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Thematic analysis of interviews exploring the perceptions of antenatal exercise in pregnant individuals and the impact of COVID-19

Hamstring muscle injury is highly prevalent in sports involving repeated maximal sprinting. Although neuromuscular fatigue is thought to be a risk factor, the mechanisms underlying the fatigue response to repeated maximal sprints are unclear. Here, we show that repeated maximal sprints induce neuromuscular fatigue accompanied with a prolonged strength loss in hamstring muscles. The immediate hamstring strength loss was linked to both central and peripheral fatigue, while prolonged strength loss was associated with indicators of muscle damage. The kinematic changes immediately after sprinting likely protected fatigued hamstrings from excess elongation stress, while larger hamstring muscle physiological cross-sectional area and lower myoblast:fibroblast ratio appeared to protect against fatigue/damage and improve muscle recovery within the first 48 h after sprinting. We have therefore identified novel mechanisms that likely regulate the fatigue/damage response and initial recovery following repeated maximal sprinting in humans.

Sprint interval training (SIT) has been proposed as a time efficient alternative to endurance training (ET) for increasing skeletal muscle oxidative capacity and improving certain cardiovascular functions. In this study we sought to make the first comparisons of the structural and endothelial enzymatic changes in skeletal muscle microvessels in response to ET and SIT. Sixteen young sedentary males (age 21 ± SEM 0.7 years, BMI 23.8 ± SEM 0.7 kg m-2) were randomly assigned to 6 weeks of ET (40-60 min cycling at ∼65%, 5 times per week) or SIT (4-6 Wingate tests, 3 times per week). Muscle biopsies were taken from the m. vastus lateralis before and following 60 min cycling at 65% to measure muscle microvascular endothelial eNOS content, eNOS serine1177 phosphorylation, NOX2 content and capillarisation using quantitative immunofluorescence microscopy. Whole body insulin sensitivity, arterial stiffness and blood pressure were also assessed. ET and SIT increased skeletal muscle microvascular eNOS content (ET 14%; P < 0.05, SIT 36%; P < 0.05), with a significantly greater increase observed following SIT (P < 0.05). Sixty minutes of moderate intensity exercise increased eNOS ser1177 phosphorylation in all instances (P < 0.05), but basal and post-exercise eNOS ser1177 phosphorylation was lower following both training modes. All microscopy measures of skeletal muscle capillarisation (P < 0.05) were increased with SIT or ET, while neither endothelial nor sarcolemmal NOX2 was changed. Both training modes reduced aortic stiffness and increased whole body insulin sensitivity (P < 0.05). In conclusion, in sedentary males SIT and ET are effective in improving muscle microvascular density and eNOS protein content. © 2013 The Authors. The Journal of Physiology © 2013 The Physiological Society.

Intramuscular triglyceride (IMTG) utilization is enhanced by endurance training (ET) and is linked to improved insulin sensitivity. This study first investigated the hypothesis that ET-induced increases in net IMTG breakdown and insulin sensitivity are related to increased expression of perilipin 2 (PLIN2) and perilipin 5 (PLIN5). Second, we hypothesized that sprint interval training (SIT) also promotes increases in IMTG utilization and insulin sensitivity. Sixteen sedentary males performed 6 weeks of either SIT (4–6, 30 s Wingate tests per session, 3 days week−1) or ET (40–60 min moderate-intensity cycling, 5 days week−1). Training increased resting IMTG content (SIT 1.7-fold, ET 2.4-fold; P < 0.05), concomitant with parallel increases in PLIN2 (SIT 2.3-fold, ET 2.8-fold; P < 0.01) and PLIN5 expression (SIT 2.2-fold, ET 3.1-fold; P < 0.01). Pre-training, 60 min cycling at ∼65% pre-training decreased IMTG content in type I fibres (SIT 17 ± 10%, ET 15 ± 12%; P < 0.05). Following training, a significantly greater breakdown of IMTG in type I fibres occurred during exercise (SIT 27 ± 13%, ET 43 ± 6%; P < 0.05), with preferential breakdown of PLIN2- and particularly PLIN5-associated lipid droplets. Training increased the Matsuda insulin sensitivity index (SIT 56 ± 15%, ET 29 ± 12%; main effect P < 0.05). No training × group interactions were observed for any variables. In conclusion, SIT and ET both increase net IMTG breakdown during exercise and increase in PLIN2 and PLIN5 protein expression. The data are consistent with the hypothesis that increases in PLIN2 and PLIN5 are related to the mechanisms that promote increased IMTG utilization during exercise and improve insulin sensitivity following 6 weeks of SIT and ET.

