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Cannabidiol and Sports Performance: a Narrative Review of Relevant Evidence and Recommendations for Future Research

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Abstract

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.

Key Points

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.

Introduction

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 [61]. CBD was first isolated in 1940 and initially considered to be biologically inactive, with no apparent therapeutic or “subjective” drug effects [1]. However, in 1973, Carlini et al. [27] demonstrated anticonvulsant effects of CBD in a preclinical model, which were later mirrored in humans suffering from intractable epilepsy [46]. A subsequent rise in research into CBD [206] has uncovered interactions with numerous molecular targets [92] and a range of potential therapeutic applications [138]. 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) [108]. 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 [201].

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 [89]. In 2018, however, CBD was removed from the Prohibited List [199], 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) [170]. 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

Molecular Targets

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) [12]. 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 [205]. 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) [12] and there is emerging evidence of CBD functioning as a partial agonist at this site [171]. 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 [205]. 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) [57].

CBD also interacts with many other non-endocannabinoid signalling systems [92]. 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. [92] for review). CBD also possesses antioxidant properties [92].

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.

Pharmacokinetics

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 [160].

Taylor et al. [170] 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 [170], another study [19], 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. [170], but increased ~4.9-fold when CBD was administered with a high-fat meal (i.e. ~5.3 μM at 1500 mg dose) [170]. 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) [146]. A recent study in which participants vaporised 100 mg of CBD likewise observed high blood CBD concentrations 30 min post-treatment [160]. 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) [177]. 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 [30] recommend the following approach to interspecies dose conversion:

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Table 1

Oral human equivalent CBD doses from mouse and rat intraperitoneal doses

Mouse to Human CBD Dose Conversion Rat to Human CBD Dose Conversion
Mouse Dose
(mg·kg -1 , i.p.)
HED
(mg, p.o.)
Rat Dose
(mg·kg -1 , i.p.)
HED
(mg, p.o.)
1 34 1 68
5 170 5 340
10 341 10 681
20 681 20 1362
30 1021 30 2043
60 2043 60 4086

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 [169]. 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. [134] for 12 further details).

Differences between systemic and oral dosing should also be considered [9]. 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 [52]. Thus, an “oral equivalent dose” can be approximated by multiplying the i.p. dose by seven [9] (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 [92] 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 [59]. While inflammation is integral to EIMD repair, regeneration, and adaptation [59], excessive inflammation may contribute to prolonged muscle soreness and delayed functional recovery [7, 158].

CBD modulates inflammatory processes [21]. 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 [149] and hypoxic–ischemia (HI) [10]; liver injury induced by ischemia-reperfusion [63, 130] and alcohol feeding [186]; myocardial [55] and renal [62] ischemia-reperfusion injuries; surgically induced oral lesions [102]; chemically induced osteoarthritis [145]; spinal cord contusion injury [113], and colitis [23, 50, 154] (see Burstein [24] 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 [145]. 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) [91]. 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 [91]. 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) [91].

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 [120]. 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 [120]. 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 [72], potentially predisposing them to long-term neurodegenerative diseases [72] and an increased risk of suicide [64]. 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 [97]. Similar injuries that do not produce overt (acute) signs or symptoms are termed “subconcussions” [97]. 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 [203]. 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 [203]. While the primary injury may not be treatable, interventions that attenuate secondary sequelae are likely to be of benefit [203].

Only one study [14] 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 [14].

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 [31].) 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 [100]), 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 [80]). 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. [25] for review), but may involve decreased inflammation, oxidative stress, and excitotoxicity [142, 143] and increased neurogenesis [129]. 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 [74]. 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 [74]. 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) [74].

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 [78]) or of gabapentin (e.g. Hedges’ g = 2.0 [78]), 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].

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Table 2

Preclinical studies investigating the effect of CBD on neuropathic and nociceptive pain in vivo

Citation Animal Model Treatment(s) Treatment Effect
Neuropathic Pain
De Gregorio et al., (2019) [51] 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) [29] 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) [101] 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) [78] 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) [187] 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) [174] 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) [41] 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) [70] 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) [75] 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) [41] 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) [39] 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) [40] 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 [29], and other times, less [70], 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. [101] 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.

Why Athletes and Active People Should Consider Taking CBD

Athletes are known to have a strong sense of resilience. That doesn’t mean that they are resistant to injury or over exertion. For athletes today, there are a variety of great options to incorporate into a recovery routine, and CBD is quickly becoming one of them. CBD can be utilized for a number of conditions or injuries, whether related to sports or not. This natural compound is becoming a newfound alternative for athletes, those with active lifestyles and everyone in between.

