Dissertations / Theses on the topic 'Resistance exercise intervention'

There is abundant evidence supporting the health benefits physical activity in cancer survival. Exercise per se is associated with positive physical and psychosocial benefits for survivors of solid tumours. There are limited available research data on blood borne cancers. Lymphoma is one such haematological cancer where survivors often experience decrements in psychosocial, physical functioning and quality of life (QoL) domains. A minority (~25%) of lymphoma survivors meet the recommended public guidelines for exercise. Further to this, the work of Bellizzi and colleagues (2009) indicates that QoL decrements often persist for years following treatment. Conventional wisdom dictates that exercise is likely to be an effective means of alleviating some adverse outcomes from blood borne cancers but this hypothesis is largely untested to date. Further to this, the theory of planned behaviour (TPB) has been shown to provide effectual model for predicting exercise behaviour amongst cancer survivors but known to differ by tumour type. Therefore, the aims of the present thesis were to determine the effects of 12-weeks of a combined aerobic and resistance training programme (CARP) on QoL and health related outcomes in Hodgkin’s lymphoma (HL) and Non-Hodgkin’s lymphoma (NHL) survivors. The thesis focused specifically on four main aims; Aim 1 the primary aim was to identify whether a 12-week CARP is effective at improving QoL in HL and NHL survivors. Secondary Aims were to; Aim 2 to determine whether a 12-week CARP is effective at improving standard measures of muscle function and cardio-respiratory fitness in HL and NHL survivors. Aim 3 to examine whether a 12-week CARP affects inflammatory environment and/or immune function in HL and NHL survivors. Aim 4 to identify whether theory of planned behaviour (TPB) may be an effectual model to predict exercise intention in HL and NHL survivors. In realising these aims, a parallel group randomised control exercise trial (RCT) was conducted with two components. Forty-one (n=41) HL and NHL survivors completed the trial at St George’s hospital, London. Participants, who had completed chemotherapy or radiation treatment (<6 months), were stratified according to tumour type and randomly assigned to either control (CON; n=21) or intervention (INT; n=20). The intervention consisted of a combination of 12-weeks supervised aerobic and resistance training (CARP) whilst the control group received usual care. The first component consisted of three measurement phases; baseline (To; n=41), post-intervention (T1; n=41) for all measurements, and 12 months follow-up (T2; n=15) for qualitative measures. A representative sample (n=6) from the intervention group took part in a focus group to explore participant perception of the impact of the CARP. QoL was assessed using the previously validated European Organization for Research and Treatment of Cancer Quality of Life (EORTC-QLQ-30) questionnaire. Secondary outcome measures consisted of health-related quality of life (HRQoL) determined by Functional Assessment of Cancer Therapy in Lymphoma (FACT-Lym); Mood disturbance and fatigue were determined using Profile of Mood States (POMS) questionnaire; anxiety and depression were determined using Hospital Anxiety and Depression scale (HADS). Participant cardiorespiratory fitness was assessed using the Balke-ware treadmill test, muscle function assessed by grip strength and muscle endurance tests. Blood was sampled using the standard venepuncture method followed by radioimmunoassay to determine interleukin 6 (IL-6) and c-reactive protein (CRP) concentrations. In order to identify determinants of exercise intention and behaviour in HL and NHL survivors, a second component to the trial utilised a validated TPB questionnaire, assessed at baseline (To; n=41), and post-intervention (T1; n=41). Data were analysed using SPSS version 18.0 using appropriate statistical functions. Statistical significance was set at p<0.05. Data are presented as means i standard deviations (S.D.). Results demonstrate that study adherence between To and T1 was 87.2% (41/47) with a large accession rates at 12 months follow up (15/41). Linear mixed models analysis was used to examine subjectively reported outcomes. Clinically relevant improvements in QoL were achieved in both groups at T1. HRQoL, a domain of QoL, increased with exercise; the improvements were both clinically relevant and statistically significant. Subscales of QoL and HRQoL that significantly improved with exercise are social function (p=0.020), emotional well-being (p=0.029), and functional well-being (p=0.025), as well as functional lymphoma specific concerns (p=0.034). Mood disturbance was unchanged in either group, physical function improved only in the control group (p=0.049). Both groups showed improved (p<0.05) physical well-being, vigour, reduced fatigue, and increase in subjectively reported amount of physical activity (IPAQ) as time passed from the end of treatment. At follow-up, HRQoL, lymphoma concerns, fatigue, and the trial outcome index significantly improved in both groups (p<0.05) from baseline; anxiety