identify key areas for future research. As direct studies of CBD and sports performance are is currently lacking, evidence for this narrative review was sourced from preclinical studies and a limited number of clinical trials in non-athlete populations. Preclinical studies have observed robust anti-inflammatory, neuroprotective and analgesic effects of CBD in animal models. Preliminary preclinical evidence also suggests that CBD may protect against gastrointestinal damage associated with inflammation and promote healing of traumatic skeletal injuries. However, further research is required to confirm these observations. Early stage clinical studies suggest that CBD may be anxiolytic in “stress-inducing” situations and in individuals with anxiety disorders. While some case reports indicate that CBD improves sleep, robust evidence is currently lacking. Cognitive function and thermoregulation appear to be unaffected by CBD while effects on food intake, metabolic function, cardiovascular function, and infection require further study. CBD may exert a number of physiological, biochemical, and psychological effects with the potential to benefit athletes. However, well controlled, studies in athlete populations are required before definitive conclusions can be reached regarding the utility of CBD in supporting athletic performance.
CBD has been reported to exert a number of physiological, biochemical, and psychological effects that have the potential to benefit athletes.
The available evidence is preliminary, at times inconsistent, and largely based on preclinical studies involving laboratory animals.
Rigorous, controlled investigations clarifying the utility of CBD in the sporting context are warranted.
Cannabis sativa contains numerous chemical compounds with potential bioactive effects, including at least 144 cannabinoids [56, 76]. The most studied of the cannabinoids are Δ 9 -tetrahydrocannabinol (Δ 9 -THC), renowned for its distinctive intoxicating effects [73, 123], and cannabidiol (CBD)—a non-intoxicating cannabinoid that is particularly enriched in industrial hemp cultivars grown for seed and fibre . CBD was first isolated in 1940 and initially considered to be biologically inactive, with no apparent therapeutic or “subjective” drug effects . However, in 1973, Carlini et al.  demonstrated anticonvulsant effects of CBD in a preclinical model, which were later mirrored in humans suffering from intractable epilepsy . A subsequent rise in research into CBD  has uncovered interactions with numerous molecular targets  and a range of potential therapeutic applications . Following successful phase 3 clinical trials [53, 54, 172], the oral CBD solution, Epidiolex®, has also recently gained Food and Drug Administration approval as a regulated prescription medication to treat certain forms of paediatric epilepsy.
Recently, interest in CBD has intensified among the general population as evidenced by an exponential rise in internet searches for ‘CBD’ in the United States (USA) . Some professional athletes (e.g. golfers, rugby players) also appear to be using CBD (e.g. ‘Team cbdMD’ https://www.cbdmd.com/), despite there being no published studies demonstrating beneficial effects on sport or exercise performance. In many jurisdictions, including the USA and Europe, access to regulated, prescription CBD (i.e. Epidiolex®) is limited to patients with intractable epilepsy. However, a wide range of low dose (e.g. 5–50 mg·d −1 ) CBD-containing “nutraceuticals” (primarily in oil or capsule form) have become readily available online and over-the-counter (e.g. pharmacies, health food stores) [20, 125]. This includes some varieties that are marketed specifically to recreational and elite athletes (e.g. cbdMD, fourfivecbd). The use of these products is likely to become even more widespread if the World Health Organization’s recommendation that CBD no longer be scheduled in the international drug control conventions is adopted by the United Nations member states .
Cannabis has been prohibited in all sports during competition since the World Anti-Doping Agency first assumed the responsibility of establishing and maintaining the list of prohibited substances in sport 15 years ago . In 2018, however, CBD was removed from the Prohibited List , presumably on the basis of mounting scientific evidence that the cannabinoid is safe and well-tolerated in humans [16, 169], even at very high doses (e.g. 1500 mg·day −1 or as an acute dose of 6000 mg) . While several recent reviews have described the impact of cannabis on athlete health and performance [99, 176, 188], the influence of CBD alone has yet to be addressed.
The aim of this narrative review was to explore evidence on the physiological, biochemical, and psychological effects of CBD that may be relevant to sport and/or exercise performance and to identify relevant areas for future research. Given the absence of studies directly investigating CBD and sports performance, this review draws primarily on preclinical studies involving laboratory animals and a limited number of clinical trials involving non-athlete populations.
