Highlights
- •Platelet mitochondrial function is an ideal bioenergetic indicator in HF patients.
- •HIIT elevates bioenergetics health index of platelet mitochondria in HF patients.
- •HIIT enhances platelet mitochondrial OCRs via increasing Complex I/II activities.
- •Aerobic fitness is positively associated with platelet mitochondrial OCRs in HF patients.
Abstract
Objective
Exercise improves cardiopulmonary fitness and reduces the risk of vascular thrombosis
in patients with cardiovascular diseases. In platelets, mitochondria carry out cellular
bioenergetics and thrombogenesis. This study aimed to elucidate the effect of high-intensity
interval training (HIIT) on systemic aerobic capacity and platelet mitochondrial bioenergetics
in patients with heart failure (HF).
Methods
Thirty-four randomly selected HF patients engaged in HIIT (3-min intervals at 40%
and 80% of VO2peak, n = 17) for 30 min/day, 3 days/week for 12 weeks, or to a control group that received
general healthcare (GHC; n = 17). Systemic aerobic capacity (i.e., peak O2 consumption, VO2peak) and platelet mitochondrial O2 consumption rate (OCR) in the HF patients were measured through automatic gas analysis
and high-resolution respirometry, respectively.
Results
The HIIT group exhibited higher VO2peak and O2 uptake efficiency slope and lower VE-VCO2 slope after 12-week intervention, compared to those of the GHC group. Moreover, the
HIIT regimen increased the maximal and reserve OCR capacities, enhanced the Complex
I- and II-mediated OCRs, and elevated the bioenergetic health index in platelet mitochondria;
however, these effects were not observed with the GHC regimen. Additionally, the VO2peak levels were positively correlated with the maximal and reserve OCR capacities and
Complex I- and II-mediated OCRs in platelet mitochondria.
Conclusion
Platelet mitochondrial function is an ideal bioenergetic indicator in patients with
HF. HIIT for 12 weeks elevates platelet mitochondrial OCRs via increasing Complex
I and II activities. Moreover, systemic aerobic capacity is positively associated
with platelet mitochondrial OCRs in HF patients.
Keywords
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References
- Pathophysiological role of cytokines in congestive heart failure.Annu. Rev. Med. 2001; 52: 15-27
- Markers of hypercoagulability and inflammation predict mortality in patients with heart failure.J. