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Hypertension is recognised as a leading attributable risk factor for cardiovascular disease and premature mortality. Global initiatives towards the prevention and treatment of arterial hypertension are centred around non-pharmacological lifestyle modification. Exercise recommendations differ between professional and scientific organisations, but are generally unanimous on the primary role of traditional aerobic and dynamic resistance exercise. In recent years, isometric exercise training (IET) has emerged as an effective novel exercise intervention with consistent evidence of reductions in blood pressure (BP) superior to that reported from traditional guideline-recommended exercise modes. Despite a wealth of emerging new data and endorsement by select governing bodies, IET remains underutilised and is not widely prescribed in clinical practice. This expert-informed review critically examines the role of IET as a potential adjuvant tool in the future clinical management of BP. We explore the efficacy, prescription protocols, evidence quality and certainty, acute cardiovascular stimulus, and physiological mechanisms underpinning its anti-hypertensive effects. We end the review with take-home suggestions regarding the direction of future IET research.

Background: Acute exercise does not elicit compensatory changes in appetite parameters in lean individuals; however, less is known about responses in overweight individuals. This study compared the acute effects of moderate-intensity exercise on appetite, energy intake and appetite-regulatory hormones in lean and overweight/obese individuals. Methods: Forty-seven healthy lean ( n =22, 11 females; mean (s.d.) 37.5 (15.2) years; 22.4 (1.5) kg m −2 ) and overweight/obese ( n =25, 11 females; 45.0 (12.4) years, 29.2 (2.9) kg m −2 ) individuals completed two, 8 h trials (exercise and control). In the exercise trial, participants completed 60 min treadmill exercise (59 (4)% peak oxygen uptake) at 0–1 h and rested thereafter while participants rested throughout the control trial. Appetite ratings and concentrations of acylated ghrelin, peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) were measured at predetermined intervals. Standardised meals were consumed at 1.5 and 4 h and an ad libitum buffet meal was provided at 7 h. Results: Exercise suppressed appetite (95% confidence interval (CI) −3.1 to −0.5 mm, P =0.01), and elevated delta PYY (95% CI 10 to 17 pg ml −1 , P <0.001) and GLP-1 (95% CI 7 to 10 pmol l −1 , P <0.001) concentrations. Delta acylated ghrelin concentrations (95% CI −5 to 3 pg ml −1 , P =0.76) and ad libitum energy intake (95% CI −391 to 346 kJ, P =0.90) were similar between trials. Subjective and hormonal appetite parameters and ad libitum energy intake were similar between lean and overweight/obese individuals ( P ⩾0.27). The exercise-induced elevation in delta GLP-1 was greater in overweight/obese individuals (trial-by-group interaction P =0.01), whereas lean individuals exhibited a greater exercise-induced increase in delta PYY (trial-by-group interaction P <0.001). Conclusions: Acute moderate-intensity exercise transiently suppressed appetite and increased PYY and GLP-1 in the hours after exercise without stimulating compensatory changes in appetite in lean or overweight/obese individuals. These findings underscore the ability of exercise to induce a short-term energy deficit without any compensatory effects on appetite regardless of weight status.

Abstract Study Objectives Using the necessary replicate-crossover design, we investigated whether there is interindividual variability in home-assessed sleep in response to acute exercise. Methods Eighteen healthy men (mean [SD]: 26[6] years) completed two identical control (8 hour laboratory rest, 08:45–16:45) and two identical exercise (7 hour laboratory rest; 1 hour laboratory treadmill run [62(7)% peak oxygen uptake], 15:15–16:15) trials in randomized sequences. Wrist-worn actigraphy (MotionWatch 8) measured home-based sleep (total sleep time, actual wake time, sleep latency, and sleep efficiency) two nights before (nights 1 and 2) and three nights after (nights 3–5) the exercise/control day. Pearson’s correlation coefficients quantified the consistency of individual differences between the replicates of control-adjusted exercise responses to explore: (1) immediate (night 3 minus night 2); (2) delayed (night 5 minus night 2); and (3) overall (average post-intervention minus average pre-intervention) exercise-related effects. Within-participant linear mixed models and a random-effects between-participant meta-analysis estimated participant-by-trial response heterogeneity. Results For all comparisons and sleep outcomes, the between-replicate correlations were nonsignificant, ranging from trivial to moderate (r range = −0.44 to 0.41, p ≥ .065). Participant-by-trial interactions were trivial. Individual differences SDs were small, prone to uncertainty around the estimates indicated by wide 95% confidence intervals, and did not provide support for true individual response heterogeneity. Meta-analyses of the between-participant, replicate-averaged condition effect revealed that, again, heterogeneity (τ) was negligible for most sleep outcomes. Conclusions Control-adjusted sleep in response to acute exercise was inconsistent when measured on repeated occasions. Interindividual differences in sleep in response to exercise were small compared with the natural (trial-to-trial) within-subject variability in sleep outcomes. Clinical trials information https://clinicaltrials.gov/study/NCT05022498. Registration number: NCT05022498. Graphical Abstract Graphical Abstract