Cannabidiol (CBD): Molecular Targets, Pharmacokinetics and Dosing
The distinctive intoxicating effects of Δ 9 -THC (as well as some of its therapeutic effects) involve the activation of CB1R (the cannabinoid type 1 receptor) . This ubiquitous receptor is expressed throughout the central nervous system, the peripheral nervous system, and in the cardiovascular system, gastrointestinal (GI) tract, skeletal musculature, liver, and reproductive organs . Unlike Δ 9 -THC, CBD is not an agonist of CB1R, although it may act as a negative allosteric modulator (NAM) at this site (i.e. decreasing the potency and/or efficacy of other ligands without activating the receptor itself) [92, 106]. Δ 9 -THC also acts as an agonist at CB2R (the cannabinoid type 2 receptor)  and there is emerging evidence of CBD functioning as a partial agonist at this site . CB2R is primarily located on immune system cells but is also expressed in the cardiovascular system, GI tract, bone, liver, adipose tissue, and reproductive organs . CBD may also influence the endocannabinoid system indirectly via the inhibition of fatty acid amide hydrolase (FAAH), a key enzyme involved in the degradation of the principle endocannabinoid signalling molecule, anandamide (AEA) [92, 110]. The inhibition of FAAH is predicted to lead to an increase in brain and plasma concentrations of AEA, which acts as a partial agonist at CB1R and CB2R, thereby increasing endocannabinoid tone [92, 110]. Increases in endocannabinoid tone may also occur as a result of CBD inhibiting AEA transport via effects on fatty acid-binding proteins (and this mechanism may have more relevance than FAAH inhibition in humans) .
CBD also interacts with many other non-endocannabinoid signalling systems . Briefly, at concentrations ≤ 10 μM, CBD has been reported to interact with the serotonin 1A [5-HT1A] receptor, the orphan G protein-coupled receptor 55, as well as the glycine, opioid, and peroxisome proliferator-activated receptors, various ion channels (e.g. the transient potential vanilloid receptor type 1 channel [TRPV1] and other transient potential vanilloid channels) and various enzymes (e.g. cyclooxygenase (COX)1 and COX2, cytochrome P450 enzymes) [11, 92] (see Ibeas et al.  for review). CBD also possesses antioxidant properties .
It is important to recognise that the molecular targets of CBD are still being established, with many of those identified in in vitro cellular assays still to be validated as occurring in vivo. As such, the functional relevance of many of these interactions remains to be established.
CBD is often consumed orally as oil; however, it can also be ingested in other forms (e.g. gel capsules, tinctures, beverages, and confectionery products) and applied topically [20, 125]. High concentration CBD “vape oils” (i.e. for use in e-cigarette devices) are also available in some countries, as are some CBD-dominant forms of cannabis (sometimes known as “light cannabis”) that can be smoked or vaporised [20, 125]. Pure, synthetic, crystalline CBD was also vaporised in a recent laboratory study .
Taylor et al.  recently conducted a comprehensive analysis of oral CBD oil pharmacokinetics in healthy participants. When administered as a single, oral dose (1500–6000 mg), the time to reach peak plasma concentrations (tmax) was ~4–5 h and the terminal half-life was ~14–17 h. Although tmax did not increase dose-dependently in this investigation , another study , involving a much lower oral dose of CBD (300 mg), did indicate a shorter tmax (i.e. ~2–3 h). Peak plasma concentrations (Cmax) were ~0.9–2.5 μM in Taylor et al. , but increased ~4.9-fold when CBD was administered with a high-fat meal (i.e. ~5.3 μM at 1500 mg dose) . Both studies observed a large amount of inter-individual variation in pharmacokinetic responses [19, 170].
The pharmacokinetics of inhaled CBD are yet to be well characterised. However, smoked “light cannabis” (with a lower Δ 9 -THC and higher CBD content than other varieties) has been reported to elicit high serum CBD concentrations at 30 min post-treatment (that decline over time) . A recent study in which participants vaporised 100 mg of CBD likewise observed high blood CBD concentrations 30 min post-treatment . As neither study collected blood samples within < 30 min of CBD administration, tmax and Cmax are unknown [146, 160].
