Moving for a Better Beat: How Exercise Benefits the Heart
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Join Dr. Louise Naylor as she dives into the benefits of exercise to optimize and maintain the cardiovascular system. Exploring the effects of exercise and exercise training on the cardiovascular system, Louise draws on real case studies to illustrate the many benefits of exercise in elite athletes right through to patients with end stage heart failure. Key Topics Include: - Developing a deeper appreciation of the importance of exercise to optimize and maintain cardiovascular health - Appreciating that all exercise isn’t all the same – different modes of exercise induce distinctly different physiological stimuli and adaptations - Understanding whether exercise is safe for everyone - The Goldilocks Principle: is there such a thing as too little or too much exercise? - Not everyone responds the same to an identical exercise program
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Moving for a Better Beat: How Exercise Benefits the Heart
- 1. Copyright 2022. All Rights Reserved. Contact Presenter for Permission Moving for a Better Beat: How Exercise Benefits the Heart Louise Naylor, PhD Professor School of Human Sciences The University of Western Australia
- 2. Prof Louise Naylor University of Western Australia
- 4. Moving for a Better Beat Exercise to optimise health All exercise is not equal Not everyone responds identically Is exercise for everybody?
- 5. Exercise to your heart’s content Exercise capacity better predictor of survival than any risk factor Myers • 2002 • NEJM Fit (<8 METs) Hypertension COPD Diabetes Smoking BMI >30 Hyperlipidemia 2.5 2.0 1.5 1.0 0.5 0.0 Relative risk of death (1.2-1.6) (0.8 – 2.1) (0.9 – 1.9) (1.1 – 1.6) (1.2 – 2.0) (1.2 - 1.8) Mod (5-8METs) (1.7 – 2.3) (1.0 – 2.7) (1.5 – 3.5) (1.6 – 2.3) (1.6 – 2.3) (1.8 – 3.0) Unfit (>5METs)
- 6. Loss Stable Gain 1 1.2 1.4 1.6 1.8 2 2.2 Loss Stable Gain Hazard ratio (all –cause mortality) Fitness Change Lee • 2011 • Circ Fitness vs fatness
- 7. Loss Stable Gain 1 1.2 1.4 1.6 1.8 2 2.2 Loss Stable Gain Hazard ratio (all –cause mortality) Fitness Change Lee • 2011 • Circ Lack of exercise responsible for twice as many deaths as obesity Fitness vs fatness
- 9. How much? Arem • 2015 • JAMA Intern Med 31% Guidelines: Minimum of 7.5 MET hrs per week of moderate or vigorous physical activity (~150 min) 20% 37%
- 10. Minimum: 15 min of moderate- intensity exercise How much? Wen • 2011 • The Lancet 31% 20% 37%
- 11. How much? Arem • 2015 • JAMA Intern Med 31% 20% 37%
- 12. Arrhythmia Blood markers Coronary Calcium Cardiac fatigue Fibrosi s Rao • 2018 • Am J Med
- 13. “Doctors, researchers, and scientists―even ancient philosophers―have long claimed exercise works like a miracle drug. Now they have proof.”
- 14. Moving for a Better Beat Exercise to optimise health Is exercise for everybody? All exercise is not equal Not everyone responds identically All exercise is not equal
- 15. All exercise is not equal Morganroth • Ann Int Med • 1975
- 18. Concentric LV hypertrophy wall diameter ↑ wall diameter
- 20. Eccentric LV hypertrophy wall ↑ wall diameter ↑ diameter
- 21. Ford • Cir Res • 1976 “cardiac muscle grows to match the workload imposed on the ventricle”
- 22. Grossman • J Clin Invest • 1975 LV pressure overload => concentric hypertrophy (increased h/R ratio) LV volume overload => eccentric hypertrophy (normal h/R ratio)
- 23. Naylor • 2008 • Sport Med
- 24. Haykowsky • 2001 • Chest 70 75 80 85 90 95 LV ES Wall stress Baseline 80% 1RM 95% 1RM 100% 1RM
- 25. Prakken • 2010 • BrJ Sport Med Bellenger • 2000 • J Cardiovasc Magn Reson Cardiac MR vs echo MRI decreases sample size requirements for detection of LV mass change by >95%
- 26. Naylor • 2008 • Sport Med
- 27. Does exercise training influence cardiac morphology? Angela Spence, Louise Naylor, Howard Carter, Christopher Buck, Lawrence Dembo, Conor Murray, Phillip Watson, David Oxborough, Keith George, Danny Green A prospective, longitudinal MRI study
- 28. Baseline Trained Detrained Endurance Training (n=10) 3 x 1 hour/wk; 24 weeks Progressive overload Individualised for intensity Resistance Training (n = 13) 3 x 1 hour/wk; 24 weeks Progressive overload Individualised for intensity Detraining 6 weeks Pre-study activity level Spence • 2011 • J Physiol
