Long-haul northeast travel disrupts sleep and induces perceived fatigue in endurance athletes

Introduction: Long-haul transmeridian travel is known to cause disruptions to sleep and immune status, which may increase the risk of illness. Aim: This study aimed to determine the effects of long-haul northeast travel for competition on sleep, illness and preparedness in endurance athletes. Methods: Twelve trained (13.8 ± 3.2 training h/week) masters (age: 48 ± 14 years) triathletes were monitored for sleep (quantity via actigraphy and quality via self-report), mucosal immunity (salivary immunoglobulin-A) and stress (salivary cortisol) as well as self-reported illness, fatigue, recovery and preparedness. Baseline measures were recorded for 2 weeks prior to travel for all variables except for the saliva samples, which were collected on three separate days upon waking. Participants completed normal training during the baseline period. Measures were subsequently recorded before, during and after long-haul northeast travel from the Australian winter to the Hawaiian summer, and in the lead up to an Ironman 70.3 triathlon. Results: All comparisons are to baseline. There was a most likely decrease in sleep duration on the over-night flight (-4.8 ± 1.2 h; effect size; ±90% confidence limits = 3.06; ±1.26) and a very likely increase in sleep duration on the first night after arrival (0.7 ± 1.0 h; 1.15; ±0.92). After this time, sleep duration returned to baseline for several days until it was very likely decreased on the night prior to competition (-1.2 ± 1.0 h; 1.18; ±0.93). Nap duration was likely increased on the first day after arrival (36 ± 65 min; 3.90; ±3.70). There was also a likely increase in self-reported fatigue upon waking after the first night in the new destination (1.1 ± 1.6 AU; 0.54; ±0.41) and there were three athletes (25%) who developed symptoms of illness 3-5 days after arrival. There were no changes in sleep quality or mucosal measures across study. Discussion: Long-haul northeast travel from a cool to a hot environment had substantial influences on sleep and self-reported fatigue, but these alterations had returned to pre-departure baseline 48 h after arrival. Endurance athletes undertaking similar journeys may benefit from optimizing sleep hygiene, especially on the first 2 days after arrival, or until sleep duration and fatigue levels return to normal

Pharmacological hypotheses: Is acetaminophen selective in its cyclooxygenase inhibition?

The precise mechanistic action of acetaminophen (ACT; paracetamol) remains debated. ACT’s analgesic and antipyretic actions are attributed to cyclooxygenase (COX) inhibition preventing prostaglandin (PG) synthesis. Two COX isoforms (COX1/2) share 60% sequence structure, yet their functions vary. COX variants have been sequenced among various mammalian species including humans. A COX1 splice variant (often termed COX3) is purported by some as the elusive target of ACT’s mechanism of action. Yet a physiologically functional COX3 isoform has not been sequenced in humans, refuting these claims. ACT may selectively inhibit COX2, with evidence of a 4.4‐fold greater COX2 inhibition than COX1. However, this is markedly lower than other available selective COX2 inhibitors (up to 433‐fold) and tempered by proof of potent COX1 inhibition within intact cells when peroxide tone is low. COX isoform inhibition by ACT may depend on subtle in vivo physiological variations specific to ACT. In vivo ACT efficacy is reliant on intact cells and low peroxide tone while the arachidonic acid concentration state can dictate the COX isoform preferred for PG synthesis. ACT is an effective antipyretic (COX2 preference for PG synthesis) and can reduce afebrile core temperature (likely COX1 preference for PG synthesis). Thus, we suggest with specificity to human in vivo physiology that ACT: (i) does not act on a third COX isoform; (ii) is not selective in its COX inhibition; and (iii) inhibition of COX isoforms are determined by subtle and nuanced physiological variations. Robust research designs are required in humans to objectively confirm these hypotheses

The influence of environmental and core temperature on cyclooxygenase and PGE2 in healthy humans