CBD is metabolised by several cytochrome P [CYP] 450 enzymes (e.g. CYP3A4, CYP2C9, CYP2C19) which convert it to a number of primary and secondary metabolites (e.g. 7-OH-CBD, 6-OH-CBD, and 7-COOH-CBD) . Complex pharmacokinetic interactions may occur when CBD is co-administered with other drugs (e.g. Δ 9 -THC) and dietary constituents (e.g. caffeine) that also utilise these enzymes [6, 163].
Interspecies Dose Conversions
Given the number of preclinical studies involving animal models that will be discussed in this review, it is important to consider interspecies dose equivalence (Table (Table1). 1 ). The USA Food and Drug Administration  recommend the following approach to interspecies dose conversion:
Oral human equivalent CBD doses from mouse and rat intraperitoneal doses
|Mouse to Human CBD Dose Conversion||Rat to Human CBD Dose Conversion|
(mg·kg -1 , i.p.)
(mg·kg -1 , i.p.)
Each HED is based on a body mass of 60 kg and calculated as per the methods described in 2.3 Dose Conversions. The highest documented acute oral CBD dose in humans is 6000 mg; the highest documented chronic oral CBD dose in humans is 1500 mg . HED: Human Equivalent Dose; i.p.: Intraperitoneal; p.o.: Oral
Where HED is the human equivalent dose and Km is a correction factor estimated by dividing the average body mass (BM) of the species (60, 0.020 and 0.150 kg for 11 humans, mice and rats respectively) and by its surface area (see: Nair, et al.  for 12 further details).
Differences between systemic and oral dosing should also be considered . Intraperitoneal (i.p.) dosing is often used in animal studies and has been reported to elicit Cmax values ~7-fold higher than oral dosing in mice . Thus, an “oral equivalent dose” can be approximated by multiplying the i.p. dose by seven  (Table (Table1). 1 ). Intravenous (i.v.) dosing will produce even higher plasma CBD concentrations; however, the authors are not aware of any published data that would facilitate conversion between i.v. and oral dosing in rodents. Please note that these values are intended as a guide only and subject to limitations (e.g. interspecies differences in drug potency and receptor expression/configuration).
Cannabidiol (CBD) in Sport and Exercise Performance
Literature Search Methodology
The clinical and preclinical literature was reviewed to identify studies investigating the effects of CBD that might be relevant within a sport and/or exercise context. The online databases PubMed (MEDLINE), Web of Science (via Thomas Reuters), and Scopus were searched between April and October of 2019 using terms such as: ‘cannabinoid’ ‘cannabidiol’, ‘CBD’ and ‘cannabis’. This review focuses primarily on effects that have been demonstrated in vivo and generally avoids attempting to predict functional effects on the basis of target-oriented in vitro data, given the numerous molecular targets of CBD  and the fact that exercise itself induces complex biochemical changes. Nonetheless, some potential interactions are noted. As our intent was to summarise evidence on a range of potentially relevant topics, rather than provide a detailed assessment of the literature, the reader will be directed to more focused reviews, where appropriate. All doses described are oral and acute (single), unless otherwise stated.
Exercise-Induced Muscle Damage—Muscle Function, Soreness, and Injury
Exercise, particularly when strenuous, unfamiliar, and/or involving an eccentric component, can cause ultrastructural damage to skeletal muscle myofibrils and the surrounding extracellular matrix [36, 59]. This exercise-induced muscle damage (EIMD) impairs muscle function and initiates an inflammatory response . While inflammation is integral to EIMD repair, regeneration, and adaptation , excessive inflammation may contribute to prolonged muscle soreness and delayed functional recovery [7, 158].
CBD modulates inflammatory processes . In preclinical models of acute inflammation, CBD has been reported to attenuate immune cell accumulation (e.g. neutrophils, lymphocytes macrophages) [102, 130, 149, 186], stimulate production of anti-inflammatory cytokines (e.g. interleukin (IL)-4, IL-10) [190, 191, 23] and inhibit production of pro-inflammatory cytokines (e.g. IL-1β, IL-6, IL-8, tumour necrosis factor (TNF)-α) [10, 50, 55, 62, 63, 113, 130, 149, 154, 186] and reactive oxygen species [62, 130, 186]. Models demonstrating such effects have included lung injury induced by chemical treatment  and hypoxic–ischemia (HI) ; liver injury induced by ischemia-reperfusion [63, 130] and alcohol feeding ; myocardial  and renal  ischemia-reperfusion injuries; surgically induced oral lesions ; chemically induced osteoarthritis ; spinal cord contusion injury , and colitis [23, 50, 154] (see Burstein  for review). Anti-inflammatory effects are generally observed at higher CBD doses in vivo (e.g. ≥ 10 mg·kg −1 , i.p.); although, lower doses (e.g. ~1.5 mg·kg −1 , i.p.) have indicated efficacy in some studies . Research investigating the effects of CBD on inflammation in humans is limited and inconclusive [94, 133].