significantly increased in the intervention and anxiety, physical well-being, and functional well-being improved in the control group. Both groups reduced physical activity at follow-up. Predicted aerobic capacity showed a trend towards an increase, whereas resting heart rate (p=0.041) abdominal muscle endurance (p=0.018) significantly improved in the [NT group with a concomitant trend for a decrease in the CON group. However, this did not reach a level of significance. Although both groups experienced worsening of pulmonary function post intervention, this only reached a level of significance in the ]NT group. No significant changes in either IL-6 or CRP were observed during the study. ANOVA and MANOVA were used to analyse physical outcomes. Regression analysis was used to determine the predictive value of the TPB variables upon intention to exercise, and TPB variables and intention upon actual behaviour. Simultaneous Multiple Regressions were used first to determine the equation for each model. Stepwise Multiple Regressions were used to examine the impact of each variable on the dependent variable to find the best model of prediction. At baseline (both INT and CON groups collapsed to one) the model predicts intention (68.6%), but prediction of variation in actual behaviour is low (36.2%); self- efficacy (13:0.495) and social support (13:0.469) predict intention to exercise among lymphoma survivors and self-efficacy (B=0.609) alone predicts actual behaviour at To. At T1, the model predicts 77.0% of the variation in intention amongst the CON group but only 14.7% of actual behaviour; attitude (B=0.864) predicted intention to behave. Amongst the exercising group, the model predicts 61.5% of the variation in intention, but only 19.2% of actual behaviour; social support (B=0.800) predicts intention to exercise. None of the determinants significantly predicted actual behaviour at T1. The current thesis presents the first data in examination of the impact of a CARP amongst post- treatment lymphoma survivors. The exercise training intervention significantly improved HRQOL and psychosocial well-being. This is noteworthy as lymphoma survivors are often burdened with reduced HRQOL and psychosocial morbidity. Although predicted aerobic fitness levels were statistically unchanged in INT following the intervention, the trend towards an improvement indicates that either an increase in exercise programme length or intensity of exercise sessions may achieve statistical improvement in future studies. The findings from this thesis indicate CARP to be effective in improving psychosocial outcomes in lymphoma survivors. At 12-month follow-up, reduced physical activity was associated with increased anxiety; functional and physical well-being did not improve despite increases seen in CON.

Resistance training is a highly utilised form of exercise that is used to develop strength, power, speed and muscular endurance. Although it is associated with many positive benefits it also has some potentially unfavourable effects. These are manifested in the form of altered muscle function through the effects of muscle fatigue and exercise induced muscle damage. Various aspects muscle fatigue and damage have been well studied, however research into the effects of these on tests of strength, power, acceleration and agility is sparse. Therefore the aim of this study was to investigate the effects of a heavy resistance intervention on the recovery of the above measures of performance. Performance of these parameters were examined through the application of functional .performance measures such as maximal voluntary isometric strength, vertical jump height, standing broad jump, 10m sprinting speed, and the Illinois Agility run. The subjects were recreationally active, but non•resistance trained, males between the age of 18 and 45. The subjects completed 10 testing sessions, four on the day of the heavy resistance intervention (prior, immediately post, 2 and 6 hours post) and 2 measurements taken 3 hours apart for the following 3 days. Results analysed via a one•way analysis of variance (ANOVA) with repeated measures, and simple contrasts to baseline were used to identify any significant relationships. Statistical significance was set at p

Black South African (SA) women are disproportionally affected by obesity and insulin resistance, which have been associated with depot-specific alterations in adipose tissue function. This thesis aimed to evaluate the differences in fatty acid (FA) composition and gene expression between abdominal (aSAT) and gluteal subcutaneous adipose tissue (gSAT), and the changes in response to exercise training in relation to body composition, hepatic fat, inflammatory and oxidative stress markers, and insulin sensitivity (SI) in obese black SA women. This research evaluated the i) FA composition of aSAT and gSAT, and red blood cell total phospholipids (RBC-TPL) and their associations with body composition, hepatic fat and SI, ii) changes in these FA profiles in response to exercise training and the relationship with changes in systemic inflammation, hepatic fat and SI; iii) effects of exercise training on systemic markers and SAT gene expression