- 29. 0 5 10 15 Endurance Resistance Change in LVM (g) * Exercise training Eccentric hypertrophy pattern in the endurance group Spence • 2011 • J Physiol
- 30. Eccentric hypertrophy with endurance training Limited hypertrophy with resistance training Naylor • 2008 • Sport Med
- 31. Moving for a Better Beat Exercise to optimise health Is exercise for everybody? All exercise is not equal Not everyone responds identically Not everyone responds identically
- 32. Is response modality specific? Resistance Training Endurance Training % LV Mass % LV Mass >50% non-responders 20% non-responders LV mass (g) Spence • 2011 • J Physiol
- 33. PHYS ED What’s the Best Exercise for You? Twins Can Provide an Answer Almost everyone responds to the right exercise program, but the right program is not genetics- dependent HEALTH Weights or Running? Which type of exercise is right for you? The effects of a workout vary from person to person. Here’s how to know what’s right for you AMERICAN JOURNAL OF PHYSIOLOGY- HEART CIRC PHYSIOL THE JOURNAL OF PHYSIOLOGY MEDICINE & SCIENCE IN SPORT & EXERCISE JOURNAL OF APPLIED PHYSIOLOGY CONTEMPORARY CLINICAL TRIALS COMMUNICATIONS
- 34. We do not train populations or even small groups. We train individuals …and twins
- 35. Monozygotic (MZ) Twins Identical twins Theoretically share 100% DNA Dizygotic (DZ) Twins Fraternal (non- identical) twins Share ~50% DNA Twin B response with training Twin A change with training MZ Twin pairs highly correlated DZ Twin pairs moderately correlated 2:1 = heritable MZ &DZ twin pairs moderately correlated Twin B response with training Twin A change with training <2:1 = environmental
- 37. Nearly every heart responds to exercise
- 38. Genetic Environmental Twin B response with training Twin A change with training Twin B response with training Twin A change with training Cross sectional data: additive genetic and shared environmental Training data: Limited genetic and mainly unshared environmental contribution
- 39. Gender ? Marsh • 2021 • MSSE Males eccentric hypertrophy following endurance training No evidence in females
- 40. Moving for a Better Beat Exercise to optimise health Is exercise for everybody? All exercise is not equal Not everyone responds identically Case Studies
- 41. Rowers Does increased LV Mass improve function? Naylor • 2005 • J Physiol
- 42. 52 Vanoverschelde • 1993 • J Appl Physiol Márton • 2022 • Eu r Heart J - Cardiovascular Imaging Cardiac function is correlated to exercise capacity Function is related to fitness
- 43. Systole: Shortens, thickens and twists… Diastole: Lengthens, un-thickens, untwists... Nottin • 2008 • Journal of Physiology• Volume 586 Cardiac function
- 44. Diastolic function Sharpe • 2006 • Am J Cardiol 0 1 2 3 4 5 6 7 8 9 10 Obese Lean E/E’ Obese Lean LV mass (g) 150 ± 7 133 ± 13 LV mass index (g/m2) 79 ± 3 83 ± 4 Reduced independent of LV morphology
- 45. Rowers Diastolic function is normal in athletes so long as the training stimulus is extant Naylor • 2005 • J Physiol
- 46. Can exercise training can reverse diastolic dysfunction? Naylor • 2008 • MSSE improved early diastolic tissue velocity, independent of changes in LV morphology Pre Trained Pre No training Age 12.2 ± 0.4 13.6 ± 0.7 Weight 84.9 ± 6.5 82.1 ± 8.3 LV Mass (g) 160.7 ± 11.6 167.14.7 165.8 165.4
- 47. Adaptations are mode specific in heart failure patients Lan • J Am Soc Echo • 2020
- 48. 63 Green • Exp Physiol • 2012 Naylor • JSAMS • 2021 Arteries also respond to exercise
- 49. Case study 1 Kristian 22yo male Medical Hx: • Marfans • Bentalls procedure • Heart failure • Cardiac transplant (prolonged bed rest secondary to complications) • Cachexia and severe deconditioning
- 50. Chasland • 2017 • MSSE Eccentric exercise
- 51. Chasland • 2017 • MSSE VO2 VCO2 CBF(?) HR SBP W Effort Eccentric exercise
- 52. Benefits of Eccentric Exercise ✓ Greater muscular workload ✓ Lower cardiorespiratory demand
- 53. Insert video 1 please Kristian
- 54. Case Study 2
- 55. Early detection of cardio- vascular disease in survivors of childhood cancer
- 56. Cardiac magnetic resonance (CMR) to detect early signals of cardiac injury Early detection of heart disease Echocardiography (3D & diastolic function) at rest & stress to unmask early functional changes