In terms of muscle-specific inflammation, one preclinical study has investigated the effect of high-dose CBD (i.e. 60 mg·kg −1 ·d −1 , i.p.) on transcription and synthesis of pro-inflammatory markers (i.e. IL-6 receptors, TNF-α, TNF-β1, and inducible nitric oxide synthase) in the gastrocnemius and diaphragm of dystrophic MDX mice (a mouse model of Duchenne muscular dystrophy) . In this investigation, CBD attenuated mRNA expression of each marker and reduced plasma concentrations of IL-6 and TNFα. Improvements in muscle strength and coordination, as well as reductions in tissue degeneration, were also reported at this dose. Lower, but still relatively high, CBD doses (20–40 mg·kg −1 ·day −1 , i.p.) had no functional benefits . Of course, it is important to recognise that EIMD and muscular dystrophy differ in their pathophysiology, and so the effects observed in MDX mice may involve mechanisms less relevant to EIMD (e.g. skeletal muscle differentiation, autophagy) .
While CBD could potentially aid in muscle recovery, other anti-inflammatory agents, such as ibuprofen (a non-steroidal anti-inflammatory drug [NSAID]) have been reported to attenuate exercise-induced skeletal muscle adaptation . The precise mechanism(s) underpinning these effects have not been fully elucidated, although it may be that the prevention of inflammation inhibits angiogenesis and skeletal muscle hypertrophy . Human trials also suggest that ibuprofen may not influence EIMD, inflammation, or soreness [144, 175]. Thus, if CBD exerts its effects via similar mechanisms, it could possibly attenuate the benefits of training without influencing muscle function or soreness. Future studies investigating this are clearly warranted to clarify such issues and elucidate the potential benefits of CBD.
Neuroprotection—Concussion and Subconcussion
Recent estimates suggest that 6–36% of high school and collegiate athletes in the USA have experienced more than one concussion , potentially predisposing them to long-term neurodegenerative diseases  and an increased risk of suicide . Concussion is a distinct form of mild traumatic brain injury (TBI) in which a biomechanical force temporarily disrupts normal brain functioning causing neurological–cognitive–behavioural signs and symptoms . Similar injuries that do not produce overt (acute) signs or symptoms are termed “subconcussions” . In TBI, the primary injury occurs as a result of the biomechanical force; secondary injury is then sustained through a complex cascade of events, including HI, cerebral oedema, increased intracranial pressure, and hydrocephalus . These processes are, in turn, related to a number of detrimental neurochemical changes, including glutamate excitotoxicity, perturbation of cellular calcium homeostasis, excessive membrane depolarisation, mitochondrial dysfunction, inflammation, increased free radicals and lipid peroxidation, and apoptosis . While the primary injury may not be treatable, interventions that attenuate secondary sequelae are likely to be of benefit .
Only one study  has investigated the biochemical and neuropsychological effects of CBD in an animal model of TBI. Here, C57BL/6 mice were given chronic CBD treatment (3 μg·day −1 , oral) 1–14 and 50–60 days post- (weight drop) brain insult. CBD attenuated the behavioural (e.g. anxious and aggressive behaviour, depressive-like behaviour, impaired social interactions, pain-related behaviours) and some of the cortical biochemical abnormalities were observed. Specifically, CBD tended to normalise extracellular glutamate, d -aspartate, and γ-aminobutyric acid concentrations in the medial prefrontal cortex, suggesting a reduction in excitotoxicity. However, neuronal damage was not measured directly in this study .
