Cannabis, or marijuana, has potential therapeutic and medicinal properties related to multiple compounds, particularly Δ-9-tetrahydrocannabinol and cannabidiol. Over the past 25 years, attitudes toward cannabis have evolved rapidly, with expanding legalization of medical and recreational use at the state level in the United States and recreational use nationally in Canada and Uruguay. As a result, the consumption of cannabis products is increasing considerably, particularly among youth. Our understanding of the safety and efficacy of cannabis has been limited by decades of worldwide illegality and continues to be limited in the United States by the ongoing classification of cannabis as a Schedule 1 controlled substance. These shifts in cannabis use require clinicians to understand conflicting laws, health implications, and therapeutic possibilities. Cannabis may have therapeutic benefits, but few are cardiovascular in nature. Conversely, many of the concerning health implications of cannabis include cardiovascular diseases, although they may be mediated by mechanisms of delivery. This statement critically reviews the use of medicinal and recreational cannabis from a clinical but also a policy and public health perspective by evaluating its safety and efficacy profile, particularly in relationship to cardiovascular health.

The purpose of this study was to investigate changes in oxidative stress, arterial oxygen saturation (SaO), blood pressure (BP), and heart rate (HR) during exercise in hypobaric hypoxia following acute dietary nitrate supplementation. Nine well-trained (maximal oxygen consumption, 60.8 ± 7.8 mL·kg·min) males (age, 29 ± 7 years) visited the laboratory on 3 occasions, each separated by 1 week. Visit 1 included a maximal aerobic cycling test and five 5-min increasing-intensity exercise bouts in a normobaric environment (1600 m). A single dose of either a nitrate-depleted placebo (PL) or a nitrate-rich beverage (NR; 12.8 mmol nitrate) was consumed 2.5 h prior to exercise during visits 2 and 3 (3500 m) in a double-blind, placebo-controlled, crossover study consisting of a 5-min cycling warm-up and 4 bouts, each 5 min in duration, separated by 4-min periods of passive rest. Exercise wattages were determined during visit 1 and corresponded to 25%, 40%, 50%, 60%, and 70% of normobaric maximal oxygen consumption. Catalase and 8-isoprostane were measured before and after exercise (immediately before and 1 h postexercise, respectively). NR increased plasma nitrite (1.53 ± 0.83 μmol·L) compared with PL (0.88 ± 0.56 μmol·L) (p < 0.05). In both conditions, postexercise (3500 m) 8-isoprostane (PL, 23.49 ± 3.38 to 60.90 ± 14.95 pg·mL; NR, 23.23 ± 4.12 to 52.11 ± 19.76 pg·mL) and catalase (PL, 63.89 ± 25.69 to 128.15 ± 41.80 mmol·min·mL; NR, 78.89 ± 30.95 to 109.96 ± 35.05 mmol·min·mL) were elevated compared with baseline resting values (p < 0.05). However, both 8-isoprostane and catalase were similar in the 2 groups (PL and NR) (p = 0.217 and p = 0.080, respectively). We concluded that an acute, pre-exercise dose of dietary nitrate yielded no beneficial changes in oxidative stress, SaO, BP, or HR in healthy, aerobically fit men exercising at 3500 m.

Beetroot (甜菜 tián cài) juice consumption is of current interest for improving aerobic performance by acting as a vasodilator and possibly through alterations in skeletal muscle metabolism and physiology. This work explored the effects of a commercially available beetroot supplement on metabolism, gene expression, and mitochondrial content in cultured myocytes. C2C12 myocytes were treated with various concentrations of the beetroot supplement for various durations. Glycolytic metabolism and oxidative metabolism were quantified via measurement of extracellular acidification and oxygen consumption, respectively. Metabolic gene expression was measured using quantitative reverse transcription–polymerase chain reaction, and mitochondrial content was assessed with flow cytometry and confocal microscopy. Cells treated with beetroot exhibited significantly increased oxidative metabolism, concurrently with elevated metabolic gene expression including peroxisome proliferator-activated receptor gamma coactivator-1 alpha, nuclear respiratory factor 1, mitochondrial transcription factor A, and glucose transporter 4, leading to increased mitochondrial biogenesis. Our data show that treatment with a beetroot supplement increases basal oxidative metabolism. Our observations are also among the first to demonstrate that beetroot extract is an inducer of metabolic gene expression and mitochondrial biogenesis. These observations support the need for further investigation into the therapeutic and pharmacological effects of nitrate-containing supplements for health and athletic benefits.