- 57. Aims of exercise rehabilitation Build and maintain lifelong exercise habits Mills • 2013 • J Pediatr
- 58. Insert video 2 please
- 60. 6MWT results
- 61. CVRG UWA email: Louise.Naylor@uwa.edu.au Aloysius David Andy Haynes Arga Raden Barb Maslen Bianca Spence Channa Marsh Danny Green Hannah Thomas Howard Carter Jaye Lewis Jesse Criddle Joao Locatelli Julie Collis Juliene Gonclaves Kristanti Wigati Lachlan McRobb Larissa Kennel Lauren McKeown Lucy Bolam Shae Richardson Discovery Translation Impact
- 62. Thank you for participating! CLICK HERE to learn more and watch the webinar
Editor's Notes
- “...athletes participating in isotonic or endurance training is associated with an increased left ventricular end-diastolic volume, but left ventricular wall thickness remains normal. In contrast... athletes participating in isometric or resistance exercises is associated with an increased left ventricular wall thickness, whereas left ventricular end-diastolic volume remains normal...”
- (increased LV mass secondary to an increase in diastolic internal cavity dimension and wall thickness)
- two specific technical issues warrant evaluation. First, only echocardiographic studies of the AH were included in a previous meta-analysis.5 Cardiac magnetic resonance (CMR) has now become the ‘gold standard’ for cardiac structural assessment. Clinically significant differences between echocardiography and CMR have been reported.11 While eccentric hypertrophy has been reported when CMR is used in endurance-trained participants,12 no concentric adaptation has been noted in resistance-trained athletes.13 Developments in CMR and echocardiography have also resulted in new regional functional indices (ie, tissue-Doppler analysis) and greater access to morphological and functional data from the right ventricle and left atrium. A second concern is the impact of body size on cardiac structure. Pluim et al,5 reported absolute cardiac dimensions in their between-group comparisons. Although informative, their data do not take into account potential differences in body size and composition between athletes and sedentary controls that might alter the interpretation of AH studies.14–17 Normalizing the increased heart weight to the increased body weight of the athletes appears to greatly reduce the increased ratio typically observed in true hypertrophy (Oakley, 2001; Haykowsky et al., 2002). Later reiterated by Systematic review and meta-analysis by Utomi in 2013 All LV structural parameters were increased in athletes compared with sedentary controls. Differences between athlete groups were only noted for LVEDD and LVEDV, which were larger in endurance athletes than in resistance athletes. There were no differences between athlete groups for IVSWT or PWT. The larger LV chamber accounted for a greater SV in endurance athletes compared with resistance athletes and controls but LVEF did not differ among all groups. Both LV E/A and LV E’ were larger in endurance athletes than in controls.
- Haykowsky threw a spanner in the works Perhaps not all questioned the effect of RT on left ventricular (LV) morphology. (https://doi.org/10.2165/00007256-200232130-00003) And it remains unequivocal even today. Of interest, nearly 40% of all RT athletes have normal LV geometry. LV gets larger, but not necessarily thicker walls. The expected concentric hypertrophy seen in Olympic weightlifters, whereas an eccentric pattern of hypertrophy is not uncommon in bodybuilders. Of course, cannot ignore that numerous RT athletes who use anabolic steroids have been shown to have significantly higher LV mass compared with drug-free sport-matched athletes.
- MRI decreases sample size requirements for detection of LV mass change by >95% (Bellenger et al., 2000), strongly suggesting that, when performing repeated measurements in training studies, MRI is a preferable technology (Myerson et al., 2002). sample sizes for HF CMR to detect a 10-ml change in end-diastolic volume (n = 12) and end-systolic volume (n = 10), a 3% change in ejection fraction (n = 15), and a 10-g change in mass was (n = 9) were substantially smaller than recently published values for two-dimensional echocardiography (reduction of 81-97%).