Other preclinical studies have investigated the impact of CBD on different animal models of acute neuronal injury, in particular, acute cerebral HI [4, 13, 31, 68, 69, 80, 81, 83, 100, 105, 127, 129, 142, 143, 153]. Studies administering a single (acute) dose of CBD shortly post-HI (e.g. ≤1 h) have produced inconsistent results. For instance, while Garberg et al. [68, 69] found no effect of CBD (1 or 50 mg·kg −1 , i.v.) on HI-induced neuronal damage in piglets, others observed neuroprotection at similar doses (e.g. 1 mg·kg −1 , i.v [105, 143]., 1 mg·kg −1 , s.c [127, 142]., and 5 mg·kg −1 , i.p .) in piglets and rats. When given chronically, or repeatedly within a short timeframe proximal to the HI event, however, CBD appears to be neuroprotective. Effective dosing strategies have varied and included initiating treatment several days pre-HI (e.g. 100 or 200 μg·day −1 , intracerebroventricular 5 days; Wistar rats ), shortly pre- and/or post-HI 1 , and up to 3 days post-HI (e.g. 3 mg·kg −1 ·day −1 , i.p. 12 days; ddY mice ). Thus, chronic CBD treatment may be more effective than acute intervention. While “pre-incident” dosing might also be beneficial, it is noted that in practice, this would require humans at risk of TBI to use CBD chronically as a prophylactic.
The precise mechanism(s) underpinning the neuroprotective effects of CBD are not completely understood (see Campos et al.  for review), but may involve decreased inflammation, oxidative stress, and excitotoxicity [142, 143] and increased neurogenesis . Preclinical studies have also demonstrated beneficial effects of CBD in other animal models of neurodegeneration (e.g. transgenic model of Alzheimer’s disease [34, 35], brain iron-overload [47, 48]). Collectively, these data suggest that research investigating the utility of CBD in ameliorating the harmful long-term effects of repeated sports concussions is warranted.
Nociceptive and Neuropathic Pain
Persistent pain is common in athletes . Nociceptive pain, which includes inflammatory pain, typically occurs with tissue damage; whereas neuropathic pain typically results from a lesion or disease in the somatosensory nervous system . Neuropathic pain is common among para-athletes with spinal cord injuries and can also arise with surgery (e.g. to treat an existing injury) or if there is repetitive mechanical and/or inflammatory irritation of peripheral nerves (e.g. as in endurance sports) .
Clinical trials investigating the combined effects of Δ 9 -THC and CBD (e.g. Sativex®) on chronic neuropathic pain have yielded promising initial results [87, 114, 151, 156]. However, the therapeutic effects of CBD administered alone have received limited clinical attention. Preclinical (in vivo) studies investigating the effects of CBD on neuropathic and nociceptive pain are summarised in Table Table2. 2 . Despite some methodological inconsistencies (e.g. the pain model, period of treatment, route of delivery), most preclinical studies appear to have observed a significant analgesic effect of CBD [29, 39–41, 51, 70, 75, 78], albeit somewhat less pronounced than the effects of Δ 9 -THC [29, 78] (e.g. Hedges’ g = 0.8 vs. 1.8 ) or of gabapentin (e.g. Hedges’ g = 2.0 ), a commonly used agent for treating neuropathic pain. Capsazepine co-treatment has also been reported to attenuate CBD-induced analgesia, suggesting that the effect may be mediated, at least in part, by the TRPV1 channel [40, 41, 51]. This mechanism is noteworthy as studies have implicated the TRPV1 in the development of mechanical hyperalgesia induced by muscle inflammation [66, 140].