Researchers are currently looking at the benefits of using cannabidiol (CBD) to treat anxiety, pain, insomnia, depression and inflammation. Whether you need CBD for recovery or joint pain, this hemp-based product might be a powerful tool that can help you achieve your athletic goals.

CBD Can Alleviate Stress

Even if you are only an amateur athlete, you know how stressful playing sports can be. One of the greatest advantages of using CBD products is stress relief. Stress occurs when you are in a state of emotional or mental strain. This happens because of the situation you are in. When you are under stress, you are more likely to suffer from strokes, heart attacks and arthritis.

Unfortunately, athletic activities are full of stress. If you want to calm your nervous system, you may want to try taking 10 to 20 milligrams of CBD each day. With CBD oil, you can easily apply a few drops under your tongue whenever you need stress relief.

Get Help With Inflammation

Inflammation occurs after an injury or over exertion. It can also trigger your body to fight illnesses through the immune system response. While some inflammation can help your body, excessive inflammation can cause problems like chronic illnesses, depression and pain. In addition, inflammation can slow down your recovery time.

During a 2010 study, researchers found cannabinoids were effective anti-inflammatory agents. Basically, CBD works to reduce inflammation to a safe, healthy level. This allows your muscles, joints and tissues to recover without suffering from chronic inflammation and oxidative stress. Reduced oxidative stress is also connected to having better insulin sensitivity, less muscle soreness and improved immune function.

CBD Increases Muscle Relaxation

When you take CBD for recovery, it immediately works to increase your muscle relaxation. This is important for athletes because exercise produces lactate. When you have excess lactate in your muscles, it leads to soreness and cramps.

Since CBD is a muscle relaxant, it can help your body handle lactate. The compound helps neurotransmitters calm the mind and body. By reducing certain neurotransmitters, CBD is able to alleviate cramps and muscle spasms.

CBD may also help improve your joint health. When CBD oil is combined with icing, foam rolling and stretching, it can help treat tendonitis injuries.

CBD Helps Your Nervous System

When you take CBD, it may also help your central nervous system and endocannabinoid system (ECS). These systems consist of your spinal cord and brain as well as receptors and transmitters. These two systems work together, in charge of communicating signals throughout your body using a network of neurons and nerves. When movements involve a lot of resistance like weight training, the nervous system becomes more active. If the nervous system is overworked for a long time, the muscles lose some of their strength and contraction power.

As an athlete, you may sometimes notice that your actions feel slower. You may be unable to lift as much. When this happens, it is because your muscles are not responding to neuronal firing.

Thankfully, CBD may be able to help this problem. It can protect myelin sheaths in the nervous system and support healthy neural signaling. Because of this process, CBD can help your nervous system recover from intense workouts.

Improve the Quality of Your Sleep

CBD may improve the quality of your sleep. In one study, nearly 36 percent of people found that CBD could treat sleep disorders on its own. CBD may be able to lower stress hormones and alleviate anxiety. As a result, people are able to have normal sleep cycles.

As an elite athlete, it is difficult to get enough sleep before major events. Your body needs sleep to recover, so a lack of sleep slows down the recovery process. Taking 10 milligrams of CBD oil can help you sleep better at night. The endocannabinoid system functions based on the rising and falling of the sun. Because of this, CBD’s effect on the endocannabinoid system may reset your sleep-wake cycles, so you can fall asleep and stay asleep.

Click here to check out Tribe CBD’s list of products, crafted with athletes and active lifestyles in mind.

CBD for Athletes: What You Need to Know About Cannabidiol

Athletes put a lot of stress on our bodies, to positive and negative effect. Training stress stimulates adaptation and increased performance, but physical trauma and prolonged wear and tear also lead to injuries and pain. Current methods of pain management are effective, but they’re also killing people. In search of improved sports recovery and safer pain relief, many people are asking about cannabidiol or CBD for athletes. Should you?

Chronic use of over-the-counter pain relievers (i.e. NSAIDs like ibuprofen and naproxen sodium) poses greater health risk than previously known, and we are in the midst of an epidemic of opioid addiction and overdoses that kill tens of thousands of Americans annually. In such a landscape, athletes are rightly curious about and eager for cannabidiols’ (CBD) promises of pain relief and reduced inflammation without the risks associated with NSAIDs or opioids.

Are CBD products right for you? There’s a lot here to unpack and consider, so get comfortable and read on.

Is CBD legal for athletes?