- the anticipated structural cardiac adaptations that develop as a function of these underlying physiological stressors. Modified from Baggish et al (1).. These studies suggest that LV hypertrophy can occur after 3 months of exercise training and as little as 3-4 h/week (13,14). Moreover, it has been suggested that 3 hours of exercise/week is required to see adaptations in the resting electrocardiogram (ECG), resting heart rate, peak VO2, and LV mass (15).
- Our results showed an increased LV mass and corresponding increase in wall thickness following the resistacne training. These adaptations were not observed in the resistance trained group. Similarly, LV end diastolic volume increased in the endurance but not resistance group LV mass and wall thickness: ↑ END training = RES - LVEDV ↑ with endurance END … increases in both LV Mass and LVEDV” As the ratio of LV mass:LVEDV unchanged following training, indicative of an ‘eccentric’ hypertrophy pattern in the END group as a result of increases in both LV mass and LVEDV. Therefore our study offers some support for the the ‘Morganroth hypothesis’ as it pertains to ENDURANCE training But cast some further doubt regarding the impact of RESISTANCE training on the heart
- (aged 29±6 years; 7 men and 5 women) CMR LV& RV Mass and volumes at baseline and after 3, 6, 9, and 12 months of training. Maximum oxygen uptake ( Vo 2 max) and cardiac output at rest and during exercise (C2 H2 rebreathing) were measured at the same time periods. Pulmonary artery catheterization was performed before and after 1 year of training, and pressure-volume and Starling curves were constructed during decreases (lower body negative pressure) and increases (saline infusion) in cardiac volume. Mean Vo 2 max rose from 40.3±1.6 to 48.7±2.5 mL/kg per minute after 1 year Prolonged and intensive endurance training in previously sedentary individuals resulted in a large increase in LV mass, approaching a level similar to that reported cross-sectionally in elite endurance athletes.8,44,45 Contrary to conventional thinking, the LV responded to the initiation of endurance training with an increase in mass without a change in volume (concentric hypertrophy); an increase in LVEDV occurred only after 6 to 9 months of progressive training, restoring the baseline mass-to-volume ratio (eccentric hypertrophy). In contrast to the LV, the RV responded to endurance training with a balanced increase in mass and volume, thereby maintaining a constant mass-to-volume ratio (eccentric hypertrophy) at all levels of training. Despite these morphological adaptations, and although maximal cardiac output and Vo2max increased substantially during the training period, they did not reach levels typically observed in trained endurance athletes.5,8 One year of intensive endurance training led to a modest increase in LV distensibility and compliance but remained substantially below that observed in elite athletes.15omen)
- Spence- Mild morphological RV adaptation occurred after 6 months of intense supervised E and R exercise training. The degree of change was slightly but not significantly larger after E training. RV changes mirrored those observed in the left ventricle. Cardiac output (CO) increases with exercise intensity to deliver oxygen to the working muscles. Although oxygen utilization by the peripheral muscle is also an important factor, the ability to augment CO remains a key determinant of exercise capacity. Exercise-induced increases in CO (often termed ‘cardiac reserve’) have most commonly been attributed to increases in heart rate, augmentation in left ventricular (LV) function and vasodilation of the systemic circulation.1,2 The fact that cardiac output is only as good as your worst ventricle is often overlooked. Given that the cardiovascular system is composed of two circulations in series, it is impossible for the output of the left ventricle (LV) to exceed that of the right ventricle (RV) and vice versa. Many texts on exercise physiology have focused on the systemic circulation to explain cardiovascular performance and limitation during exercise but there is reasonably compelling physiological evidence to suggest that it may be the RV that is placed under greatest stress during exercise and is most likely to be the Achilles’ heel that limits augmentation of CO. Relative to the LV, increases in load are greater for RV and the contractile force may be insufficient to maintain the increases of output required during intense sustained exercise. This review will discuss novel concepts of exercise physiology, highlighting the evolving evidence implicating the RV as a key determinant of exercise capacity, a potential stress point for exercise-induced injury and a chamber that undergoes disproportionate remodelling in the setting of athletic training. Detriment in EF seen in LV, perhaps more pronounced in the Right side of the heart. Studies assessing ventricular function immediately following ultraendurance exercise (ranging ∼50 km to 160.93 km or I think that is somewhere around 30 to 100 miles) reported attenuated EF in both LV and RV, with larger