Preclinical studies investigating the effect of CBD on neuropathic and nociceptive pain in vivo
|De Gregorio et al., (2019) ||Wistar rats||SNI||5 mg·kg -1 ·d -1 , s.c. 7 d||CBD sig. decreased mechanical allodynia on Tx day 7.|
|Casey et al., (2017) ||C57BL/6 mice||CCI||30 mg·kg -1 , s.c.||CBD sig. decreased mechanical allodynia 2 h, but not 0.5, 1, 4 or 6 h, post-Tx compared to baseline.|
|0.01, 0.1, 1, 10 or 100 mg·kg -1 , s.c.||CBD dose-dependently decreased mechanical and cold allodynia.|
|King et al., (2017) ||C57BL/6 mice||CT (Paclitaxel)||0.625–20 mg·kg -1 , i.p. 15 min prior to CT on days 1, 3, 5 and 7||1 and 20 mg·kg -1 CBD sig. attenuated the development of mechanical allodynia measured on Tx days 9 and 14, but not 21.|
|CT (Oxaliplatin)||1.25–10 mg·kg -1 , i.p. 15 min prior to CT on days 1, 3, 5 and 7||1.25–10 mg·kg -1 CBD sig. attenuated the development of mechanical allodynia measured on Tx days 2, 4, 7 and 10.|
|CT (Vincristine)||1.25–10 mg·kg -1 , i.p. 15 min prior to CT on days 1, 3, 5 and 7||CBD did not attenuate the development of CT-induced mechanical allodynia measured on Tx days 5, 10, 15 and 22.|
|Harris et al., (2016) ||C57BL/6 mice||CT (Cisplatin)||2 mg·kg -1 , i.p.||CBD sig. decreased tactile allodynia 1 h post-Tx.|
|0.5, 1 or 2 mg·kg -1 , i.p. 30 min prior to CT every second day for 12 d||CBD did not attenuate the development of CT-induced tactile allodynia measured on Tx days 6, 10 and 12.|
|Ward et al., (2014) ||C57BL/6 mice||CT (Paclitaxel)||2.5 or 5 mg·kg -1 ·d -1 , i.p. 15 min prior to CT on days 1, 3, 5 and 7||2.5 and 5 mg·kg -1 ·d -1 CBD attenuated the development of CT-induced mechanical allodynia.|
|Toth et al., (2010) ||CD1 mice||STZ Diabetes||0.1, 1 or 2 mg·kg -1 ·d -1 , i.n. 3 months||1 and 2 mg·kg -1 ·d -1 CBD sig. attenuated the development of thermal and tactile hypersensitivity compared to 0.1 mg·kg -1 ·d -1 CBD.|
|2 mg·kg -1 ·d -1 , i.n. 1 month||CBD did not alleviate developed thermal or tactile hypersensitivity.|
|1, 10 or 20 mg·kg -1 ·d -1 , i.p. 3 months||20 mg·kg -1 ·d -1 CBD sig. attenuated the development of thermal and tactile hypersensitivity compared to 1 mg·kg -1 ·d -1 CBD.|
|20 mg·kg -1 ·d -1 , i.p. 1 month||CBD did not alleviate developed thermal or tactile hypersensitivity.|
|Costa et al., (2007) ||Wistar rats||CCI||2.5, 5, 10 or 20 mg·kg -1 ·d -1 , oral 7 d||5, 10 and 20 mg·kg -1 ·d -1 CBD sig. decreased thermal and mechanical hyperalgesia on Tx day 7.|
|Nociceptive (Inflammatory) Pain|
|Genaro et al., (2017) ||Wistar rats||Incision||0.3, 1, 3, 10 or 30 mg·kg -1 , i.p.||3 mg·kg -1 CBD sig. decreased mechanical allodynia between 30- and 150-min post-Tx; 10 mg·kg -1 CBD sig. decreased mechanical allodynia 60 min post-Tx, only.|
|Hammell et al., (2016) ||Sprague-Dawley rats||FCA||0.6, 3.1, 6.2 or 62.3 mg·kg -1 ·d -1 , t.c. 4 d||6.2 and 62.3 mg·kg -1 CBD sig. decreased pain-related behaviour on Tx day 4 and thermal hyperalgesia on Tx days 2, 3 and 4.|
|Costa et al., (2007) ||Wistar rats||FCA||20 mg·kg -1 ·d -1 , oral 7 d||CBD sig. decreased thermal and mechanical hyperalgesia on Tx day 7.|
|Costa et al., (2004) ||Wistar rats||Carrageenan||5, 7.5, 10, 20 and 40 mg·kg -1 , oral||5, 7.5, 10, 20 and 40 mg·kg -1 ·d -1 CBD sig. decreased thermal hyperalgesia 1–5 h post-Tx.|
|Costa et al., (2004) ||Wistar rats||Carrageenan||10 mg·kg -1 , oral||CBD sig. decreased thermal hyperalgesia 1 h post-Tx.|
The ‘Treatment Effects’ described are in comparison to a vehicle condition, unless otherwise stated
CBD Cannabidiol, CCI Chronic Constriction Injury, CT Chemotherapy, FCA Freund’s Complete Adjuvant, i.n. Intranasal, i.t. Intrathecal, s.c. Subcutaneous, SNI Spared Nerve Injury, STZ Streptozotocin, t.c. Transcutaneously, Tx Treatment
It is important to recognise that the analgesic effect of CBD likely depends on several factors, including the treatment dose and the type of pain involved. Indeed, low doses of CBD (e.g. ≤ 1 mg·kg −1 , i.p.) do not consistently attenuate pain [29, 41, 70, 75, 101]; while higher doses are sometimes found to be more , and other times, less , efficacious than moderate doses in preclinical studies (Table (Table3). 3 ). This highlights the importance of determining a therapeutic dose for CBD in analgesia. Data from King et al.  also demonstrate the selectivity of the response, indicating that CBD only effective in attenuating the development of neuropathic pain induced by certain chemotherapeutic agents (i.e. paclitaxel and oxaliplatin but not vincristine). Thus, placebo-controlled trials of CBD in treating pain in clinical populations and athletes are warranted.