Coronary artery disease (CAD) is the leading cause of global death. Diagnosis and treatment for CAD often involves angiography and/or angioplasty. However, the radial artery catheterization required during both procedures may result in acute artery dysfunction/damage, mainly due to endothelial disruption. Whilst exercise training typically enhances endothelial function, and is therefore generally recommended for CAD patients, animal studies indicated paradoxical exercise-induced vasoconstriction post-catheterization. It is not currently known if there is an acute period when exercise is detrimental due to catheter-induced damage. Chapter 4 has demonstrated that catheterization in CAD patients results in impaired flow-mediated dilation (FMD), but that arterial responses to handgrip exercise (HE) are preserved 1 week post-catheterization. This finding suggests that the impact of endothelial disruption may be stimulus specific, with redundant mechanisms likely to preserve exercise-mediated vasodilator responses in the face of catheterization-mediated damage. Chapter 6 showed that catheterization in young healthy males with a fully functional endothelium resulted in reduced FMD, including completely abolished FMD (≤0%) in approximately 1/5th of participants. This exaggerated response in healthy subjects, compared to CAD patients, raises the question of whether individuals with a priori endothelial dysfunction are more or less susceptible to catheterization-induced arterial risk. Given the association between endothelial dysfunction and CAD progression, Chapter 5 explored relationships between FMD and arterial responses to exercise with the protein content of eNOS, NAD(P)Hox subunit 2, NFκB, ET-1, nitrotyrosine, the senescence markers (p53, p21, p16) and eNOS Ser1177 phosphorylation in endothelial cells (EC)s obtained from the radial arteries of CAD patients. FMD was positively associated with eNOS Ser1177 phosphorylation, and protein content of p21 and p16, whereas no associations were found between FMD and markers of oxidative stress, vasoconstriction or inflammation. HE-induced dilation was not associated with any of the EC proteins, or FMD. A number of associations were observed between the expression of atherogenic risk-modulating proteins, providing novel insight into the molecular mechanisms related to vascular function in CAD. Lastly, Chapter 7 provided novel molecular insights into how elevated shear stress induced by exercise benefits endothelial function in humans. In particular, it has been shown that a ~5-fold increase in shear stress induced by 30 minutes of HE resulted in upregulation of eNOS Ser1177 phosphorylation, whereas no effect was reported in PECAM-1 Tyr713 activation in ECs obtained from radial artery of young healthy well-trained males. As such, this study suggests that PECAM-1 activation is not involved in the vascular response to prolonged elevations in shear stress. In conclusion, this thesis provided important information regarding the impact of catheterization on arterial function, showing preserved exercise-induced dilation in CAD patients following catheterization damage. This suggests early onset of exercise-based rehabilitation after catheterization procedures is safe, although this should be confirmed in other cohorts and in a larger sample. In addition, this thesis demonstrated novel insights into the molecular mechanisms related to arterial function in CAD, suggesting that progressive endothelial dysfunction in CAD may be more dependent on NO production than NO scavenging. Finally, this thesis provided novel data regarding the mechanism by which ECs sense elevated shear stress, suggesting no involvement of PECAM-1 in exercise-induced NO production.

Within the laboratory setting, high intensity interval training (HIIT) can elicit physiological adaptations similar to traditional moderate intensity continuous training (MICT) with the important advantage of a reduced total exercise volume and time commitment. However, researchers have argued that HIIT is not a viable public health strategy because it is too demanding to be maintained by non-athletic populations (Biddle and Batterham, 2015). The aim of this thesis was to investigate the effect of real-world HIIT interventions on adherence and cardio-metabolic health risk factors. Furthermore this thesis investigates the feasibility and perceptual responses to home-based wholebody HIIT as a strategy to remove many of the major barriers to exercise. In Chapter 3, 82 previously sedentary males (n=26) and females (n=56) aged 18-65 (28±10 y, BMI 25±3 kg.m-2) participated in the study. In a randomised cross-over design, whereby participants completed either 6 weeks of 30HIT (4-8x30s sprint with 120s active recovery) and 6-weeks of 60HIT (6-10x60s sprint with 60s active recovery). Participants then completed a 4-week washout period before completing the alternative intervention. Training sessions were completed on a Wattbike, 3 times per week. VO2peak, body composition (DXA), glycaemic control (oral glucose tolerance test (OGTT) and arterial stiffness (aortic pulse wave velocity (aPWV)) were assessed pre and post each 6-week training phase. VO2peak increased post intervention in 30HIT and 60HIT (P0.05). In Chapter 4, 154 patients (males: n=88), females: n=66) who were eligible for a UK exercise referral scheme (ERS) (inactive and at least one health risk factor) were recruited. Participants chose either 12-weeks ERS (encouraged to achieve 150min/wk of moderate-intensity exercise, with reduced cost gym membership) or Home-based HIIT (4-9x1min intervals interspersed with 1 min rest, using body weight exercises). Adherence and compliance to the programme were monitored using a heart rate monitor. VO2peak, body composition (DXA), glycaemic control (OGTT) and arterial stiffness (aPWV) was recorded at baseline, post-intervention (12-weeks) and 3-months postintervention (follow-up). Perceptions of the programme were evaluated using an online interview. 56% (n=87) of eligible participants chose Home-based HIIT in preference to ERS. At baseline Home-based HIIT had a lower VO2peak than ERS (P=0.034). ERS and Home-based HIIT had a similar adherence (HIIT 39%, ERS 53% P=0.298) and compliance to the prescribed programme (HIIT 30%, ERS 47% P=0.331). VO2peak increased post-intervention (P