of inflammation and oxidative stress; and iv) regional differences in transcriptome profiles of aSAT and gSAT pre- and post-exercise training. Forty-five IsiXhosa women (30-40kg/m2 , 20-35 years) were randomized into control (n=22) or exercise groups (n=23; 12-week aerobic-resistance training, 40-60 min/session, 4 days/week). Pre and postintervention measurements included: anthropometry, body composition, cardiorespiratory fitness, dietary intake, SI, hepatic fat, systemic markers and SAT gene expression of adipokines, inflammation and oxidative stress, RBC-TPL and SAT fatty acids profiles, and untargeted SAT gene expression analyses. The main findings showed differences in the circulating (RBC-TPL) and stored (SAT) FA composition, which reflected in different associations between these FA profiles and SI. Moreover, the changes in FA composition in response to exercise training were depot-specific, with the changes in RBC-TPL correlating with a decrease in systemic inflammation and hepatic fat. Exercise training alleviated systemic oxidative stress and induced increased gSAT inflammatory genes, reflecting SAT remodelling. These changes coincided with a reduction in gynoid fat and were not associated with increased SI. Furthermore, there were unique depot-specific gene expression signatures relating to embryonic development at baseline and more diverse functional-related processes at post-training. This generated novel candidate genes potentially implicated in the relationship between body fat distribution and metabolic status in obese black SA women.

Syftet med denna studie var att undersöka effekten av 6 veckors styrketräning med så kallad Nordic Hamstring Exercise (NHE) i jämförelse med Razor Hamstring Curl (RHC) med avseende på hamstringsmuskulaturens styrka och rörlighet hos unga fotbollsspelare.   43 fotbollsspelande ungdomar från två olika lag rekryterades till studien varav 40 slutförde den. Deltagarna var av manligt kön och hade en medelålder på 17.2 ± 0.6. De randomiserades till två olika interventionsgrupper, NHE och RHC, där de fick utföra tilldelad övning under träningstid under sex veckor. Mätning av hamstrings rörlighet och isometrisk utvärdering av hamstrings muskelstyrka i 90°-, 45°- och 0°- knävinkel utfördes innan och efter intervention. Parade t-test och Wilcoxon signed rank test användes för att testa förändringen inom grupp och ANCOVA användes för att se skillnaderna mellan grupperna.    NHE-gruppen hade en signifikant ökning av muskelstyrkan i samtliga testvinklar. RHC gruppen hade signifikant ökning i endast två av tre testvinklar. Mätningen i 0° visade ingen signifikant ökning av muskelstyrkan. Rörligheten hade en signifikant ökning i båda interventionsgrupperna. När interventionsgrupperna testades mot varandra så hade NHE gruppen en signifikant högre ökning av muskelstyrkan i 0° mätningen jämfört med RHC gruppen. Ingen signifikant skillnad uppmärksammades i de andra testvinklarna eller i ökningen av rörligheten.   Både NHE- och RHC-träning under 6 veckor resulterade i signifikant ökning av muskelstyrka och rörlighet i hamstringsmuskulaturen hos unga fotbollsspelare. NHE resulterade dock i en signifikant större ökning av muskelstyrkan i ett större rörelseomfång än RHC-övningen. Baserat på resultaten i denna studie är NHE den föredragna metoden att inkludera i framtida träningsprogram.

A narrative review of quantitative studies was conducted to critically appraise and synthesise the current evidence for resistance exercise as a way to improve the psychosocial well-being of older adults. Fifteen articles, which met the inclusion criteria, were retrieved. The data were synthesized and critiqued according to methodological features. The results suggest that resistance exercise can significantly improve the psychosocial well-being of older adults and may be particularly effective for clinically unwell older adults. However, a cautious interpretation should be made when analysing the results, due to the diversity of resistance exercise used. Suggestions for future research were considered. A mixed-method approach combing both quantitative and qualitative methods was adopted for the empirical paper. Twenty-three participants were recruited through a larger study, a randomised controlled eight-week trial comparing resistance training with a treatment-as-usual group. Questionnaires were used to analyse the effect of exercise on quality of life and mental health of older adults. Results showed no significant differences between the groups. Interviews were conducted post intervention with nine participants who had been allocated to the resistance exercise group. Interview transcripts were analysed using thematic analysis. Six main themes were created to describe the participants’ experience: adjustment to illness; capabilities/limitations of body/ability; maintaining life’s qualities; impact of exercise; undertaking a research programme and being a helper. The analysis suggests that resistance exercise can improve mood, bodily confidence, social contact with others and generate routine and purpose. The findings also suggest that those who are not effectively supported may not continue with their exercise routine.

