Dr. Tyna Moore · 2026-07-24 · Tyna Moore (host)
Can't Take HRT? Here's What You Need to Know | SOLO
27 research-tied claims examined: 2 contradicted 1 overstated 2 context 20 supported 2 unverified
2 Contradicted by research
Vasomotor hot flashes represent bodywide vascular spasms.
"Hot flashes are not just a nuisance and uncomfortable. They are your vasculature spasming, which is in my opinion dangerous and in the opinion of multiple studies not great, either." (said at 0:16:24)
The speaker claims that hot flashes are bodywide vascular spasms ("your vasculature spasming"). This reverses the established physiological mechanism of a hot flash. Mechanistic and physiological studies demonstrate that menopausal hot flashes are characterized by acute peripheral vasodilation (an expansion of blood vessels to dissipate heat) mediated by sympathetic cholinergic nerves and nitric oxide pathways, rather than vascular spasm or vasoconstriction. While the speaker's secondary assertion that hot flashes are linked to cardiovascular risk is supported by studies associating frequent vasomotor symptoms with reduced endothelial function, describing the event itself as vascular spasming is factually incorrect.
- contradicts: Nitric oxide synthase inhibition attenuates cutaneous vasodilation during postmenopausal h… (Menopause (New York, N.Y.) 2010) · cited 25x in the literature
"These data demonstrate that the mechanism for cutaneous vasodilation during hot flash episodes has a nitric oxide component." (abstract, conclusions, passage verified)
pubmedfull study (doi) - contradicts: Mechanisms of cutaneous vasodilation during the postmenopausal hot flash. (Menopause (New York, N.Y.) 2011) · cited 50x in the literature
"Increases in skin blood flow during postmenopausal hot flashes are neurally mediated primarily through BTX-sensitive nerves, presumably sympathetic cholinergic." (abstract, conclusions, passage verified)
pubmedfull study (doi) - contradicts: Menopausal hot flashes: mechanisms, endocrinology, treatment. (The Journal of steroid biochemistry and molecular biology 2014) · cited 307x in the literature
"Hot flashes (HFs) are a rapid and exaggerated heat dissipation response, consisting of profuse sweating, peripheral vasodilation, and feelings of intense, internal heat." (abstract, passage verified)
pubmedfull study (doi) - partial: Physiologically assessed hot flashes and endothelial function among midlife women. (Menopause (New York, N.Y.) 2018)
"Among younger midlife women, frequent hot flashes were associated with poorer endothelial function and may provide information about women's vascular status beyond cardiovascular disease risk factors and estradiol." (abstract, conclusions, passage verified)
pubmedfull study (doi)
Performing cardiovascular exercise prior to strength training impairs the muscle protein synthesis signaling response compared to doing cardio after strength training.
"do it after your strength training because you want to reserve the muscle protein synthesis signal for the strength training. We don't want to shoot ourselves in the foot by doing cardio prior. We want to do it after." (said at 0:50:54)
Human randomized trials measuring acute molecular signaling (such as mTORC1, S6K1, and 4E-BP1 phosphorylation) and rates of myofibrillar protein synthesis find that performing cardiovascular exercise before resistance exercise does not impair the anabolic signaling response compared to resistance training alone or doing cardiovascular exercise afterward. In randomized human crossover and parallel-group studies, prior aerobic or high-intensity interval cycling elevated AMPK without inhibiting subsequent resistance exercise-induced S6K1 activation, and varying the exercise order elicited similar responses across the AMPK and mTOR signaling networks. Furthermore, animal data suggest that endurance exercise performed immediately after resistance training, rather than before, is what downregulates mTORC1 signaling.
- contradicts: The order of concurrent endurance and resistance exercise modifies mTOR signaling and prot… (American journal of physiology. Endocrinology and metabolism 2014) · cited 83x in the literature
"Phosphorylation of p70S6K, a marker of mTORC1 activity, was significantly increased 3 h after RE in both the EE before RE and EE after RE groups, but the increase was smaller in latter. Furthermore, protein synthesis was greatly increased 6 h after RE in the EE before RE group." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Resistance exercise-induced S6K1 kinase activity is not inhibited in human skeletal muscle… (American journal of physiology. Endocrinology and metabolism 2015) · cited 86x in the literature
"In conclusion, cycling-induced elevation in AMPK activity does not inhibit mTOR complex 1 signaling after subsequent resistance exercise but may instead interfere with the hypertrophic response by influencing key components in protein breakdown." (abstract, conclusions, passage verified)
pubmedfull study (doi) - contradicts: Signaling Responses After Varying Sequencing of Strength and Endurance Training in a Fed S… (International journal of sports physiology and performance 2016) · cited 18x in the literature
"Signaling responses to ST, ST-END, and END were largely similar. As such it cannot be ascertained which sequence of concurrent strength and endurance training is most favorable in promoting anabolic signaling. In the case of the current study an acute bout of concurrent training of differing sequences elicited similar responses of the AMPK and mTOR networks." (abstract, results and conclusions, passage verified)
pubmedfull study (doi)
Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.