Aims: The aims of this study were to investigate: the effects of home-HIIT and home-MICT completed in a postprandial state compared to a non-exercise control period on; i) hypoglycaemia ii) time in range (TIR), and iii) glycaemic variability (GV), for up to 48-hours post exercise in a free-living environment in adults with Type 1 diabetes. A secondary aim was to investigate whether acute changes following exercise influenced 14-day glycaemic control. Methods: 11 adults with Type 1 diabetes (male n=4, female n=7, age 26 ± 7 years, BMI 25.43 ± 4.29 kg.m2, Type 1 diabetes duration 10 ± 8 years) completed a randomised crossover study consisting of three 14-day interventions; 1) home-HIIT, 2) home-MICT and 3) non-exercise control (CON). During exercise intervention the effect of six exercise sessions on subsequent glycaemic control was assessed for up to 48-hours post exercise. CON data was time matched to home-HIIT. Glycaemic control was measured using an Abbot Freestyle Libre flash glucose monitor. Dietary intake and insulin dose were also assessed. Results: Neither home-HIIT or home-MICT increased time spent in serious, clinically significant hypoglycaemia (< 3.0 mmol/L) compared to CON at any period during the 48 hours post exercise (P > 0.05). TIR in home-HIIT was significantly greater during the period immediately after exercise compared to CON (11% [0, 22], P = 0.043) and significantly greater compared to home-MICT during the awake periods on the day following (10% [2, 18], P = 0.013) and second day following exercise (11% [3, 20], P = 0.014). GV, assessed as coefficient of variation (CV) was increased during the nocturnal period on the second day following home-MICT compared to CON (CV = 4% [1, 7] P = 0.008) and home-HIIT (CV = -5% [-8, 2], P = 0.005). This increase in GV translated into an increased nocturnal GV over the 14-day day intervention period in home-MICT compared to home-HIIT (CV = -4% [-8, 0], P = 0.034). Conclusion: In conclusion, both home-HIIT and home-MICT are safe exercise modalities for people with Type 1 diabetes but Home-HIIT may provide more beneficial effects on glycaemic control compared to home-MICT. This study provides novel evidence that exercise affects glycaemic control for up to 48-hours post exercise in people with Type 1 diabetes.

In this paper a three-dimensional isotropic fractional viscoelastic model is examined. It is shown that if different time scales for the volumetric and deviatoric components are assumed, the Poisson ratio is time varying function; in particular viscoelastic Poisson ratio may be obtained both increasing and decreasing with time. Moreover, it is shown that, from a theoretical point of view, one-dimensional fractional constitutive laws for normal stress and strain components are not correct to fit uniaxial experimental test, unless the time scale of deviatoric and volumetric are equal. Finally, the model is proved to satisfy correspondence principles also for the viscoelastic Poisson’s ratio and some issues about thermodynamic consistency of the model are addressed.