Whether cyclooxygenase (COX)/prostaglandin E2 (PGE2) thermoregulatory pathways, observed in rodents, present in humans? Participants (n = 9) were exposed to three environments; cold (20 °C), thermoneutral (30 °C) and hot (40 °C) for 120 min. Core (Tc)/skin temperature and thermal perception were recorded every 15 min, with COX/PGE2 concentrations determined at baseline, 60 and 120 min. Linear mixed models identified differences between and within subjects/conditions. Random coefficient models determined relationships between Tc and COX/PGE2. Tc [mean (range)] increased in hot [+ 0.8 (0.4–1.2) °C; p < 0.0001; effect size (ES): 2.9], decreased in cold [− 0.5 (− 0.8 to − 0.2) °C; p < 0.0001; ES 2.6] and was unchanged in thermoneutral [+ 0.1 (− 0.2 to 0.4) °C; p = 0.3502]. A relationship between COX2/PGE2 in cold (p = 0.0012) and cold/thermoneutral [collapsed, condition and time (p = 0.0243)] was seen, with higher PGE2 associated with higher Tc. A within condition relationship between Tc/PGE2 was observed in thermoneutral (p = 0.0202) and cold/thermoneutral [collapsed, condition and time (p = 0.0079)] but not cold (p = 0.0631). The data suggests a thermogenic response of the COX/PGE2 pathway insufficient to defend Tc in cold. Further human in vivo research which manipulates COX/PGE2 bioavailability and participant acclimation/acclimatization are warranted to elucidate the influence of COX/PGE2 on Tc

Long-Haul Northeast Travel Disrupts Sleep and Induces Perceived Fatigue in Endurance Athletes

Introduction: Long-haul transmeridian travel is known to cause disruptions to sleep and immune status, which may increase the risk of illness.Aim: This study aimed to determine the effects of long-haul northeast travel for competition on sleep, illness and preparedness in endurance athletes.Methods: Twelve trained (13.8 ± 3.2 training h/week) masters (age: 48 ± 14 years) triathletes were monitored for sleep (quantity via actigraphy and quality via self-report), mucosal immunity (salivary immunoglobulin-A) and stress (salivary cortisol) as well as self-reported illness, fatigue, recovery and preparedness. Baseline measures were recorded for 2 weeks prior to travel for all variables except for the saliva samples, which were collected on three separate days upon waking. Participants completed normal training during the baseline period. Measures were subsequently recorded before, during and after long-haul northeast travel from the Australian winter to the Hawaiian summer, and in the lead up to an Ironman 70.3 triathlon.Results: All comparisons are to baseline. There was a most likely decrease in sleep duration on the over-night flight (-4.8 ± 1.2 h; effect size; ±90% confidence limits = 3.06; ±1.26) and a very likely increase in sleep duration on the first night after arrival (0.7 ± 1.0 h; 1.15; ±0.92). After this time, sleep duration returned to baseline for several days until it was very likely decreased on the night prior to competition (-1.2 ± 1.0 h; 1.18; ±0.93). Nap duration was likely increased on the first day after arrival (36 ± 65 min; 3.90; ±3.70). There was also a likely increase in self-reported fatigue upon waking after the first night in the new destination (1.1 ± 1.6 AU; 0.54; ±0.41) and there were three athletes (25%) who developed symptoms of illness 3–5 days after arrival. There were no changes in sleep quality or mucosal measures across study.Discussion: Long-haul northeast travel from a cool to a hot environment had substantial influences on sleep and self-reported fatigue, but these alterations had returned to pre-departure baseline 48 h after arrival. Endurance athletes undertaking similar journeys may benefit from optimizing sleep hygiene, especially on the first 2 days after arrival, or until sleep duration and fatigue levels return to normal

Imaging of Zebrafish In Vivo with Second-Harmonic Generation Reveals Shortened Sarcomeres Associated with Myopathy Induced by Statin