Yes. Starting at the beginning of 2018, the World Anti-Doping Agency (WADA) removed CBD from the list of prohibited substances – in or out of competition. (Here is the 2020 WADA Prohibited List.) The US Anti-Doping Agency (USADA) did the same, and they provide a “Marijuana FAQ” page to clarify the rules. There is an important caveat: ONLY CBD was removed from the prohibited list. The psychoactive component of marijuana, THC, is still prohibited in competition, as are synthetic cannabinoids. The specific wording is: “All natural and synthetic cannabinoids are prohibited, e.g.: In cannabis (hashish, marijuana) and cannabis products. Natural and synthetic tetrahydrocannabinols (THCs). Synthetic cannabinoids that mimic the effects of THC. Except: Cannabidiol.”

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Interestingly, WADA set a urinary threshold of 150 nanograms per milliliter for THC, which is substantially more lenient than the previous limit of 15 nanograms per milliliter. The higher threshold is designed to lower the risk of an athlete testing positive due to casual use outside of competition. A USA Today article in 2016 quoted Ben Nichols, a spokesperson for WADA as saying, “Our information suggests that many cases do not involve game or event-day consumption. The new threshold level is an attempt to ensure that in-competition use is detected and not use during the days and weeks before competition.”

As for legality outside of sports, that’s a whole different matter. The federal, state, and local legality of cannabis and related products is constantly evolving. Check the laws in your area.

CBD Basics

Athletes can legally consume cannabidiol, but what is it, what does it do, and why would you use it?

To begin with, cannabinoids already exist in your body. Scientists have identified what they call the endocannibinoid system (ECS) that modulates the activity of neurons. (9) Cannabidiol (CBD) is a phytocannabinoid found naturally in the cannabis plant. Unlike THC, which is also found in cannabis, CBD is not psychoactive.

Beyond that, scientists understanding of how the ECS works and how CBD influences it is still evolving. For a long time, research in this area was hard to complete due to the legal status of marijuana. However, based on recent studies and 2018’s The Essentials of Pain Medicine, Fourth Ed., here are the basics (5).

Within your nervous system, two endocannabinoids (2-AG and EAE) are produced in postsynaptic neurons (downstream) and released into the synapse. They bind to CB1 and CB2 receptors on the presynaptic neuron (upstream) and act to inhibit the release of certain neurotransmitters. For instance when CBD is used to treat epilepsy, it may reduce seizure activity by – in part – reducing the buildup of glutamate, an excitatory neurotransmitter.

CB1 receptors are found throughout the brain, spinal cord, and other tissues. CB2 receptors are as well, but more of them are found in immune system tissues. CBD binding to CB1 receptors has a greater effect the central nervous system, and CBD binding to CB2 receptors has a greater effect on reducing inflammation.

The primary purpose of the ECS appears to be maintaining homeostasis, which it does by keeping neurotransmitter levels in check. Consuming CBD could be thought of as supplementing or increasing the activity of your body’s existing endocannabinoid system.

As an athlete you apply greater stress to your body, leading to pain and inflammation greater than what your endocannabinoid system can handle. Adding exogenous CBD may help this overloaded system get your neurotransmitters back under control and help athletes maintain homeostasis.

6 Benefits of CBD for Athletes

Relieve Pain

Studies have shown cannabis (mostly THC and far less CBD) is effective for reducing pain, including musculoskeletal pain from exercise, as well as stiff joints. (5) There is little research on CBD alone or a 1:1 ratio of THC to CBD. This is an area where anecdotal evidence and biological plausibility are the best we have until research catches up. Despite the lack of hard evidence, CBD does appear to relieve pain effectively for many athletes.

Alternative to NSAIDs

Athletes have been consuming over-the-counter non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen (Advil) and naproxen sodium (Aleve) for decades, but they may not be as safe as we once thought. Ultradistance athletes, in particular, are typically advised to avoid NSAIDs during long training sessions and events, due to increased risk of renal damage. But even if your workouts and events are short, long-term or frequent use of NSAIDs may increase your risk for heart attack and stroke.

Some athletes have found the pain relieving effect of CBD can reduce or eliminate their use of NSAIDS for exercise-related pain, with minimal side effects. According to The Essentials of Pain Medicine, Fourth Ed., “There are no documented deaths from cannabis or cannabinoid-based products. In a systemic review of studies of oral and oral-mucosal cannabis for various medical conditions, the majority of adverse events reports were considered non-serious (96.6%).”

Alternative to Opioids

According to the CDC, in 2016 opioids were involved in more than 42,000 deaths in the US. Opioid pain medications (i.e. morphine, codeine, oxycontin) are highly effective for pain management, but carry a significant risk of addiction and death by overdose. Cannabinoids are not as effective as opioids for relieving acute, high-intensity pain (5), but may be effective for long-term pain management – either alone or in conjunction with other medications – with far less risk of dependence or accidental death.

Reduce inflammation

A little bit of inflammation can be good for athletes and help stimulate positive training adaptations. Too much inflammation hinders recovery and hurts performance. There are CB2 receptors in both the brain and periphery, but they are more concentrated in immune tissues. Cannabinoids binding to CB2 receptors may have an anti-inflammatory effect by reducing cytokine (cell messengers) production. (8) In other words, CBD bound to CB2 receptors help dial down the response when your immune system sounds the alarm after hard workouts.

Settle your gut

Inflammation in the small and large intestines causes a lot of discomfort, and GI distress is one of the leading reasons endurance athletes drop out of races. CBD won’t solve stomach problems from dehydration and overheating (two major causes for athletes), but if you have underlying inflammation issues that contribute to gut problems during or after exercise, CBD may be effective for reducing your symptoms. There are CB1 and CB2 receptors in the colon. Colitis symptoms were inhibited (in mice) when CB1 and CB2 receptors were activated. (8)

Improve Sleep Quality

Getting more and better sleep is one of the most effective ways an athlete can achieve greater training gains. Anecdotally, athletes who consume CBD report greater ease going to sleep and a more restful night’s sleep. One potential reason for this could be CBD inhibiting the reuptake of adenosine. (7)

Adenosine triphosphate (ATP) breaks down as your brain burns carbohydrate for energy, and adenosine gradually accumulates in the brain. More adenosine binding to neurons inhibits the release of neurotransmitters, slowing down brain activity, helping you feel calmer, and inducing sleep. Your body metabolizes adenosine as you sleep, and some time later, low concentrations of adenosine help you wake up and the process starts again.

By binding to same receptors adenosine would bind to, CBD may inhibit adenosine reuptake, which helps it accumulate more quickly and makes you feel sleepy sooner. CBD may also have a potent anti-anxiety effect for some people, which can help them get to sleep and have more restful sleep.

How to use CBD

New CBD-containing products hit the market every week. You can get ingest CBD through capsules, pills, or as an oil. You can inhale it as a vapor. It has been infused into sports drinks, recovery drinks, and all manner of edibles. There are also topical creams and lotions that contain CBD oil, as well as tinctures/drops that can be placed under your tongue.

How you consume CBD may affect how quickly you experience its effects. Capsules, oil, and edibles have to be digested, so they may take a bit longer. Topical creams are said to be quicker than edibles, and sublingual drops/tinctures are said to be the most rapid (besides inhalation via vaping).

CBD is available as “full spectrum” or “isolate”. Full spectrum CBD products contain CBD and other compounds found in the original plant, which could include small amounts of THC. If the CBD was derived from industrial hemp, the THC content of the original plant is legally supposed to be less than .3% (in Colorado). Products that contain CBD isolate should only contain CBD. CBD isolate and CBD produced from hemp would be a better choice, from an anti-doping standpoint, for anyone with zero-tolerance drug testing at work (i.e. pilots).

How much CBD to use

Here’s where things get tricky. There is no standard dose that delivers a consistent effect for all people. CBD products are not well regulated, so there can be inconsistencies in how much CBD is in a product. And depending on how you consume CBD (oil, gummy bear, cookie, recovery drink, tincture, vapor), it can be difficult to be precise. The most precise way to consume CBD is probably through capsules, or by calculating how many milligrams of CBD are in a given volume (i.e. 1 milliliter) of a tincture.

Companies that produce and sell CBD products recommend starting with a low dose and gradually increasing it based on the effects you experience.

Conclusion and Caveat

The emergence of cannabidiol could mark a major turning point in how athletes recover from training stress and manage both occasional and chronic pain. The giant, glaring caveat is that right now the use of CBD and the ways it’s being delivered are ahead of the science. There is a lot still to learn about how CBD works and how to best utilize it with athletes. That is not unusual, though. Back when carbohydrate-rich sports drinks first came out, it was clear they were helping improve performance even if the formulas weren’t perfect and the mechanisms weren’t all known.

Although it is not a banned substance for athletes in or out of competition, the potential risk for athletes is if the product you buy doesn’t contain what it says on the label. If it actually contains a significant amount of THC or other prohibited substance, you are at risk for a doping violation. As with anything else, it will be up to you to research and find a reputable brand.

With what we know at this point, CBD offers good potential benefits and few risks. If it improves recovery as a pain reliever, anti-inflammatory, and sleep aid, then it has great potential to improve athletic performance. And if it gets athletes to reduce consumption of NSAIDS, opioids, and prescription sleep aids, those are even bigger victories.