Introduction: Laboratory-based High intensity interval training (HIIT) is an efficacious time-saving exercise modality resulting in similar adaptations to traditional moderate-intensity continuous training. Recently, Home-based HIIT, involving bodyweight exercises, has gained popularity in the literature, as it overcomes additional barriers such as limited access to facilities and appropriate equipment. However, literature in to home-based HIIT is still sparse, and little is known about how manipulating interval duration, interval number and work-to-rest ratio could influence the efficacy and effectiveness of such interventions. Aims: Two separate but related studies were conducted. The aim of study 1 was to investigate the acute physiological, perceptual, and motivational responses to five home-based HIIT protocols with various work-to-rest ratios (specifically 1:1, 1:2 and 1:4) and interval durations (30s or 60s). The aim of study 2 was to implement and compare two of the HIIT protocols investigated in study one to identify the ideal interval duration for improving cardiorespiratory fitness (CRF) and health in sedentary individuals. Methods: In Study 1, 10 healthy participants (age = 25±4 yrs, BMI = 22.7±1.4kg.m2) completed a randomised cross-over study, whereby each participant completed five bodyweight HIIT protocols, four using 30s intervals (30:30x6 (30s interval interspersed with 30s rest, completed 6 times), 30:60x6, 30:120x6 and 30:30x12) and one using 60s intervals (60:60x6). A total of 12 exercises were implemented, examples included burpees, mountain climbers, and jumping jacks. Blood lactate, heart rate (HR), feeling scale (FS), enjoyment and perceived competence were measured in response to each protocol. In Study 2, 28 healthy sedentary participants (age = 29±10 yrs, BMI = 25.3±3.9 kg.m2) completed a randomised cross-over design, whereby each participant completed 6 weeks of 30:120HIIT (4-8x30s with 120s rest) and 60:60HIIT (6-10x60s with 60s rest). In addition to the 12 exercises implemented in study 1, a further 6 were added in study 2. CRF, body composition (bioimpedance), blood pressure and aortic pulse wave velocity were assessed pre and post each intervention, with a 4-6-week wash-out period between interventions. Results: Study 1 (acute phase), established that 60:60x6 and 30:30x12 resulted in significantly higher change in blood lactate and HR responses compared to 30:30x6, 30:60x6, and 30:120x6 (P0.05). Study 2 (chronic phase) demonstrated that CRF increased following both 30:120HIIT and 60:60HIIT (P0.05). Conclusion: This is the first study to directly compare different home-based HIIT protocols by manipulating interval durations and work-to-rest ratios. Home-based HIIT protocols consisting of 30:120HIIT and 60:60HIIT improved CRF and aPWV after 6 weeks in sedentary individuals, despite 30:120HIIT producing significantly lower lactate and heart rate responses whilst also showing less aversive perceptions during an acute bout of exercise to that of 60:60HIIT.

New strategies are urgently needed to increase physical activity participation in the increasingly sedentary population to combat the rising rates of obesity and metabolic disease. The aim of this thesis was to provide evidence that practical high-intensity interval training (HIT) strategies can remove many of the major exercise barriers for obese individuals and people with type 1 diabetes that could potentially increase physical activity participation. Secondly, this thesis aimed to provide mechanistic evidence to explain the physiological effectiveness of HIT as a means to reduce the risk of cardio-metabolic disease. In Chapters 4 and 5, 32 obese adults with at least 3 additional cardiovascular disease (CVD) risk factors completed one of three 12-week training programmes 3x/week: Home-HIT (n=9); Laboratory-based supervised HIT (Lab-HIT; n=10) or home-based moderate intensity continuous training (Home-MICT; n=13). Changes in V ̇O2peak, insulin sensitivity, body composition, flow-mediated dilation (FMD) and aortic pulse wave velocity (PWV) were assessed. Muscle biopsies were taken to assess changes in capillarisation, mitochondrial density, intramuscular triglyceride (IMTG) content and eNOS and GLUT4 protein expression using quantitative immunofluorescence microscopy. Adherence and compliance (Home-HIT 96±3% & 99±1%; Home-MICT 88±4% & 100±0%; Lab-HIT 97±1% & 100±0%, respectively) to training did not differ between groups. Training increased V ̇O2peak and Matsuda insulin sensitivity index (P

Introduction: Aerobic exercise capacity outperforms established clinical risk factors such as smoking, hypertension, obesity and diabetes in predicting all-cause mortality (Myer et al., 2004). ‘Lack of time’ is the most commonly cited barrier to sufficient amounts of physical activity (Trost et al., 2002). High intensity interval training (HIT) is a time-efficient alternative to moderate intensity continuous training (MICT), but the feasibility for exercise-naïve individuals has been questioned. Success has depended on vigorous encouragement by the researchers and the presence of expensive specialised cycle ergometers. Aim: To investigate whether two popular HIT protocols (30HIT and 60HIT) can increase aerobic exercise capacity without verbal encouragement or specialised cycle ergometers, such that HIT interventions can be delivered in a real life setting independent of instructors. Methods: Twenty-eight previously sedentary males (n=6) and females (n=22) aged 18-55 participated (28±2 y, BMI 25±1 kg.m2). In a randomised counterbalanced cross-over design, participants completed either 6 weeks of 30HIT (4-8x30s with 120s active recovery) or 60HIT (6-10x60s with 60s active recovery). Training sessions were completed on a Wattbike, 3 times per week. Participants were told to reach > 80% of maximal heart rate (HRmax). VO2peak and Watt max were assessed pre and post each intervention, with a 4-6 weeks wash-out period between interventions. Results: VO2peak increased post intervention in 30HIT (37±1 to 38±1 ml.min-1.kg-1) and 60HIT (35±1 to 38±1 ml.min-1.kg-1). There was a significant main effect of training on VO2peak (P < 0.001), with no difference between training modes (P=0.849). When normalized to Watt max those participants producing higher peak power output (PPO) improved their VO2peak significantly more than those producing a low PPO, irrespective of group (30HIT P