Jessica M. Scott

The health benefits of interactive video game exercise.

The purpose of this study was to evaluate the effectiveness of interactive video games (combined with stationary cycling) on health-related physical fitness and exercise adherence in comparison with traditional aerobic training (stationary cycling alone). College-aged males were stratified (aerobic fitness and body mass) and then assigned randomly to experimental (n = 7) or control (n = 7) conditions. Program attendance, health-related physical fitness (including maximal aerobic power (VO2 max), body composition, muscular strength, muscular power, and flexibility), and resting blood pressure were measured before and after training (60%-75% heart rate reserve, 3 d/week for 30 min/d for 6 weeks). There was a significant difference in the attendance of the interactive video game and traditional training groups (78% +/- 18% vs. 48% +/- 29%, respectively). VO2 max was significantly increased after interactive video game (11% +/- 5%) but not traditional (3% +/- 6%) training. There was a significantly greater reduction in resting systolic blood pressure after interactive video game (132 +/- 6 vs. 123 +/- 6 mmHg) than traditional (131 +/- 7 vs. 128 +/- 8 mmHg) training. There were no significant changes in body composition after either training program. Attendance mediated the relationships between condition and changes in health outcomes (including VO2 max, vertical jump, and systolic blood pressure). The present investigation indicates that a training program that links interactive video games to cycle exercise results in greater improvements in health-related physical fitness than that seen after traditional cycle exercise training. It appears that greater attendance, and thus a higher volume of physical activity, is the mechanism for the differences in health-related physical fitness.

Cardiopulmonary Function and Age-Related Decline Across the Breast Cancer Survivorship Continuum

PURPOSE To evaluate cardiopulmonary function (as measured by peak oxygen consumption [VO(2peak)]) across the breast cancer continuum and its prognostic significance in women with metastatic disease. PATIENTS AND METHODS Patients with breast cancer representing four cross-sectional cohorts--that is, (1) before, (2) during, and (3) after adjuvant therapy for nonmetastatic disease, and (4) during therapy in metastatic disease--were studied. A cardiopulmonary exercise test (CPET) with expired gas analysis was used to assess VO(2peak). A Cox proportional hazards model was used to estimate the risk of death according to VO(2peak) category (< 15.4 v ≥ 15.4 mL · kg(-1) · min(-1)) with adjustment for clinical factors. RESULTS A total of 248 women (age, 55 ± 8 years) completed a CPET. Mean VO(2peak) was 17.8 ± a standard deviation of 4.3 mL · kg(-1) · min(-1), the equivalent of 27% ± 17% below age-matched healthy sedentary women. For the entire cohort, 32% had a VO(2peak) less than 15.4 mL · kg(-1) · min(-1)--the VO(2peak) required for functional independence. VO(2peak) was significantly different across breast cancer cohorts for relative (mL · kg(-1) · min(-1)) and absolute (L · min(-1)) VO(2peak) (P = .017 and P < .001, respectively); VO(2peak) was lowest in women with metastatic disease. In patients with metastatic disease (n = 52), compared with patients achieving a VO(2peak) ≤ 1.09 L · min(-1), the adjusted hazard ratio for death was 0.32 (95% CI, 0.16 to 0.67, P = .002) for a VO(2peak) more than 1.09 L · min(-1). CONCLUSION Patients with breast cancer have marked impairment in VO(2peak) across the entire survivorship continuum. VO(2peak) may be an independent predictor of survival in metastatic disease.

Effect of Exercise Training on Peak Oxygen Consumption in Patients with Cancer: A Meta-Analysis