Childhood and adolescent obesity is a significant problem in Australia and it has reached alarming levels. While most studies have suggested that increased levels of physical activity, combined with improved nutrition can improve body composition and health of children who are obese or overweight, the majority of these programs have used aerobic-based interventions. Despite the abundant research on the role of which parents and schools can play in the prevention of obesity in children, the use of resistance training in youth and health promotion is a fairly new concept, and one that needs further study.

It has long been known that in addition to disruptions in glucose homeostasis, individuals with insulin resistance have a breakdown in lipid dynamics, often manifested by elevated levels of circulating fatty acids (FA) together with accumulation of lipids in insulin-sensitive tissues, including skeletal muscle. However, little is known about how common therapies used to treat insulin resistant individuals (such as Rosiglitazone and exercise training) improve skeletal muscle lipid and glucose metabolism. Thus, the primary aim of the studies undertaken for this thesis was to enhance our understanding of the mechanisms by which Rosiglitazone and exercise training improve skeletal muscle lipid metabolism and insulin sensitivity in two distinct models of insulin resistance. The first investigation determined the effect of chronic Rosiglitazone treatment on the accumulation of lipid metabolites and enzymatic regulators of lipid metabolism in the skeletal muscle of obese Zucker rats. The observation that Rosiglitazone treatment exacerbated the accumulation of muscle ceramide and diacylglycerol in skeletal muscle, while improving glucose tolerance led to the conclusion that this insulin sensitising drug improves insulin sensitivity by mechanisms other than reduction of fatty acid metabolites in this tissue. Accordingly, the second investigation sought to identify an alternative mechanism by which Rosiglitazone treatment may improve skeletal muscle insulin sensitivity. It was found that Rosiglitazone restored AMP-activated protein kinase (AMPK) á2 activity in the skeletal muscle of obese Zucker rats, providing a potential peroxisome proliferator activated receptor (PPAR) ã-independent mechanism by which this drug may mediate its insulinsensitising actions. The final experiment undertaken for this thesis determined the independent and interactive effects on Rosiglitazone and exercise training on various aspects of skeletal muscle glucose and lipid metabolism in a model of diet-induced insulin resistance, the high-fat fed rat. Exercise training, but not Rosiglitazone treatment restored skeletal muscle insulin sensitivity in high-fat fed rats. Improvements in insulin sensitivity with exercise training were associated with increased FA oxidation, increased AMPK activity and a normalisation of the expression of the Akt substrate, AS160. In contrast, Rosiglitazone treatment was associated with increased FA uptake and decreased insulin-stimulated glucose uptake in skeletal muscle. Exercise prevented the accumulation of skeletal muscle lipids in Rosiglitazone-treated animals when the two treatments were combined. In summary, the results from the studies undertaken for this thesis provide novel information regarding the mechanisms by which two insulinsensitising therapies, exercise training and Rosiglitazone treatment, act to improve glucose and lipid metabolism in skeletal muscle.It has long been known that in addition to disruptions in glucose homeostasis, individuals with insulin resistance have a breakdown in lipid dynamics, often manifested by elevated levels of circulating fatty acids (FA) together with accumulation of lipids in insulin-sensitive tissues, including skeletal muscle. However, little is known about how common therapies used to treat insulin resistant individuals (such as Rosiglitazone and exercise training) improve skeletal muscle lipid and glucose metabolism. Thus, the primary aim of the studies undertaken for this thesis was to enhance our understanding of the mechanisms by which Rosiglitazone and exercise training improve skeletal muscle lipid metabolism and insulin sensitivity in two distinct models of insulin resistance. The first investigation determined the effect of chronic Rosiglitazone treatment on the accumulation of lipid metabolites and enzymatic regulators of lipid metabolism in the skeletal muscle of obese Zucker rats. The observation that Rosiglitazone treatment exacerbated the accumulation of muscle ceramide and diacylglycerol in skeletal muscle, while improving glucose tolerance led to the conclusion that this insulin sensitising drug improves insulin