reductions on the RV. Why? The greater vulnerability of the right heart is likely caused by reduced wall thickness, with exercise-induced relative increases in wall stress being substantially larger for the RV vs LV (±125% vs ±4%, respectively). Accumulating evidence suggests that the adverse effects of both short-term intense PA and cumulative EEE are most evident in the right-side cardiac chambers (RV and RA). At rest, average cardiac output in an average size human is approximately 5 L·min−1, and this typically increases by five-fold to about 25 L·min−1 during vigorous ET. During chronic long-term exposure to prolonged, high-intensity ET, this increased cardiac output may place more strain on the thinner wall, smaller, right-side cardiac chambers compared with the left side of the heart. Following a marathon, for example, approximately 30% of runners develop acute dilation of cardiac structures, especially the RV and RA, and dysfunction of the RV and ventricular septum. During the postrace period, the cardiac geometric dimensions are restored, but with this recurrent stretch of the chambers and reestablishment of chamber geometry, some individuals may be prone to the development of chronic structural changes, including chronic dilation of the LA, RA, and RV, as well as patchy myocardial scarring in response to the recurrent volume load and excessive cardiac strain. Although these abnormalities are typically asymptomatic and resolve over 24 to 72 h, if they accrue over many years, they may predispose to potentially serious arrhythmias, such as AF and/or VA (18,27–30,32). In one prospective study of 25 runners (12 men and 13 women), Trivax et al. (39) found that running a marathon caused acute dilation of the RA and RV, with a sudden fall in RV ejection fraction (EF). Similarly La Gerche et al. (14) studied 40 highly trained aerobic athletes after competing in EEE events (marathons, mean time 3 h; half Ironman triathlons, mean time 5.5 h; full Ironman, mean time 11 h; and Alpine Cycling race, mean time 8 h). On postrace echocardiograms, they noted increases in RV volume and reduced RVEF (but not LVEF) (Fig. 2) and found elevations in biomarkers (troponin and BNP), which correlated with the fall in RVEF. These abnormalities in cardiac structure returned entirely to baseline within the first few weeks and are noted more typically in races of long duration. Of this cohort, 5 of the 40 (12.5%) had myocardial scarring detected on cardiac magnetic resonance imaging (MRI), as demonstrated by late gadolinium enhancement (LGE). Therefore these studies suggest that intense EEE induces RV dysfunction, which largely spares the LV (except for possibly the ventricular septum shared by both ventricles). Even when short-term RV recovery appears to be complete, potentially long-term ET and competition in EEE races may lead to myocardial fibrosis eventually, which potentially could predispose malignant VA.
- two specific technical issues warrant evaluation. First, only echocardiographic studies of the AH were included in a previous meta-analysis.5 Cardiac magnetic resonance (CMR) has now become the ‘gold standard’ for cardiac structural assessment. Clinically significant differences between echocardiography and CMR have been reported.11 While eccentric hypertrophy has been reported when CMR is used in endurance-trained participants,12 no concentric adaptation has been noted in resistance-trained athletes.13 Developments in CMR and echocardiography have also resulted in new regional functional indices (ie, tissue-Doppler analysis) and greater access to morphological and functional data from the right ventricle and left atrium. A second concern is the impact of body size on cardiac structure. Pluim et al,5 reported absolute cardiac dimensions in their between-group comparisons. Although informative, their data do not take into account potential differences in body size and composition between athletes and sedentary controls that might alter the interpretation of AH studies.14–17 Normalizing the increased heart weight to the increased body weight of the athletes appears to greatly reduce the increased ratio typically observed in true hypertrophy (Oakley, 2001; Haykowsky et al., 2002). Later reiterated by Systematic review and meta-analysis by Utomi in 2013 All LV structural parameters were increased in athletes compared with sedentary controls. Differences between athlete groups were only noted for LVEDD and LVEDV, which were larger in endurance athletes than in resistance athletes. There were no differences between athlete groups for IVSWT or PWT. The larger LV chamber accounted for a greater SV in endurance athletes compared with resistance athletes and controls but LVEF did not differ among all groups. Both LV E/A and LV E’ were larger in endurance athletes than in controls.
- To provide more explanation The first question was informed by recent studies from our lab that indicated RES and END differed in response profiles. But this study was limited because subjects only performed one mode of exercise meaning that selection bias may have played a role in the groups.