BACKGROUND We conducted a meta-analysis to determine the effects of supervised exercise training on peak oxygen consumption (VO(2peak)) in adults with cancer. METHODS A literature review using Ovid MEDLINE (1950-2010), the Cochrane Central Register of Controlled Trials (1991-2010), AMED (1985-2010), Embase (1988-2010), PubMed (1966-2010), Scopus (1950-2010), and Web of Science (1950-2010) was performed to identify randomized controlled trials examining the effects of supervised exercise training on measurement of VO(2peak) (via gas exchange analysis) in adults with cancer. Studies were selected using predetermined criteria, and two independent reviewers extracted data. Weighted mean differences (WMDs) were calculated using random effect models. RESULTS Six studies evaluated VO(2peak) involving a total of 571 adult cancer patients (exercise, n = 344; usual care control, n = 227). Pooled data indicated that exercise training was associated with a statistically significant increase in VO(2peak) (WMD, 2.90 ml·kg(-1)·min(-1); 95% confidence interval [CI], 1.16-4.64); however, significant heterogeneity was evident in this estimate (I(2), 87%). Usual care (control) was associated with a significant decline in VO(2peak) from baseline to postintervention (WMD, -1.02 ml·kg(-1)·min(-1); 95% CI, -1.46 to -0.58; I(2), 22%). Sensitivity analyses indicated superior improvements in VO(2peak) for studies conducted for a shorter duration (<4 months) and following the completion of adjuvant therapy (p-values < .001). Exercise training was not associated with a higher incidence of adverse events, although safety was not rigorously monitored or reported. CONCLUSIONS Supervised exercise training is associated with significant improvements in VO(2peak) following a diagnosis of early-stage cancer, with minimal adverse events.

Cancer Therapy–Induced Cardiac Toxicity in Early Breast Cancer Addressing the Unresolved Issues

The landscape of early breast cancer has changed dramatically with significant advancements in early screening and diagnosis and curative-intent therapies. Indeed, breast cancer–specific survival has improved by 20% during the past 30 years, and 5-year survival is now 98% for early-stage disease.1 As a consequence, the risk and nature of adjuvant therapy–induced immediate and late-occurring cardiovascular injury have similarly evolved. In women with early breast cancer, particularly those >65 years of age, cardiovascular disease (CVD) is now the predominant cause of mortality as indicated by Surveillance, Epidemiology, and End Results (SEER)–Medicare linked data.2 Additionally, these women are also at increased risk of CVD compared with age-matched women without a history of breast cancer.3 Significant cardiac safety concerns about anticancer therapy were first described by Von Hoff and colleagues,4 identifying dose-dependent and progressive left ventricular (LV) dysfunction manifesting as symptomatic heart failure in patients receiving anthracyclines. From this work and others,5,6 anthracycline-induced cardiac toxicity7,8 is now a well-recognized adverse side effect. More recently, randomized trials have demonstrated that human epidermal growth factor receptor 2 (HER2)–directed monoclonal antibodies (ie, trastuzumab) and newer multitargeted small-molecule inhibitors interfere with molecular pathways crucial to normal cardiac homeostasis,9 resulting in relatively high incidences of subclinical and overt cardiac toxicity.10 Although cardiac toxicity with newer therapies has demonstrated reversibility,11 recovery of LV function after treatment cessation is uncertain at this time.12 Thus, to identify those individuals at high risk of cardiac toxicity, baseline measurement of LV ejection fraction (LVEF) is recommended by the American College of Cardiology (ACC) and American Heart Association (AHA) as standard of care for all breast cancer patients being considered for potentially cardiac-toxic treatment regimens.13,14 In addition, measurement …

Modulation of Anthracycline-Induced Cardiotoxicity by Aerobic Exercise in Breast Cancer Current Evidence and Underlying Mechanisms

