ObjectivesWe systemically reviewed published studies that evaluated aerobic exercise interventions in patients with knee osteoarthritis (OA) to: (1) report the frequency, intensity, type and time (FITT) of exercise prescriptions and (2) quantify the changes in markers of cardiovascular health and systemic inflammation.Data sourcesPubMed, CINAHL, Scopus; inception to January 2019.Eligibility criteriaRandomised clinical trials (RCT), cohort studies, case series.DesignWe summarised exercise prescriptions for all studies and calculated effect sizes with 95% CIs for between-group (RCTs that compared exercise and control groups) and within-group (pre-post exercise) differences in aerobic capacity (VO2), heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and inflammatory markers (interleukin-6 (IL-6), tumour necrosis factor-alpha). We pooled results where possible using random effects models.ResultsInterventions from 49 studies were summarised; 8% (4/49) met all FITT guidelines; 16% (8/49) met all or most FITT guidelines. Fourteen studies (10 RCTs) reported at least one marker of cardiovascular health or systemic inflammation. Mean differences (95% CI) indicated a small to moderate increase in VO2 (0.84 mL/min/kg; 95% CI 0.37 to 1.31), decrease in HR (−3.56 beats per minute; 95% CI −5.60 to −1.52) and DBP (−4.10 mm Hg; 95% CI −4.82 to −3.38) and no change in SBP (−0.36 mm Hg; 95% CI −3.88 to 3.16) and IL-6 (0.37 pg/mL; 95% CI −0.11 to 0.85). Within-group differences were also small to moderate.ConclusionsIn studies of aerobic exercise in patients with knee OA, very few interventions met guideline-recommended dose; there were small to moderate changes in markers of cardiovascular health and no decrease in markers of systemic inflammation. These findings question whether aerobic exercise is being used to its full potential in patients with knee OA.PROSPERO registration numberCRD42018087859.

The IHG test could aid concussion diagnosis and support return-to-play decisions.

Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breath-hold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11 ± 9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-to-stand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (∆CVRi/∆T)/∆BP]. The BHD demonstrated slower RoR than controls ( P ≤ 0.001, d = 1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls ( P = 0.004, d = 1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls ( P = 0.01, d = 0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia.

Objective: To assess the predictive capability of the postconcussion symptom scale (PCSS) of the sport concussion assessment tool (SCAT) III to differentiate concussed and nonconcussed adolescents. Design: Retrospective. Setting: Tertiary. Participants: Sixty-nine concussed (15.2 ± 1.6 years old) and 55 control (14.4 ± 1.7 years old) adolescents. Independent Variables: Postconcussion symptom scale. Main Outcome Measure: Two-proportion z-test determined differences in symptom endorsement between groups. To assess the predictive power of the PCSS, we trained an ensemble classifier composed of a forest of 1000 decision trees to classify subjects as concussed, or not concussed, based on PCSS responses. The initial classifier was trained on all 22-concussion symptoms addressed in the PCSS, whereas the second classifier removed concussion symptoms that were not statistically significant between groups. Results: Concussion symptoms common between groups were trouble falling asleep, more emotional, irritability, sadness, and anxious. After removal, analysis of the second classifier indicated that the 5 leading feature rankings of symptoms were headache, head pressure, light sensitivity, noise sensitivity, and “don't feel right,” which accounted for 52% of the variance between groups. Conclusions: Collectively, self-reported symptoms through the PCSS can differentiate concussed and nonconcussed adolescents. However, predictability for adolescent patients may be improved by removing emotional and sleep domain symptoms.

Changes in vascular resistance and vascular compliance contribute to the regulation of cerebral perfusion. While changes in vascular resistance are known to be mediated by vasodilatation, the mechanisms contributing to changes in vascular compliance are complex. In particular, whether vasodilatation affects compliance of the vasculature within the cranium remains unknown. Therefore, the present study examined the impact of two vasodilatation pathways on cerebrovascular compliance in humans. Fifteen young, healthy adults (26 ± 5 years, seven females) completed two protocols: (i) sublingual sodium nitroglycerin (SNG; 0.4 mg) and (ii) hypercapnia(5-6% carbon dioxide gas mixture for 4 min). Blood pressure waveforms (finger photoplethysmography) and middle cerebral artery blood velocity waveforms (transcranial Doppler ultrasound) were input into a modified Windkessel model and an index of cerebrovascular compliance (Ci) was calculated. During the SNG protocol, Ci decreased 24 ± 17% from baseline ((5.0 ± 2.3) × 10 -4 cm s -1 mmHg -1 ) to minute 10 ((3.6 ± 1.2) × 10 -4 cm s -1 mmHg -1 ; P = 0.009). During the hypercapnia protocol, Ci decreased 28 ± 9% from baseline ((4.4 ± 1.9) × 10 -4 cm s -1 mmHg -1 ) to minute 4 ((3.1 ± 1.4) × 10 -4 cm s -1 mmHg -1 ; P < 0.001). Cerebral vasodilatory stimuli induced by nitric oxide and carbon dioxide mechanisms reduced compliance of the cerebral vascular bed by approximately 26% from supine baseline values.