- (L min−1) results displayed as cross-sectional (A) and response (△) to resistance (RES) (B) and endurance (END) (C) training. Individual results for twin A and twin B are represented (left) as the higher and lower result within a twin pair, respectively, with each individual within a pair joined by a line. The respective intraclass correlations (r) for monozygotic (MZ) and dizygotic (DZ) twin pairs are shown above. A boxplot of the absolute differences for each twin pair (twin A – twin B) for MZ and DZ, respectively, is also shown (right). Comparison between the effects of training within twin pairs For response to exercise training, significant rMZ but not rDZ were present for leg press response to RES and response to END for in L min−1. Subsequent analysis revealed a predominant C (0.64; 95% CI = 0.39–0.90) contribution to change in leg press to RES and an even proportion of C (0.43; 95% CI = 0.14–0.72) and E (0.57; 95% CI = 0.28–0.86) for (L min−1) change in response to END training.
- Our final question pertains to whether response to exercise has a genetic contribution. To answer this question we utilised a classical twin study using MZ and DZ twin pairs. MZ twins theoretically share 100% of their DNA and DZ twins share ~50% of their DNA. Additionally, both MZ and DZ twins share the same pregnancy environment and usually the same childhood external environment which makes them more closely matched than normal siblings. Keeping this in mind, if there is a 2:1 ratio of exercise response where MZ pairs are highly correlated and DZ pairs are moderately correlated then response is said to be highly heritable, or genetically influenced. However, if MZ and DZ pairs are similarly correlated and the ratio is less than 2:1 then response is more environmentally influenced.
- To answer our concordance question each individuals response to RES and END are plotted against each other as you can see here. End= increased LVM and not shown EDV, no change with RES LVM & EDV - Higher proportion of individuals responded to END than RES Nature or nurture? Cross sectional
- To answer our concordance question each individuals response to RES and END are plotted against each other as you can see here. Change in Superscript
- Our results indicate that in response to END, increased LVM and EDV changes characteristic of an eccentric pattern of hypertrophy were evident in males, but less so in females. Although both sexes increased LVM, only males increased EDV. This was a consistent finding whether data were expressed in absolute terms or as percent change from baseline. These data suggest that females exhibit blunted eccentric hypertrophy in response to END. With respect to RES training, EDV was unaltered in either males or females, and the decrease in LVM in males in absolute terms was not apparent when data were presented as a percentage change from baseline. These data for RES reinforce our previous findings (15), indicating that RES training, undertaken in previously inactive subjects at levels consistent with guideline-based exercise prescription, is not associated with concentric hypertrophy in either males or females.
- What if you found a magic fountain of youth that helps you live longer, be happier and even healthier. And to be even more extravagant, what you can not only prevent but also use this to treat CVD, cancer and dementia? There are many claims for miracle cures, companies and even celebrities will try to sell you supplements, herbal remedies, magic creams, all sorts of things promising to improve your health and wellbeing. While some of these are effective, none are as potent or has the same amount of robust research evidence behind them as exercise However, the answer may be so simple that you may not even think of it. Moving more. If exercise were a drug, it would be a miracle cure. The evidence for the impact of regular amounts of exercise in the prevention and treatment of common conditions is overwhelming. So you probably knew that, but who is actually getting their daily dose of exercise? why is this not common knowledge and why is it so hard to translate into action? Today I start of by summarising for you the plethora of benefits of exercise for CV health. When you hear exercise, you may be thinking of going out for a jog like this guy in this photo. He looks happy enough listening to his music and jogging happily. But if we cotinut with this analogy of exericse as a medicine, pharmaceutical I will be looking at the dose, type of