sensitivity by mechanisms other than reduction of fatty acid metabolites in this tissue. Accordingly, the second investigation sought to identify an alternative mechanism by which Rosiglitazone treatment may improve skeletal muscle insulin sensitivity. It was found that Rosiglitazone restored AMP-activated protein kinase (AMPK) á2 activity in the skeletal muscle of obese Zucker rats, providing a potential peroxisome proliferator activated receptor (PPAR) ã-independent mechanism by which this drug may mediate its insulinsensitising actions. The final experiment undertaken for this thesis determined the independent and interactive effects on Rosiglitazone and exercise training on various aspects of skeletal muscle glucose and lipid metabolism in a model of diet-induced insulin resistance, the high-fat fed rat. Exercise training, but not Rosiglitazone treatment restored skeletal muscle insulin sensitivity in high-fat fed rats. Improvements in insulin sensitivity with exercise training were associated with increased FA oxidation, increased AMPK activity and a normalisation of the expression of the Akt substrate, AS160. In contrast, Rosiglitazone treatment was associated with increased FA uptake and decreased insulin-stimulated glucose uptake in skeletal muscle. Exercise prevented the accumulation of skeletal muscle lipids in Rosiglitazone-treated animals when the two treatments were combined. In summary, the results from the studies undertaken for this thesis provide novel information regarding the mechanisms by which two insulinsensitising therapies, exercise training and Rosiglitazone treatment, act to improve glucose and lipid metabolism in skeletal muscle.

Parmi les mécanismes possibles de l'insulinorésistance associée à l'obésité figurent une altération de la production d'adipokines par le tissu adipeux (TA). Dans une première partie, nous avons étudié des patients obèses soumis à des programmes nutritionnels ou d'activité physique. Les données phénotypiques ont été reliées à l'expression de gènes du TA potentiellement impliqués dans la sensibilité à l'insuline. Nous avons confirmé qu'un entraînement en condition aérobie ou en force améliorait la sensibilité à l'insuline et démontré que ces interventions ne modifiaient pas l'expression génique dans le TA sous-cutané ou les niveaux plasmatiques d'adiponectine, d'interleukine 6, d'interleukine 1 beta et de tumor necrosis factor alpha mais diminuaient les concentrations circulantes de leptine. Différentes phases d'un programme de perte de poids améliorent la sensibilité à l'insuline et diminuent transitoirement les concentrations plasmatiques de la protéine de liaison du rétinol RBP4. Les niveaux d'ARNm ne sont diminués qu'après la première phase à très basses calories. Nos résultats montrent que les adipokines, excepté peut-être la leptine, ne semblent pas des médiateurs des changements d'insulinosensibilité induits par une intervention diététique ou l'exercice physique. Dans une seconde partie, nous avons exploré le rôle des PPARs (peroxysome proliferator-activated receptors) sur la sécrétion de protéines par le TA sous-cutané humain. Il apparaît que les PPARs régulent la production de facteurs sécrétés provenant de différents types cellulaires du TA. Cet ensemble d'études contribuent à notre compréhension des relations entre adipokines et sensibilité à l'insuline
Obesity is associated with insulin resistance (IR) and type 2 diabetes mellitus. Among possible mechanisms leading to IR are increased plasma levels of free fatty acids and altered levels of adipokines secreted from adipose tissue (AT). In the first part of the work, we studied obese patients during different nutritional and physical activity interventions. Phenotypic data were related to the expression of AT genes potentially involved in the regulation of insulin sensitivity (IS) and/or low-grade inflammation. We confirmed that aerobic and dynamic strength training improved IS and demonstrated that these interventions do not promote changes in subcutaneous AT gene expression or in plasma levels of adiponectin, interleukin-6, interleukin-1 beta and tumor necrosis factor-alpha, but decrease circulating leptin level. Very low calorie diet followed by low calorie diet and weight maintenance period enhanced IS in obese women and diminished retinol-binding protein 4 (RBP4) in plasma, but RBP4 mRNA levels were reduced only after very low calorie diet. Our findings indicate that the investigated adipokines, except potentially leptin, might not be mediators of changes in IS induced by lifestyle interventions. In the second part of the work, we investigated the role of peroxisome proliferator-activated receptors (PPARs) on the protein secretion by human subcutaneous AT. .

A greater understanding of critical periods of body weight regulation, including pregnancy, may aid in efforts to optimize weight management strategies for the mother and her baby. The gestational period has been implicated to play, in the child, a vital role in the developmental origins of obesity and other cardiometabolic diseases later in life. Therefore, we initially examined existing literature on the role of maternal obesity and its link to pediatric obesity and documented the known underlying physiological mechanisms responsible for this relationship while suggesting potential intervention targets that may improve maternal-fetal outcomes. In a second paper, we aimed to quantify maternal predictors of large for gestational age (LGA) neonates in the Ottawa and Kingston (OaK) birth cohort with specific hypotheses verifying the independent contribution of maternal prepregnancy body mass index (BMI) and excessive gestational weight gain (GWG) to fetal overgrowth. This paper also highlights the clinical utility of the revised 2009 Institute of Medicine GWG guidelines and discusses the potential role of physiological factors underlying the observed associations between BMI, excessive GWG and LGA neonates. As a follow-up to our population-level analysis (i.e., OAK cohort), papers three and four highlight how the insulin-like growth factor (IGF) axis, a vital regulator of growth and development, may be compromised at the molecular level in cases of maternal obesity (paper 3) and excessive GWG (paper 4). In paper 3 we show that maternal obesity is associated with attenuated expression of IGF binding protein-4 (IGFBP4) in umbilical cord blood and discuss how this may preferentially promote fetal adipogenesis. The effects of excessive GWG on IGF axis protein expression are addressed in paper four where we show that excessive weight gain during pregnancy is associated with increased expression of IGFBP3 in maternal circulation in normoglycemic term pregnancies. In this paper we discuss the potential inhibitory role of IGFBP3 on adipogenesis and how it relates to glucose intolerance during pregnancy. Recognizing that both obesity and excessive GWG can alter physiological processes in mother and her baby, appropriate evidence-based interventions are warranted to best optimize outcomes. In paper five, we discuss the results of a study which sought to assess patient information channels and knowledge of nutrition and physical activity during pregnancy with the intent that these findings be applied to best design efficacious strategies that cater to the needs of our target group of pregnant women. In our analysis we show that the majority of pregnant women studied would be willing to participate in a lifestyle intervention for their own personal health and that of their child. Of great interest was the observation that most women were not informed of the importance of pregnancy-specific energy intake, or made aware of their own healthy GWG targets. Additionally, many of the respondents reported receiving no information pertaining to appropriate physical activity recommendations; despite the fact that the vast majority of participants consider this lifestyle modality to be safe during their pregnancy. Finally in paper six, we build on the results of our previous work and evaluate the risks and benefits of physical activity during pregnancy on maternal-fetal outcomes through a review of the literature and note that engaging in non-sedentary pursuits during gestation may aid in maternal weight regulation, protect against metabolic disorders and optimize neonatal birth weight and body composition. Overall, the collective nature of the papers presented in this dissertation provides qualitative and quantitative evidence to support not only the complexity of body weight regulation in the mother and her baby, but also highlights potential avenues for intervention that may improve maternal-fetal outcomes during this critical period.

In this work we have developed three ordinary differential equation models of biological systems: body mass change in response to exercise, immune system response to a general inflammatory stimulus, and the immune system response in atherosclerosis. The purpose of developing such computational tools is to test hypotheses about the underlying biological processes that drive system outcomes as well as possible real medical interventions. Therefore, we focus our analysis on understanding key interactions between model parameters and outcomes to deepen our understanding of these complex processes as a means to developing effective treatments in obesity, sarcopenia, and inflammatory diseases. We develop a model of the dynamics of muscle hypertrophy in response to resistance exercise and have shown that the parameters controlling response vary between male and female group means in an elderly population. We further explore this individual variability by fitting to data from a clinical obesity study. We then apply logistic regression and classification tree methods to the analysis of between- and within-group differences in underlying physiology that lead to different long-term body composition outcomes following a diet or exercise program. Finally, we explore dieting strategies using optimal control methods. Next, we extend an existing model of inflammation to include different macrophage phenotypes. Complications with this phenotype switch can result in the accumulation of too many of either type and lead to chronic wounds or disease. With this model we are able to reproduce the expected timing of sequential influx of immune cells and mediators in a general inflammatory setting. We then calibrate this base model for the sequential response of immune cells with peritoneal cavity data from mice. Next, we develop a model for plaque formation in atherosclerosis by adapting the current inflammation model to capture the progression of macrophages to inflammatory foam cells in response to cholesterol consumption. The purpose of this work is ultimately to explore points of intervention that can lead to homeostasis.