Superior Cardiovascular Effect of Aerobic Interval Training Versus Moderate Continuous Training in Heart Failure Patients: A Randomized Study

Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Nidaros, Sør-Trøndelag, Norway
Circulation (Impact Factor: 14.43). 07/2007; 115(24):3086-94. DOI: 10.1161/CIRCULATIONAHA.106.675041
Source: PubMed


Exercise training reduces the symptoms of chronic heart failure. Which exercise intensity yields maximal beneficial adaptations is controversial. Furthermore, the incidence of chronic heart failure increases with advanced age; it has been reported that 88% and 49% of patients with a first diagnosis of chronic heart failure are >65 and >80 years old, respectively. Despite this, most previous studies have excluded patients with an age >70 years. Our objective was to compare training programs with moderate versus high exercise intensity with regard to variables associated with cardiovascular function and prognosis in patients with postinfarction heart failure.
Twenty-seven patients with stable postinfarction heart failure who were undergoing optimal medical treatment, including beta-blockers and angiotensin-converting enzyme inhibitors (aged 75.5+/-11.1 years; left ventricular [LV] ejection fraction 29%; VO2peak 13 mL x kg(-1) x min(-1)) were randomized to either moderate continuous training (70% of highest measured heart rate, ie, peak heart rate) or aerobic interval training (95% of peak heart rate) 3 times per week for 12 weeks or to a control group that received standard advice regarding physical activity. VO2peak increased more with aerobic interval training than moderate continuous training (46% versus 14%, P<0.001) and was associated with reverse LV remodeling. LV end-diastolic and end-systolic volumes declined with aerobic interval training only, by 18% and 25%, respectively; LV ejection fraction increased 35%, and pro-brain natriuretic peptide decreased 40%. Improvement in brachial artery flow-mediated dilation (endothelial function) was greater with aerobic interval training, and mitochondrial function in lateral vastus muscle increased with aerobic interval training only. The MacNew global score for quality of life in cardiovascular disease increased in both exercise groups. No changes occurred in the control group.
Exercise intensity was an important factor for reversing LV remodeling and improving aerobic capacity, endothelial function, and quality of life in patients with postinfarction heart failure. These findings may have important implications for exercise training in rehabilitation programs and future studies.