- Vigorous exercise training induces hypertrophy of the left ventricle, an adaptation commonly referred to as ‘athlete's heart’ (Maron, 1986). In patients with cardiovascular disease, left ventricular (LV) hypertrophy is associated with diastolic dysfunction, characterized by impaired ventricular relaxation and filling which manifest on echocardiographic assessment as Doppler velocity abnormalities (Ommen & Nishimura, 2003). However, exercise training is cardioprotective, being associated with decreased cardiovascular mortality and morbidity in both primary (Paffenbarger et al. 1993; Blair et al. 1995) and secondary prevention settings (Joliffe et al. 2003) and, in contrast with the situation in patients with cardiovascular disease, LV hypertrophy associated with athletic training is likely to be a benign or beneficial adaptation which does not impact on ventricular relaxation in the same manner as ‘pathological’ hypertrophy. Previous studies indicate that, despite significant ventricular hypertrophy, athletes possess normal (MacFarlane et al. 1991; Yeater et al. 1996) or enhanced diastolic function (Douglas et al. 1986; George et al. 1999; Caso et al. 2000), compared to matched controls. However, these studies relied exclusively upon cross-sectional comparisons and, to our knowledge, no studies have investigated changes in LV diastolic function in athletes studied longitudinally in response to exercise training. The purpose of the current study was therefore to assess cardiac structural and functional adaptations to exercise training in elite level athletes across a typical training cycle, which is at the end of the ‘off-season’ and following 3 and 6 months of intensive training. Men’s Coxless Four- 4th David Dennis (WA) Robert Jahrling (NSW) Tom Laurich (NSW) David McGowan (WA) Men’s Coxed Eight- Bronze Stuart Reside (WA) Stephen Stewart (NSW) Geoff Stewart (NSW) James Stewart (NSW) Michael McKay (Vic) Bo Hanson (NSW) Stefan Szczurowski (WA) Stuart Welch (NSW) Cox: Michael Toon (QLD Men’s Lightweight Coxless Four- Silver Simon Burgess (Tas) Glen Loftus (WA) Ben Cureton (WA) Anthony Edwards (Vic) Women’s Quad Scull Bronze Amber Bradley (WA) Rebecca Sattin (WA) Dana Faletic (Tas) Kerry Hore (Tas) Women’s Eight 6th Sally Victoria Roberts (NSW) Monique Heinke (NSW) Jodi Winter (NSW) Sarah Outhwaite (WA); Catriona Oliver (VIC) Sally Robbins (WA) Julia Wilson (NSW) Jo Lutz (WA) Cox: Katie Foulkes (VIC)
- Does bigger = better? So, it makes sense that there is a relationship between diastolic function and VO2 observed Long-term, intense exercise training induces adaptive changes in cardiac structure and function that enable the heart to meet the haemodynamic demands of the increased cardiac output during effort.1,2 This physiological remodelling leads to enhanced myocardial contractility, which represents the intrinsic ability of the myocardium to shorten independently of loading conditions, and as such, is the target feature of the clinical evaluations of the athlete's heart. Vanoverschelde and colleagues examined the relationship between LV diastolic function and exercise capacity in healthy men and women who were either sedentary or endurance trained athletes. Stepwise multiple regression analysis identified the ratio of early to late transmitral filling being the sinlge most significant correlate to exercise capacity (VO2max). Sixty-six healthy normal volunteers (40 men, 26 women; mean age 36 t 14 yr, range 20-76 yr) served as subjects in the present study. Fifty-seven of the subjects were sedentary (32 men, 25 women; mean age 36 t 13 yr, range 20-76 yr). Although some of them were participat- ing in low-intensity recreational activities, none had been exercising >3 h/wk. Nine subjects were endurance athletes (8 men, 1 woman; mean age 37 t 8 yr, range 26-51 yr) who were training 215 h/wk (mostly running and cycling). VO2 max ranged from 25 to 58 ml.kg-1 x min-1 in sedentary subjects and from 44 to 60 ml.kg-1 x min-1 in athletes. Similarly Marton assessed GLS and VO2 in elite swimmers, training for more than 20hrs per week and showed these values are related in humans The potential importance of enhanced diastolic function in the development of maximal SV,26 as well as putative mechanisms (preload or intrinsic relaxation properties), requires further evaluation. And this may be explained by ? Enhanced diastolic function increases maximal SV?? During exercise as the heart beats over 150 beats/min, there is just above 100ms to fill the entire LV. Under these conditions, the maintenance of adequate LV diastolic filling is extrememly important to maintain performance. In fact diastolic filling becomes more important than systolic ejection rates. In patients with heart disease, who have a reduced LV relaxation even at rest, and adapts poorly to exercise, filling rates may be too low to achieve adequate filling and CO during exercise. - ↑HR and ↑ myocardial contractility = ↑CO - Diastolic filling becomes more important than systolic ejection rates - Acute bouts of exercise are associated with enhanced diastolic filling during exercise
- During systole the cardiomyocytes contract, inducing a normal strain, including longitudinal shortening (ie from base to apex) There is also circumfrencial shortening, which is shortening in the plane perpendicular to radial and to the longitudinal axis, and at the same time, radial thinning which occurs perpendicular to the epicardium and to the longitudinal axis. TDI measures the velocity of selected segments of the LV myocardium, and therefore assesses wall movement, which is indicative of relaxation and contraction (Ommen et al. 2003). Two distinct modalities are available; pulsedwave TDI utilises a modified pulsed Doppler system with the sample volume placed conventionally at the level of the mitral valve annulus. Although longitudinal myocardial velocities can be obtained from six myocardial wall segments, the basal septal segment is most commonly interrogated. Colour