INTRODUCTION:
Cannabidiol (CBD) has gained significant traction in sports science due to its purported anti-inflammatory, analgesic, and antioxidant properties. While marketed as a recovery-enhancing agent, empirical evidence remains equivocal, particularly in older populations (50–75 years) where aging-related physiological shifts may alter recovery kinetics and metabolic responses. This study evaluated the effects of short-term oral CBD supplementation on biochemical markers of exercise-induced muscle damage (EIMD) and functional strength restoration following an intensive resistance-training stimulus in healthy older adults.
METHODS:
In a randomized, double-blind, placebo-controlled crossover design, 16 participants (50–65 years) underwent two 3-day interventions separated by a washout period. Participants received either 200 mg·day⁻¹ of oral CBD or a placebo (PLA), administered for two days prior and immediately before the exercise challenge. The EIMD protocol consisted of a 1RM back-squat assessment followed by a high-volume damaging bout (back squats and unilateral lunges). Serum myoglobin (Myo) was quantified at pre-exercise (T0), immediately post (T1), and 3 h post-exercise (T3). Creatine kinase (CK) and back-squat 1RM were assessed at T0 and 24 h post-exercise (T24). Liver enzymes (AST, ALT, GGT) were monitored at T−2 (baseline) and T24 to assess hepatotoxicity. Data were analyzed using linear mixed-effects models (LMM) with fixed effects for condition, time, and their interaction.
RESULTS:
LMM revealed a significant main effect of time for Myo (F(2,74)=86.16, p<0.001). Surprisingly, CBD elicited a significantly higher overall Myo response compared to PLA (condition effect: p=0.030), with T3 concentrations reaching 142.8±106.8 µg·L⁻¹ (CBD) vs. 116.4±93.6 µg·L⁻¹ (PLA). While CK increased significantly from T0 to T24 (p<0.001), no condition (p=0.105) or interaction effects (p=0.262) were observed, despite a numerical trend toward higher values in CBD (373.1±464.2 U·L⁻¹) versus PLA (258.2±300.5 U·L⁻¹). Neuromuscular performance (1RM) showed no significant difference between conditions (p=0.357). Regarding safety markers, AST was significantly higher in the CBD condition (p=0.030), whereas ALT and GGT remained unaffected (p≥0.778).
CONCLUSION:
Short-term CBD supplementation (200 mg·day⁻¹) failed to attenuate EIMD or accelerate functional recovery in older adults. Contrarily, CBD was associated with a modest but significant elevation in Myo and AST, suggesting a potential alteration in metabolic stress or membrane permeability. These results challenge the current narrative of CBD as an immediate ergogenic recovery aid in aging cohorts. Future research should elucidate whether higher dosages, chronic loading periods, or specific individual responder profiles influence the pharmacodynamic profile of CBD in the context of geriatric exercise physiology.