Anthracycline-containing chemotherapy (eg, doxorubicin) is well known to cause dose-dependent, progressive cardiac damage clinically manifest as decreased left ventricular (LV) ejection fraction and, ultimately, heart failure (HF) (Table 1).1,2 Unfortunately, the only clinically accepted method to minimize injury is dose modification and/or therapy discontinuation.3 An important current challenge in breast cancer management is therefore to maximize the benefits of doxorubicin while minimizing cardiac damage. Identification and examination of new interventions to prevent and/or treat doxorubicin-induced cardiotoxicity are urgently required. View this table: Table 1. Stages of Doxorubicin-Induced Cardiotoxicity Aerobic exercise is a nonpharmacological therapy that promises to attenuate doxorubicin-induced cardiotoxicity. Aerobic exercise is well documented to improve systolic and diastolic function and attenuate pathological cardiac remodeling, resulting in improved exercise tolerance and resistance to fatigue during exertion in patients with HF.4,5 The cardioprotective properties of aerobic exercise in the context of doxorubicin have, in contrast, received scant attention. It is not generally used in cancer patients despite its lack of “side effects” and the paucity of alternative strategies to prevent/treat doxorubicin-associated cardiac damage. As a first step in the possible use of exercise in cancer patients, we reviewed the mechanisms of doxorubicin-induced cardiotoxicity and the available evidence supporting the utility of aerobic exercise to prevent/treat cardiac injury. We also explored the molecular mechanisms that may underlie the cardioprotective properties of aerobic exercise. These findings have implications for future research regarding the application and effectiveness of exercise and doxorubicin treatment in humans. The mechanisms underlying the antitumor function of anthracyclines have been described previously.6–8 Among the proposed mechanisms of cardiac injury, doxorubicin-induced generation of reactive oxygen species (ROS)9,10 is a central mediator of numerous direct and indirect cardiac adverse consequences (for review, see Minotti et al11). In the present report, we …

Determinants of Exercise Intolerance in Patients with Heart Failure and Reduced or Preserved Ejection Fraction

This mini-review summarizes the literature regarding the mechanisms of exercise intolerance in patients with heart failure and reduced or preserved ejection fraction (HFREF and HFPEF, respectively). Evidence to date suggests that the reduced peak pulmonary oxygen uptake (pulm V̇o₂) in patients with HFREF compared with healthy controls is due to both central (reduced convective O₂ transport) and peripheral factors (impaired skeletal muscle blood flow, decreased diffusive O₂ transport coupled with abnormal skeletal morphology, and metabolism). Although central and peripheral impairments also limit peak pulm V̇o₂ in HFPEF patients compared with healthy controls, emerging data suggest that the latter may play a relatively greater role in limiting exercise performance in these patients. Unlike HFREF, currently there is limited evidence-based therapies that improve exercise capacity in HFPEF patients, therefore future studies are required to determine whether interventions targeted to improve peripheral vascular and skeletal muscle function result in favorable improvements in peak pulm and leg V̇o2 and their determinants in HFPEF patients.

Arterial compliance in young children: the role of aerobic fitness:

Background Reduced arterial compliance is reflective of vascular dysfunction, which promotes the atherosclerotic process, and is therefore an important predictor of vascular disease. In adults, obesity, age, aerobic fitness, oestrogens and race influence arterial compliance. Although stature and blood pressure are known to influence compliance in children, other determinants are less established. This investigation sought to determine the predictors of arterial compliance in children, assess the extent to which aerobic fitness is related to compliance, and compare compliance between girls and boys. Methods Participants (99 children aged 9-11 years, 55 boys) were assessed for aerobic fitness, physical activity level, blood pressure, body mass, percentage fat mass, height, maturity and arterial compliance (large and small). Predictors of compliance were determined using stepwise regression. Second, children were divided into quartiles according to fitness, and arterial compliance was compared using analysis of covariance (ANCOVA). Finally, differences in compliance between girls and boys were assessed using ANCOVA. Results We found that fitness, blood pressure and height accounted for 37% of the variance in large artery compliance. Mass, fitness, maturity and blood pressure accounted for 44% of the variance in small artery compliance. Children in the highest fitness quartile had greater compliance than children in the two lowest quartiles, by as much as 34%. There were no differences in compliance between girls and boys after adjusting for covariates. Discussion These data show that aerobic fitness is associated with arterial compliance in 9-11-year-old children, supporting the concept that physical fitness may exert a protective effect on the cardiovascular system.