TDI utilises the modified colour Doppler system and measures mean myocardial velocities rather than peak velocities derived from the pulsed-wave method. Conventionally, longitudinal velocities are measured offline and are obtained from different levels and regions of the myocardium. For both methods, myocardial velocities corresponding to early diastole (E0) and late diastole (A0) are reported. Data suggest that E0 is inversely related to s (Border et al. 2003). TDI measures were proposed as relatively independent of preload (Sohn et al. 1997), but this remains controversial (Prasad et al. 2007). Mitral annulus tissue velocity is dependent on LV length (Batterham et al. 2008) and thus consideration of normalisation of data is germane. Combining E trans-mitral flow with E0 mitral annular velocity (E/E0) correlates with pulmonary wedge pressure (Nagueh et al. 1997; Ommen et al. 2003; Border et al. 2003; Burgess et al. 2006). TDI can also facilitate the measurement of regional time intervals throughout diastole. Despite the fact that TDI can assess regional LV function during diastole, the issue of angle-dependency limits assessment to longitudinal motion and only a few wall segments for radial movement analysis. In an attempt to generate data for regional motion in multiple planes of movement, strain and strain rate analysis have been developed (Marwick 2006). Unlike tissue velocities, strain is not affected by translation and tethering, as a result of not being related to transducer position. Tissue-Doppler strain (Fig. 5) has been used in clinical studies (Kukulski et al. 2002), but is still limited by standard Doppler technical issues (e.g. angle dependency). Speckle-tracking analysis of 2D images (Fig. 6) can also provide strain and strain rate data with the benefit of angle-independence (Marwick 2006) and is used to 123Eur J Appl Physiol (2010) 108:1–14 5 Fig. 5 An exemplar scan from a colour tissue-Doppler assessment of regional wall strain and strain rate in the apical four-chamber view (note the apical LV view and longitudinal tissue strain traces measured in the septal and free wall at the mid-wall level) Fig. 6 An exemplar scan of myocardial speckle tracking assessment of regional wall strain and strain rate in the para-sternal short-axis view (note the short axis LV view at the level of the papillary muscle and the circumferential strain traces from six LV wall segments) generate longitudinal, radial and circumferential strain and systolic and early diastolic strain rate data. Generation of rotational strain and strain rate at the base and apical levels of the LV has further precipitated the assessment of twist (torsion) and untwist data (Helle-Valle et al. 2005). TDIand speckle tracking-derived strain data in diastole have been validated against tagged MRI (Becker et al. 2006). The application of speckle tracking-derived strain and strain rate to the assessment of diastolic function in CV disease (Ishii et al. 2009) and with the imposition of acute and chronic exercise (George et al. 2009) may develop rapidly. In summary, echocardiographic interrogation of LV diastolic function can be achieved via a number of common techniques and measures (E, A, E/A, VP, E0, E0/A0, E/E0) that are summarised in Table 1. Continuing technical development has seen more assessment modes (strain, strain rates, untwisting rates) that may provide a more complete assessment of LV diastolic function in both athletes and patients. Whilst a key limitation of echocardiography has been the lack of pressure measures affecting the LV, studies have calculated the intra-ventricular pressure gradient (IVPG) by applying the Euler equation to trans-mitral colour flow M-mode data (Greenberg et al. 2001). This in turn may facilitate further advances in our understanding of LV diastolic function. Acute aerobic exercise and diastolic function in humans General considerations for short bouts of acute exercise Acute exercise places a significant demand on the CV system to increase blood flow to deliver oxygen and nutrients to metabolically active tissues. As stated by Libonati (1999), in a closed circulation, the increase in : cardiac output Q in response to exercise is matched by enhanced LV diastolic filling, otherwise increased l
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- ~175,000 new cases of childhood cancer each year worldwide, and rising Data from Australia shows increasing prevalence of CCSS However, with advances in care, death rates from childhood cancer has fallen over the past 30 years. Now In Australia survival rates from childhood cancer are currently 85% at 5 years and 75% at 20 years. ~75% of survivors of childhood cancers experience at least one serious long term side effect, with 56% of all survivors developing a heart abnormality. Frequently, evolving cardiovascular changes do not cause symptoms, remaining latent until manifesting as advanced disease, which is both difficult and costly to treat. This emphasizes the importance of early recognition of cardiac abnormalities for improved quality of life and reduced cost to the health care system.
- On her discharge “2 weeks post heart transplant No complications”
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