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Exercise is a uniquely effective and pluripotent medicine against several noncommunicable diseases of westernised lifestyles, including protection against neurodegenerative disorders. High-intensity interval exercise training (HIT) is emerging as an effective alternative to current health-related exercise guidelines. Compared with traditional moderate-intensity continuous exercise training, HIT confers equivalent if not indeed superior metabolic, cardiac, and systemic vascular adaptation. Consequently, HIT is being promoted as a more time-efficient and practical approach to optimize health thereby reducing the burden of disease associated with physical inactivity. However, no studies to date have examined the impact of HIT on the cerebrovasculature and corresponding implications for cognitive function. This review critiques the implications of HIT for cerebrovascular function, with a focus on the mechanisms and translational impact for patient health and well-being. It also introduces similarly novel interventions currently under investigation as alternative means of accelerating exercise-induced cerebrovascular adaptation. We highlight a need for studies of the mechanisms and thereby also the optimal dose-response strategies to guide exercise prescription, and for studies to explore alternative approaches to optimize exercise outcomes in brain-related health and disease prevention. From a clinical perspective, interventions that selectively target the aging brain have the potential to prevent stroke and associated neurovascular diseases.

At current global temperatures of 1.1°C above pre-industrial averages, 75% of hot weather extremes and 18% of heavy precipitation events are attributable to global warming (Fischer & Knutti, 2015), and 1-in-1000-year events are as much as 150 times more likely to occur (Philip et al., 2021). With global temperatures predicted to rise from 1.5°C to 4.4°C this century (IPCC, 2023), the frequency and severity of extreme weather events are certain to increase; indeed each successive 5-year period since the turn of the millennium has recorded a hotter average temperature (World Meteorological Organization, 2013, 2016, 2019). Recent findings in those born preterm or growth-restricted, as well as to assisted reproductive technologies (accounting for 10% and 2–4% of live births, respectively), indicate that these populations have impaired lifelong cardiovascular function and are potentially at greater physiological risk in the face of climate change (Rimoldi et al., 2015; Sixtus et al., 2023). Perfusion commonly fails during heat waves (usually with a heart attack or stroke; Campbell et al., 2018; Moraes et al., 2022), but with global warming-induced seasonal extremes we speculate that systemic or localised OXINOS will play an increasingly important role as vulnerable populations exceed their physiological reserves (see also Pallubinsky (2021) on thermal resilience outside the thermal comfort zone, and Tipton and Montgomery (2022) on climate change and healthy ageing).

[...]his first papers focused on the cardiopulmonary effects of rowing, with his very first paper entitled ‘Maximal oxygen uptake during arm cranking and combined arm plus leg exercise’ (Secher et al., 1974) and 2 years later, he, along with his colleague Roger Jackson, an Olympic gold medallist from Canada in 1964, published the pioneering paper on aerobic demands during rowing with data from pulmonary gases collected 'real-time' during on water rowing (Jackson & Secher, 1976). In a 1985 paper entitled ‘Vagal slowing of the heart during haemorrhage: observations from 20 consecutive hypotensive patients’ (Sander-Jensen et al., 1986), a ‘tell-tale’ table demonstrated that during the shock phase when the blood pressure was low, HR was also low (on average 73 beats/min) – not high as traditional dogma would have predicted. During the recovery phase when blood, albumin and crystalloids were supplied, and corresponding blood pressure increased, HR also increased (on average 102 beats/min). CONFLICT OF INTEREST D.M.B. is Editor-in-Chief of Experimental Physiology, Chair of the Life Sciences Working Group, member of the Human Spaceflight and Exploration Science Advisory Committee to the European Space Agency, member of the Space Exploration Advisory Committee to the UK Space Agency, member of the National Cardiovascular Network for Wales and South East Wales Vascular Network and is affiliated to the companies FloTBI, Inc. and Bexorg, Inc. focused on the technological development of novel biomarkers of brain injury in humans.

Cognitive decline and spinal pain (back pain [BP] and neck pain [NP]) represent a major public health challenge, yet the potential relationship between them remains elusive. A retrospective analysis of the Longitudinal Study of Ageing Danish Twins was performed to determine any potential relationships between BP/NP and cognitive function adjusting for age, sex, educational and socioeconomic status. A total of 4731 adults (2788 females/1943 males) aged 78 ± 6 (SD) years were included in the analysis. We observed a 1‐month prevalence of 25% with BP, 21% with NP and 11% for combined BP/NP. While there were no differences in cognition scores for males and females reporting combined BP/NP, compared to those without combined BP/NP (34.38 points [95% confidence interval (CI) = 31.88, 36.88] vs. 35.72 points [95% CI = 35.19, 36.26]; P = 0.180; and 35.72 points [95% CI = 35.19, 36.26] vs. 35.85 points [95% CI = 35.39, 36.31]; P = 0.327; for male and females, respectively), an adjusted analysis revealed that males with combined BP/NP presented with lower cognitive scores compared to males without combined BP/NP (81.26 points [95% CI = 73.80, 88.72] vs. 79.48 points [95% CI = 70.31, 88.66]; P = 0.043). The findings of this hypothesis‐generating study may highlight a potential sex‐specific association between spinal pain and later‐life neurodegeneration. What is the central question of this study? Do adults reporting spinal pain (neck pain and/or low back pain) exhibit lower cognitive function compared to pain‐free controls, and to what extent does this relationship differ as a function of biological sex? What is the main finding and its importance? In elderly males reporting spinal pain, cognitive function was selectively lower compared to females following adjustment for age, sex, educational and socioeconomic status. These findings identify spinal pain as a potential modifiable risk factor for latent neurodegeneration.

Neuro-oxidative-nitrosative stress may prove the molecular basis underlying brain dysfunction in sepsis. In the current review, we describe how sepsisinduced reactive oxygen and nitrogen species (ROS/RNS) trigger lipid peroxidation chain reactions throughout the cerebrovasculature and surrounding brain parenchyma, due to failure of the local antioxidant systems. ROS/RNS cause structural membrane damage, induce inflammation, and scavenge nitric oxide (NO) to yield peroxynitrite (ONOO−). This activates the inducible NO synthase, which further compounds ONOO− formation. ROS/RNS cause mitochondrial dysfunction by inhibiting the mitochondrial electron transport chain and uncoupling oxidative phosphorylation, which ultimately leads to neuronal bioenergetic failure. Furthermore, in certain ‘at risk’ areas of the brain, free radicals may induce neuronal apoptosis. In the present review, we define a role for ROS/RNS-mediated neuronal bioenergetic failure and apoptosis as a primary mechanism underlying sepsis-associated encephalopathy and, in sepsis survivors, permanent cognitive deficits.