How CBD Can Improve Your Performance in the Gym, Outdoors, and in Your Daily Life
In the span of just a few years, CBD has exploded in the wellness world. In seemingly the blink of an eye, it went from, “CBD? That’s weed, right?”, to being featured in bougie supplement shops that look like Apple stores all across the country. Today, CBD is available in in a dizzying array of shapes and styles: lotions, tinctures, capsules, baked goods, coffee—it’s even in pet food. The market is booming and you’ve likely heard anecdotal evidence of CBD in one form or another helping someone with pain relief, recovery, sleep, or stress. Athletes, in particular, are increasingly touting its wonder-like properties.
So, what’s the deal with CBD, and should you be considering it as part of your nutritional, training, or recovery regime?
CBD is a cannabinoid, but not the one that creates the high you associate with inhaling or ingesting marijuana—that’s THC. While full spectrum CBD products will typically contain small amounts of THC, to be legally sold across the U.S., CBD oils must contain less than 0.03%THC, which is well below the necessary amount to produce any psychoactive response. Broad spectrum CBD products and CBD isolates have no detectable THC at all.
The CBD you keep hearing about is derived from hemp plants, not marijuana, and the two cannabinoids are only cousins in the big cannabis family tree. Another member of the family? Beer’s resinous bitter-maker, hops—when you tip back a pint that smells vaguely of weed, that’s because hops, marijuana, and hemp all share aromatic oils called terpenes. So, yes, holidays at the Cannabis house are probably a good time.
But none of that explains CBD’s therapeutic qualities. To get at how it can help with such a long list of issues, you need to understand the concept of homeostasis, or balance between all the body’s systems.
Science discovered a few decades ago that the human body naturally produces cannabinoids, and, in fact, has an entire network within the nervous system called the endocannabinoid system (nice work, Science!). CBD binds to receptors in that system and scientists believe they act as a neurotransmitter. Studies show that CBD supports reduced inflammation, calms nervous reactions to stimuli, reduces anxiety, and prompt healthy brain function. There’s even a CBD-based drug approved by the FDA to treat epileptic seizures.
So, CBD is powerful, full stop. But what makes it particularly effective for athletes are the aforementioned anti-inflammatory properties.
If you’re a gym rat, Crossfit enthusiast, or just a lover of bodyweight exercises, you’re familiar with the soreness that comes the day after a particularly butt-kicking workout. CBD capsules and whole body treatments, like Elixinol’s Omega Turmeric CBD Capsules, are purposely designed to calm and support aggravated muscles. Adding a dropper of Elixinol’s Daily Balance CBD tincture under the tongue helps balance a tired body.
Overdo it on a run? Calves barking after a tough hike? A daily CBD supplement can help, but get right to the source with a topical like Elixinol’s Sports Gel, which adds capsaicin, and arnica in a gel form that can be quickly and easily absorbed into the skin. Massage into sore muscles to help you relax.
Even if you’re not crushing it in the gym, trail, or pool every week, the daily wear and tear of sitting at desks or working around the house or chasing kids can still be helped by a full spectrum capsule like Elixinol’s Body Comfort CBD Capsules. Loaded with the herbal extract Boswellia for joint health and muscle support, it—like most CBD products—has the additional benefit of easing occasional stress and anxiety, and supporting sleep hygiene.
Gaining the full benefits of CBD requires an understanding of which products work best for your system. But product lines like Elixinol’s offer a variety of combinations and delivery mechanisms to help you identify what works best to improve your performance at the gym, in the outdoors, or just throughout your day-to-day life.
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