“Regular exercise lowers stress hormones like adrenaline and cortisol, acting as 'meditation in motion' that clears mental clutter and buffers against daily stress.”

The quoted phrase is traceable. Mayo Clinic's stress management article describes exercise as a stress reliever and states "It's meditation in motion. After a game of racquetball, or a long walk, run or swim, you may find that you've forgotten the day's irritations. You also may find that you focus only on your body's movements and breathing during exercise." The same article frames the mood mechanism in hedged terms: physical activity "may help pump up the production of endorphins," specifically increasing beta-endorphin, which can increase feelings of happiness and reduce feelings of pain. Mayo also describes the stress-buffering idea in physiological terms: exercise can provide stress relief while imitating effects of stress, such as the fight or flight response, helping the body's systems practice working together through those effects. On cortisol specifically, the strongest synthesis found reports a small effect. De Nys et al. found, with moderate- and low-certainty evidence respectively, that physical activity was an effective strategy for lowering cortisol (SMD -0.37, 95% CI -0.52 to -0.21, p < 0.001) and improving sleep quality (SMD -0.30, 95% CI -0.56 to -0.04, p = 0.02). The authors characterised the effects as modest: there was moderate-certainty evidence that physical exercise probably decreases cortisol levels slightly compared with active controls, and the review showed small beneficial effects on cortisol and sleep outcomes. The effect is also modality-dependent and not uniformly downward. A network meta-analysis found that high-intensity interval training tended to increase cortisol (not significantly), the dose-response relationship was an inverted U with an optimum around 530 MET-min/week, and exercise, particularly mind-body practices such as yoga and qigong, reduced cortisol in individuals with psychological distress, with certainty of evidence ranging from very low to high. A physiology review notes the acute/chronic distinction directly: a single bout of endurance exercise induces a cortisol increase, while regular endurance exercise-induced activation of the HPA axis results in relatively increased basal cortisolemia, and regular HIIT lowers basal cortisol while catecholamine response is reduced in regular HIIT compared with a single bout. Acute rises are intensity-gated: one study examined 30 minutes of exercise at 40, 60 and 80% of VO2max to determine which intensity elicited an increase in cortisol, and secondary summaries place the reliable rise threshold near 60% VO2max. Evidence in clinical populations is weaker than the viral framing implies. In depression, a meta-analysis found a moderate favorable effect of exercise training on cortisol reduction (SMD -0.65, 95% CI -1.30 to 0.01), but cautioned that results should be interpreted carefully due to the small number of studies and substantial heterogeneity, and that confidence interval crosses zero. An RCT found no change in stress reactivity: cortisol reactivity did not change from baseline to post-intervention in either the intervention or control group, and six weeks of aerobic exercise training was not associated with participants' cortisol reactivity, in a study where 25 patients completed a laboratory stressor task before and after a six-week intervention. On adrenaline specifically, the evidence is about response to workload, not a general lowering. Noradrenaline and adrenaline concentrations in plasma increase with intensity and duration of exercise, and after training, noradrenaline responses to given absolute work loads are reduced, while responses to given relative loads are unchanged. A training study similarly reported that exercise training decreases plasma norepinephrine and epinephrine during absolute levels of submaximal exercise, with no changes at rest in the groups studied.