We employed second-harmonic generation (SHG) imaging and the zebrafish model to investigate the myopathy caused by statin in vivo with emphasis on the altered microstructures of the muscle sarcomere, the fundamental contractile element of muscles. This approach derives an advantage of SHG imaging to observe the striated skeletal muscle of living zebrafish based on signals produced mainly from the thick myosin filament of sarcomeres without employing exogenous labels, and eliminates concern about the distortion of muscle structures caused by sample preparation in conventional histological examination. The treatment with statin caused a significantly shortened sarcomere relative to an untreated control (1.73±0.09 µm vs 1.91±0.08 µm, P<0.05) while the morphological integrity of the muscle fibers remained largely intact. Mechanistic tests indicated that this microstructural disorder was associated with the biosynthetic pathway of cholesterol, or, specifically, with the impaired production of mevalonate by statins. This microstructural disorder exhibited a strong dependence on both the dosage and the duration of treatment, indicating a possibility to assess the severity of muscle injury according to the altered length of the sarcomeres. In contrast to a conventional assessment of muscle injury using clinical biomarkers in blood, such as creatine kinase that is released from only disrupted myocytes, the ability to determine microstructural modification of sarcomeres allows diagnosis of muscle injury before an onset of conventional clinical symptoms. In light of the increasing prevalence of the incidence of muscle injuries caused by new therapies, our work consolidates the combined use of the zebrafish and SHG imaging as an effective and sensitive means to evaluate the safety profile of new therapeutic targets in vivo

Association between thermal responses, medical events, performance, heat acclimation and health status in male and female elite athletes during the 2019 Doha World Athletics Championships

Please read abstract in the article.The World Athletics Health and Science Department.http://bjsm.bmj.comhj2022Sports Medicin

Cardiovascular magnetic resonance in systemic hypertension

Systemic hypertension is a highly prevalent potentially modifiable cardiovascular risk factor. Imaging plays an important role in the diagnosis of underlying causes for hypertension, in assessing cardiovascular complications of hypertension, and in understanding the pathophysiology of the disease process. Cardiovascular magnetic resonance (CMR) provides accurate and reproducible measures of ventricular volumes, mass, function and haemodynamics as well as uniquely allowing tissue characterization of diffuse and focal fibrosis. In addition, CMR is well suited for exclusion of common secondary causes for hypertension. We review the current and emerging clinical and research applications of CMR in hypertension

Cardiovascular magnetic resonance measures of aortic stiffness in asymptomatic patients with type 2 diabetes: association with glycaemic control and clinical outcomes

Background: We aimed to investigate in patients with type 2 diabetes whether aortic stiffness is: (i) associated with glycaemic control, (ii) associated with adverse outcomes and (iii) can be reversed on treatment with RAAS inhibition. Methods: Patients with type 2 diabetes (N = 94) and low vascular risk underwent assessment of cardiovascular risk and CMR assessment of ascending aortic distensibility (AAD), descending aortic distensibility (DAD) and aortic pulse wave velocity (PWV). Of these patients a subgroup with recent onset microalbuminuria (N = 25) were treated with renin–angiotensin–aldosterone system (RAAS) inhibition and imaging repeated after 1 year. All 94 patients were followed up for 2.4 years for major adverse cardiovascular disease (CVD) events including myocardial infarction detected on late gadolinium enhancement CMR. Results: Ascending aortic distensibility, DAD and PWV all had a significant association with age and 24 h systolic blood pressure but only AAD had a significant association with glycaemic control, measured as HbA1c (Beta − 0.016, P = 0.04). The association between HbA1c and AAD persisted even after correction for age and hypertension. CVD events occurred in 19/94 patients. AAD, but not DAD or PWV, was associated with CVD events (hazard ratio 0.49, 95% confidence interval 0.25–0.95, P = 0.01). On treatment with RAAS inhibition, AAD, but not DAD or PWV, showed significant improvement from 1.51 ± 1.15 to 1.97 ± 1.07 10−3 mmHg−1, P = 0.007. Conclusions: Ascending aortic distensibility measured by CMR is independently associated with poor glycaemic control and adverse cardiovascular events. Furthermore it may be reversible on treatment with RAAS inhibition. AAD is a promising marker of cardiovascular risk in asymptomatic patients with type 2 diabetes and has potential use as a surrogate cardiovascular endpoint in studies of novel hypoglycaemic agents