Acute exercise suppresses appetite and alters food‐cue reactivity, but the extent exercise‐induced changes in cerebral blood flow (CBF) influences the blood‐oxygen‐level‐dependent (BOLD) signal during appetite‐related paradigms is not known. This study examined the impact of acute running on visual food‐cue reactivity and explored whether such responses are influenced by CBF variability. In a randomised crossover design, 23 men (mean ± SD: 24 ± 4 years, 22.9 ± 2.1 kg/m2) completed fMRI scans before and after 60 min of running (68% ± 3% peak oxygen uptake) or rest (control). Five‐minute pseudo‐continuous arterial spin labelling fMRI scans were conducted for CBF assessment before and at four consecutive repeat acquisitions after exercise/rest. BOLD‐fMRI was acquired during a food‐cue reactivity task before and 28 min after exercise/rest. Food‐cue reactivity analysis was performed with and without CBF adjustment. Subjective appetite ratings were assessed before, during and after exercise/rest. Exercise CBF was higher in grey matter, the posterior insula and in the region of the amygdala/hippocampus, and lower in the medial orbitofrontal cortex and dorsal striatum than control (main effect trial p ≤ .018). No time‐by‐trial interactions for CBF were identified (p ≥ .087). Exercise induced moderate‐to‐large reductions in subjective appetite ratings (Cohen's d = 0.53–0.84; p ≤ .024) and increased food‐cue reactivity in the paracingulate gyrus, hippocampus, precuneous cortex, frontal pole and posterior cingulate gyrus. Accounting for CBF variability did not markedly alter detection of exercise‐induced BOLD signal changes. Acute running evoked overall changes in CBF that were not time dependent and increased food‐cue reactivity in regions implicated in attention, anticipation of reward, and episodic memory independent of CBF. We investigated the impact of a single running bout on cerebral blood flow (CBF) and food cue reactivity using functional magnetic resonance imaging (fMRI) in healthy men. Running did not alter the time‐course of grey matter or regional CBF up to 30 min after exercise cessation but increased food cue reactivity in brain regions implicated in attention, reward and episodic memory retrieval. Exercise‐related BOLD signal changes were detected in the presence of underlying CBF.

Breakfast omission induces compensatory eating behaviour at lunch, but often reduces daily energy intake. This study investigated the effect of breakfast omission on within-day subjective appetite, energy expenditure, substrate utilisation, and appetite hormone profiles, in response to standardised feeding and exercise. Eight male, habitual breakfast eaters completed two randomised trials. Subjects arrived overnight fasted (0 h), and either consumed (BC) or omitted (BO) a standardized breakfast (mean standard deviation [SD]) (3085 [217] kJ). Lunch (4162 [510] kJ) and dinner (4914 [345] kJ) were provided at 4.5 and 10 h, respectively and subjects performed 60 min fixed-intensity cycling (50% VO2 peak) at 8 h. Blood samples were collected at 0, 4.5, 6, and 8 h, with expired air and subjective appetite sensations (hunger, fullness, desire to eat (DTE), and prospective food consumption [PFC]) collected throughout. Heart rate and perceived exertion were measured during exercise. Hunger, DTE and PFC were greater and fullness lower during BO (P < 0.05) between breakfast and lunch, with no differences after lunch (P > 0.193). Resting energy expenditure was greater at 2.5 h during BC (P < 0.05) with no other differences between trials (P > 0.156). Active glucogon-like peptide-1 (GLP-17-36) was greater (P < 0.05) and acylated ghrelin tended to be greater (P = 0.078) at 4.5 h during BC. Heart rate was greater on BO (P < 0.05) during exercise. The results of this laboratory-controlled study suggest that the effects of breakfast omission are transient and do not extend beyond lunch, even when the negative energy balance created by breakfast omission is sustained via standardised feeding and exercise. •Appetite responses to breakfast omission/consumption were compared.•Lunch and dinner intake were standardized.•Subjective appetite was not different between trials after lunch.•GLP-17-36 and acylated ghrelin were not different between trials after lunch.•The effects of breakfast omission appear transient and do not extend beyond lunch.

Intermittent energy restriction (IER) involves short periods of severe energy restriction interspersed with periods of adequate energy intake, and can induce weight loss. Insulin sensitivity is impaired by short-term, complete energy restriction, but the effects of IER are not well known. In randomised order, fourteen lean men (age: 25 (sd 4) years; BMI: 24 (sd 2) kg/m2; body fat: 17 (4) %) consumed 24-h diets providing 100 % (10 441 (sd 812) kJ; energy balance (EB)) or 25 % (2622 (sd 204) kJ; energy restriction (ER)) of estimated energy requirements, followed by an oral glucose tolerance test (OGTT; 75 g of glucose drink) after fasting overnight. Plasma/serum glucose, insulin, NEFA, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) and fibroblast growth factor 21 (FGF21) were assessed before and after (0 h) each 24-h dietary intervention, and throughout the 2-h OGTT. Homoeostatic model assessment of insulin resistance (HOMA2-IR) assessed the fasted response and incremental AUC (iAUC) or total AUC (tAUC) were calculated during the OGTT. At 0 h, HOMA2-IR was 23 % lower after ER compared with EB (P<0·05). During the OGTT, serum glucose iAUC (P<0·001), serum insulin iAUC (P<0·05) and plasma NEFA tAUC (P<0·01) were greater during ER, but GLP-1 (P=0·161), GIP (P=0·473) and FGF21 (P=0·497) tAUC were similar between trials. These results demonstrate that severe energy restriction acutely impairs postprandial glycaemic control in lean men, despite reducing HOMA2-IR. Chronic intervention studies are required to elucidate the long-term effects of IER on indices of insulin sensitivity, particularly in the absence of weight loss.

ObjectiveFamilial hypercholesterolaemia (FH) elevates low-density lipoprotein cholesterol (LDL-C) and increases cardiovascular disease (CVD) risk. This study aimed to provide evidence for the feasibility of conducting a randomised controlled trial to evaluate the efficacy of an intervention designed to improve diet and physical activity in families with FH.DesignA parallel, randomised, waitlist-controlled, feasibility pilot trial.SettingThree outpatient lipid clinics in the UK.ParticipantsFamilies that comprised children (aged 10–18 years) and their parent with genetically diagnosed FH.InterventionFamilies were randomised to either 12-week usual care or intervention. The behavioural change intervention aimed to improve dietary, physical activity and sedentary behaviours. It was delivered to families by dietitians initially via a single face-to-face session and then by four telephone or email follow-up sessions.Outcome measuresFeasibility was assessed via measures related to recruitment, retention and intervention fidelity. Postintervention qualitative interviews were conducted to explore intervention acceptability. Behavioural (dietary intake, physical activity and sedentary time) and clinical (blood pressure, body composition and blood lipids) outcomes were collected at baseline and endpoint assessments to evaluate the intervention’s potential benefit.ResultsTwenty-one families (38% of those approached) were recruited which comprised 22 children and 17 adults with FH, and 97% of families completed the study. The intervention was implemented with high fidelity and the qualitative data revealed it was well accepted. Between-group differences at the endpoint assessment were indicative of the intervention’s potential for improving diet in children and adults. Evidence for potential benefits on physical activity and sedentary behaviours was less apparent. However, the intervention was associated with improvements in several CVD risk factors including LDL-C, with a within-group mean decrease of 8% (children) and 10% (adults).ConclusionsThe study’s recruitment, retention, acceptability and potential efficacy support the development of a definitive trial, subject to identified refinements.Trial registration numberISRCTN24880714.

Background/Objectives: Long-term success of weight loss diets might depend on how the appetite regulatory system responds to energy restriction (ER). This study determined the effect of 24 h severe ER on subjective and hormonal appetite regulation, subsequent ad libitum energy intake and metabolism. Subjects/Methods: In randomised order, eight overweight or obese males consumed a 24 h diet containing either 100% (12105 (1174 kJ; energy balance; EB) or 25% (3039 (295) kJ; ER) of estimated daily energy requirements (EER). An individualised standard breakfast containing 25% of EER (3216 (341) kJ) was consumed the following morning and resting energy expenditure, substrate utilisation and plasma concentrations of acylated ghrelin, glucagon-like peptide-1 (GLP-1 7–36 ), glucose-dependant insulinotropic peptide (GIP 1–42 ), glucose, insulin and non-esterified fatty acid (NEFA) were determined for 4 h after breakfast. Ad libitum energy intake was assessed in the laboratory on day 2 and via food records on day 3. Subjective appetite was assessed throughout. Results: Energy intake was not different between trials for day 2 (EB: 14946 (1272) kJ; ER: 15251 (2114) kJ; P =0.623), day 3 (EB: 10580 (2457) kJ; 10812 (4357) kJ; P =0.832) or day 2 and 3 combined ( P= 0.693). Subjective appetite was increased during ER on day 1 ( P <0.01), but was not different between trials on day 2 ( P >0.381). Acylated ghrelin, GLP-1 7–36 and insulin were not different between trials ( P >0.104). Post-breakfast area under the curve (AUC) for NEFA ( P <0.05) and GIP 1–42 ( P <0.01) were greater during ER compared with EB. Fat oxidation was greater ( P <0.01) and carbohydrate oxidation was lower ( P <0.01) during ER, but energy expenditure was not different between trials ( P =0.158). Conclusions: These results suggest that 24 h severe ER does not affect appetite regulation or energy intake in the subsequent 48 h. This style of dieting may be conducive to maintenance of a negative EB by limiting compensatory eating behaviour, and therefore may assist with weight loss.

The fat mass and obesity-associated gene (FTO) rs9939609 A-allele is linked to obesity and dyslipidemia, yet the independent influence of this polymorphism on blood lipids remains equivocal. We examined the influence of the FTO rs9939609 polymorphism on fasting and postprandial blood lipids in individuals homozygous for the risk A-allele or T-allele with similar anthropometric and demographic characteristics. 12 AA and 12 TT males consumed a standardized meal after fasting overnight. Blood samples were collected at baseline (−1.5 h), before the meal (0 h), and for five hours postprandially to measure lipid, glucose, and insulin concentrations. Time-averaged total area under the curve (TAUC) values (0–5 h) were calculated and compared between genotypes. Fasting triacylglycerol (TG), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, non-esterified fatty acid (NEFA), glucose, and insulin concentrations were similar between groups (p ≥ 0.293). TAUC for TG was similar in AAs and TTs (95% confidence interval (CI) −0.52 to 0.31 mmol/L/h; p = 0.606). Likewise, TAUC values were similar for NEFA (95% CI −0.04 to 0.03 mmol/L/h; p = 0.734), glucose (95% CI −0.41 to 0.44 mmol/L/h; p = 0.951), and insulin (95% CI −6.87 to 2.83 pmol/L/h; p = 0.395). Blood lipids are not influenced by the FTO rs9939609 polymorphism, suggesting the FTO-dyslipidemia link is mediated by adiposity and weight management is important in preventing FTO-related lipid variations.

OBJECTIVES:To undertake a process-evaluation of a structured health intervention for truckers (SHIFT) implemented in a sample of UK lorry drivers. METHODS:A combination of “debrief interviews,” focus groups and one-to-one interviews, in addition to observations and reflections of the two lead researchers were used to collect data on the acceptability of SHIFT from a group of 16 lorry drivers and four transport managers. RESULTS:The SHIFT program was considered relevant and acceptable to lorry drivers. It provided them with health information tailored to their specific health needs, long-lasting tools and techniques, which helped to raise their awareness of key health issues and helped to stimulate lifestyle changes during their daily routine. CONCLUSION:This process-evaluation suggests that the SHIFT program should now be evaluated on a larger scale and tested through fully randomized controlled trials.