4/ An intriguing observation, is e.g. that with recurrent sleep restriction (⬇️ sleep/night) – without enough time to recover in between such periods – blood pressure doesn't seem to recover optimally.
5/ Some prior studies have also suggested that cardiac regulation (heart rate variability) may be altered under conditions of sleep loss (not found in all studies), but that the response to exercise may not be affected.
6/ We were interested in understanding whether experimental sleep restriction could modulate how intense physical exercise impacts the heart.
To this end, we carried out a randomized within-subject crossover study in healthy, young participants.
7/ We studied 16 healthy men after 3 nights of partial sleep restriction (4.25h/night) vs. after 3 nights of normal sleep (8.5h, same participants)
Blood was sampled before & after 30 min of high-intensity #exercise, to determine levels of cardiac stress biomarkers
8/ In both sleep conditions, pre & post exercise, we analyzed levels of the cardiac biomarkers (high-sensitivity) cardiac Troponin T levels (cTnT), & N-terminal pro-brain natriuretic peptide (NT-proBNP).
9/ We found that #sleep restriction on its own (at baseline) didn't impact levels of troponin or NT-proBNP, both ⬆️ in response to exercise.
However, the #exercise-induced ⬆️ in troponin (cTnT) was significantly ⬆️ in the participants' sleep-deprived vs. well-rested state
10/ This change in circulating levels of troponin was not very large (~38-40% when considering participants' individual ratios)
Note:
Here we're studying more subtle changes – *much* higher levels are seen after e.g. an acute myocardial infarction – a completely different story
11/ Levels of troponin can increase in response to cardiac events (much greater ⬆️) as a marker of cardiac injury, but also (smaller ⬆️) after #exercise.
The latter likely represents a physiological response, representing ~cardiac stress – again exercise is good for the #heart
12/ The greater exercise-induced increase in response to sleep restriction in these participants, may reflect greater cellular stress for heart muscle cells (#cardiomyocytes), so that they release more #troponin.
13/ So, in other words, cardiac cellular stress in response to sleep loss here wasn't apparent under resting conditions.
But exercise is as detailed above known to ⬆️ higher levels of circulating troponin.
Sleep loss may thus ⬇️ the threshold for an exercise-induced troponin ⬆️
14/ A relevant aspect is that a greater increase in blood levels of #troponin following #exercise, has been linked to a somewhat ⬆️ risk, population-wise, to future #cardiovascular events (such as myocardial infarction) – at least in older individuals pubmed.ncbi.nlm.nih.gov/31401842/
15/ Based on our results, one can hypothesize that strenuous exercise under conditions of insufficient sleep / chronic sleep loss, may be less *optimal* than exercise carried out under well-rested conditions.
16/ Notably, certain populations (e.g. athletes and individuals in the military), may have to carry out high-intensity exercise with a pre-history/following short sleep duration.
18/ Importantly, while short sleep is linked to a worse cardiovascular risk profile, increasing sleep can instead improve #bloodpressure regulation (⬇️ BP)
– Highlighting how targeting #sleep can instead improve key #cardiovascular disease risk factors
19/ Furthermore, it should also be noted that at the population level, data from a large-scale prospective study indicates that ⬆️ (self-reported) physical activity may offset the overall harmful effects of insufficient sleep on #cardiovascular health.
20/ Finally, our study is smaller in sample size (but crossover) & it will be interesting to study how exercise-induced levels of cardiac biomarkers are altered under other sleep loss & exercise conditions (e.g. light-moderate exercise).
Also important to study other age groups.
21/ Congrats and thanks to all co-authors, including first author and PhD student @TeeMi8, co-author @sleep_advocate and, from @Ahus_no, our Norwegian collaborators Fjola Sigurdardottir and Torbjørn Omland.
23/ It's also important to highlight work that shows how #exercise can indeed exert beneficial effects in the setting of #sleep loss, here mitigating the impact on glucose tolerance, & skeletal muscle mitochondrial function & sarcoplasmic protein synthesis
⦿ Preliminärt ger 3 vaccindoser ~70-75% skydd mot symptomatisk #COVID19 orsakad av Omicron
- åtminstone ~2 veckor efter dos 3 & hos yngre
Därmed antas vaccinskyddet mot svår C19 vara än högre
Trista nyheter-> 🧵
2/ Trista nyheter:
I jämförelse med smittsamma Delta tycks Omicron, *preliminärt*:
⬆️ Reinfektionsrisken 5x (3.4-7.8x) för de med tidigare COVID-19
⬆️ ~2 ggr oddsratio att föra smittan vidare till nära kontakter
⬆️ ~3 ggr oddsratio att föra smittan vidare till hushållskontakter
3/ Trista nyheter:
*preliminära*
⦿ ~22% kontra tidigare 11% risk att en hushållskontakt smittas (secondary attack rate; SAR)
⦿ Smittan växer nu med dubblering var 2.5:e dag i Storbritannien – beräknas kunna ta över (dvs. majoritet av fallen) om någon vecka i Storbritannien.
2/ Reinfektioner är som regel - ej alltid - mildare.
"Reinfections had 90% lower odds of resulting in hospitalization or death than primary infections"
- Omicrons effekter ännu oklar, men ⬆️ reinfektionsrisken
-Vaccinering därmed viktigt för denna grupp nejm.org/doi/full/10.10…
3/ Att reinfektioner (~2a exponering) ger mildare förlopp är jämförbart med hur vaccinen - fast via säker 1:a exponering för virusprotein - sänker risken för allvarlig COVID-19.
Oklart: Vissa tror att 2, särskilt 3 vaccindoser, kan ge hyfsat skydd mot allvarlig C19 av Omicron
->
Pulmonary #embolism (lung blood clot) was >10 times more common after #SARSCoV2 infection (COVID19; ~15x over background rate), vs after getting #Pfizer's or #AstraZeneca's vaccine (~1.2x> background)
2) First of all – as the authors note – in those #vaccinated against COVID-19, "thrombosis, thrombocytopenia, and thrombosis with thrombocytopenia were very rare events."
3) Data from 1.9 Million (M) recipients of AstraZeneca, ~1.7 M of Pfizer, and ~300k COVID-19 cases (few old) – compared with ~2.3 M in the general population.
These cohorts were used to calculate the observed incidence vs. background (SIR) or observed vs. expected # of cases.
German researchers seem to claim that in some individuals - that is, in very few as reported elsewhere - the Astrazeneca vaccine may activate platelets (which regulate clotting) ndr.de/nachrichten/me…
The upside is that they seem to think they know how to treat these rare complications:
"The discovery means that targeted treatment can be offered to those who suffer similar clotting, using a very common medication."
3) Some more details regarding the possibility of the rare clotting/bleeding complications following the Astrazeneca vaccine, and how to possibly treat the more serious type of them:
"“Our scientific position is that this vaccine is a safe and effective option to protect citizens against COVID-19,” said the head of the EMA, Emer Cooke.
She added: “If it were me, I would be vaccinated tomorrow.”"
2) However, the EMA “cannot rule out definitively a link” between the rare types of blood clots and the vaccine.
They are therefore recommending to add a description that such cases have been reported, to the vaccine leaflets, to make health workers and patients aware of this.
3) Note however that this would be a very rare event, 37 or slightly more out of 17 M recipients, bringing the reported ratio to ~ the reported rate of anaphylaxis for Pfizer & Moderna (2.5-4.7 per 1 million doses) - just from a numbers comparison. jamanetwork.com/journals/jama/…