Cardiovascular consequences of completing a 160-km ultramarathon

PURPOSES To comprehensively investigate the cardiovascular consequences of a 160-km ultramarathon using traditional echocardiography, speckle tracking imaging, cardiac biomarkers, and heart rate variability (HRV) and to examine the relationship between the changes in these variables. METHODS We examined athletes before an ultramarathon and reassessed all finishers immediately after the race. Left ventricular (LV) systolic (ejection fraction [EF], systolic blood pressure/end-systolic volume [SBP/ESV] ratio) and diastolic (ratio of early [E] to late [A], filling E:A) measurements were assessed using traditional echocardiography, whereas myocardial peak strain and strain rate were analyzed using speckle tracking. Cardiac biomarkers measured were cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-pro-BNP). HRV indices were assessed using standard frequency and time domain measures. RESULTS Twenty-five athletes successfully completed the race (25.5 +/- 3.2 h). Significant pre- to postrace changes in EF (66.8 +/- 3.8 to 61.2 +/- 4.0 %, P < 0.05) and E:A ratio (1.62 +/- 0.37 to 1.35 +/- 0.33, P < 0.05) were reported. Peak strain was significantly decreased in all planes, with the largest reduction occurring circumferentially. NT-pro-BNP concentrations increased significantly (28 +/- 17.1 vs 795 +/- 823 ng x L, P < 0.05), whereas postrace cTnT were elevated in just five athletes (20%). No significant alterations in HRV were noted postrace. Reductions in LV function were not significantly associated with changes in cardiac biomarkers and/or HRV. CONCLUSIONS Although the stress of an ultramarathon resulted in a mild reduction in LV function and biomarker release, the mechanisms behind such consequences remain unknown. It is likely that factors other than myocardial damage or strong vagal reactivation contributed to postexercise decreases in LV function after an ultramarathon.

Left ventricular torsion and untwisting during exercise in heart transplant recipients

Left ventricular (LV) rotation is the dominant deformation during relaxation and links systole with early diastolic recoil. LV torsion and untwisting rates during submaximal exercise were compared between heart transplant recipients (HTRs), young adults and healthy older individuals to better understand impaired diastolic function in HTRs. Two dimensional and colour M‐mode echocardiography with speckle‐tracking analysis were completed in eight HTRs (age: 61 ± 9 years), six recipient age‐matched (RM, age: 60 ± 11 years), and five donor age‐matched (DM, age: 35 ± 8 years) individuals (all males) at rest and during submaximal cycle exercise. LV peak torsion, peak rate of untwisting and peak intraventricular pressure gradients (IVPGs) were examined. LV torsion increased with exercise in DMs (6.5 ± 5.6 deg, P < 0.05), but not in RMs (−2.6 ± 7.0 deg) or HTRs (−0.9 ± 4.4 deg). The change from rest to exercise in the peak rate of untwisting was significantly greater for DMs (−2.1 ± 0.5 rads s−1, P < 0.05) compared to RMs (−0.7 ± 1.3 rads s−1) and HTRs (−0.2 ± 0.9 rads s−1). The amount of untwisting occurring prior to mitral valve opening substantially declined with exercise in RMs and HTRs only. The change in IVPGs was 1.3‐fold greater in DMs versus HTRs or RMs (P > 0.05). Peak LV torsion and untwisting are blunted during exercise in HTRs and RMs compared to DMs. These factors may contribute to the impaired diastolic filling found in HTRs during exercise. Similarities between HTRs and RMs during exercise suggest functional accelerated ageing of the cardiac allograft.

A framework for prescription in exercise-oncology research

The field of exercise‐oncology has increased dramatically over the past two decades, with close to 100 published studies investigating the efficacy of structured exercise training interventions in patients with cancer. Of interest, despite considerable differences in study population and primary study end point, the vast majority of studies have tested the efficacy of an exercise prescription that adhered to traditional guidelines consisting of either supervised or home‐based endurance (aerobic) training or endurance training combined with resistance training, prescribed at a moderate intensity (50–75% of a predetermined physiological parameter, typically age‐predicted heart rate maximum or reserve), for two to three sessions per week, for 10 to 60 min per exercise session, for 12 to 15 weeks. The use of generic exercise prescriptions may, however, be masking the full therapeutic potential of exercise treatment in the oncology setting. Against this background, this opinion paper provides an overview of the fundamental tenets of human exercise physiology known as the principles of training, with specific application of these principles in the design and conduct of clinical trials in exercise‐oncology research. We contend that the application of these guidelines will ensure continued progress in the field while optimizing the safety and efficacy of exercise treatment following a cancer diagnosis.