Download full-text


Available from: Arnt E Tjønna,
483 Reads
  • Source
    • "Another important factor in the effective translation of preclinical findings to humans is the exercise intervention design. While preclinical and clinical experimental studies demonstrate that high intensity aerobic exercise results in greater cardiac benefits than moderate or low intensity [150] [151], the strenuous exercise prescription applied in most preclinical studies (five days a week, moderate to high intensity, 20–90 minutes) would likely not be tolerable for humans undergoing chemotherapy treatment [152]. One rodent study implemented a more clinically feasible and practical exercise prescription and doxorubicin treatment protocol involving 20 minutes of low intensity exercise, performed five days per week during chronic low dose doxorubicin treatment [23]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Thanks to increasingly effective treatment, breast cancer mortality rates have significantly declined over the past few decades. Following the increase in life expectancy of women diagnosed with breast cancer, it has been recognized that these women are at an elevated risk for cardiovascular disease due in part to the cardiotoxic side effects of treatment. This paper reviews evidence for the role of exercise in prevention of cardiovascular toxicity associated with chemotherapy used in breast cancer, and in modifying cardiovascular risk factors in breast cancer survivors. There is growing evidence indicating that the primary mechanism for this protective effect appears to be improved antioxidant capacity in the heart and vasculature and subsequent reduction of treatment-related oxidative stress in these structures. Further clinical research is needed to determine whether exercise is a feasible and effective nonpharmacological treatment to reduce cardiovascular morbidity and mortality in breast cancer survivors, to identify the cancer therapies for which it is effective, and to determine the optimal exercise dose. Safe and noninvasive measures that are sensitive to changes in cardiovascular function are required to answer these questions in patient populations. Cardiac strain, endothelial function, and cardiac biomarkers are suggested outcome measures for clinical research in this field.
    Journal of Oncology 09/2015; 2015(6). DOI:10.1155/2015/917606
  • Source
    • "We found average peak HR at the end of each of the four peak workload phases (180.9 ± 5.6 b·min -1 = 95.4 %HR max ) was not significantly different from 95 %HR max from IET (180.2 ± 4.1 b·min -1 ). The peak power output at 95 %HR max we used as P peak for long HIIE in our study represented the upper limit of the range of 85 -95 %HR max for the original 4 x 4 HIIE model applied in both healthy (Helgerud et al., 2007) and diseased populations (Wisloff et al., 2007). However, exercise intensities of 90 %HR max -or even intensities of 85 %HR max , particularly in patients suffering from cardiovascular diseases treated with beta blockers (Hofmann et al., 2005; Wonisch et al., 2003) -might just as well correspond to workloads above the second turn point and induce an accordingly high acute physiological response (Hofmann et al., 2001). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Objectives: The acute physiological processes during “aerobic” high-intensity interval exercise (HIIE) and their regulation are inadequately studied. The main goal of this study was to investigate the acute metabolic and cardiorespiratory response to long and short HIIE compared to continuous exercise (CE) as well as its regulation and predictability. Methods: Six healthy well-trained sport students (5 males, 1 female; age: 25.7 ± 3.1 years; height: 180.4 ± 4.3 cm; weight: 76.7 ± 6.4 kg; VO2max: 4.33 ± 0.7 l•min-1) performed a maximal incremental exercise test (IET) and subsequently three different exercise sessions matched for mean load (Pmean) and exercise duration (28 min): 1) long HIIE with submaximal peak workloads (Ppeak = power output at 95 % of maximum heart rate), peak workload durations (tpeak) of 4 min, and recovery durations (trec) of 3 min, 2) short HIIE with Ppeak according to the maximum power output (Pmax) from IET, tpeak of 20 s, and individually calculated trec (26.7 ± 13.4 s), and 3) CE with a target workload (Ptarget) equating to Pmean of HIIE. Results: In short HIIE, mean lactate (Lamean) (5.22 ± 1.41 mmol•l-1), peak La (7.14 ± 2.48 mmol•l-1), and peak heart rate (HRpeak) (181.00 ± 6.66 b•min-1) were significantly lower compared to long HIIE (Lamean: 9.83 ± 2.78 mmol•l-1; Lapeak: 12.37 ± 4.17 mmol•l-1, HRpeak: 187.67 ± 5.72 b•min-1). No significant differences in any parameters were found between short HIIE and CE despite considerably higher peak workloads in short HIIE. Conclusions: The acute metabolic and peak cardiorespiratory demand during “aerobic” short HIIE was significantly lower compared to long HIIE and regulable via Pmean. Consequently, short HIIE allows a consciously aimed triggering of specific and desired or required acute physiological responses.
    Journal of sports science & medicine 03/2015; 14(1):29-36. · 1.03 Impact Factor
  • Source
    • "The overall goal of HF therapy is to relieve symptoms, decrease hospitalization rates and prevent premature death. Regular physical activity has been shown to improve the quality of life in patients with stable chronic HF, reverse pathological remodeling and improve heart function of patients with systolic HF, although patient non-adherence remains a major challenge (reviewed in De Maeyer et al. 2013; Piña et al. 2003; Wisloff et al. 2007). Implantable devices such as cardioverter defibrillators and LV assist devices have been shown to reduce the risk of sudden death or improve survival, but limited economic resources affect the usage of device therapy (reviewed in McMurray 2010). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The onset of heart failure is typically preceded by cardiac hypertrophy, a response of the heart to increased workload, a cardiac insult such as a heart attack or genetic mutation. Cardiac hypertrophy is usually characterized by an increase in cardiomyocyte size and thickening of ventricular walls. Initially, such growth is an adaptive response to maintain cardiac function; however, in settings of sustained stress and as time progresses, these changes become maladaptive and the heart ultimately fails. In this review, we discuss the key features of pathological cardiac hypertrophy and the numerous mediators that have been found to be involved in the pathogenesis of cardiac hypertrophy affecting gene transcription, calcium handling, protein synthesis, metabolism, autophagy, oxidative stress and inflammation. We also discuss new mediators including signaling proteins, microRNAs, long noncoding RNAs and new findings related to the role of calcineurin and calcium-/calmodulin-dependent protein kinases. We also highlight mediators and processes which contribute to the transition from adaptive cardiac remodeling to maladaptive remodeling and heart failure. Treatment strategies for heart failure commonly include diuretics, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers and β-blockers; however, mortality rates remain high. Here, we discuss new therapeutic approaches (e.g., RNA-based therapies, dietary supplementation, small molecules) either entering clinical trials or in preclinical development. Finally, we address the challenges that remain in translating these discoveries to new and approved therapies for heart failure.
    Archive für Toxikologie 02/2015; 89(9). DOI:10.1007/s00204-015-1477-x · 5.98 Impact Factor
Show more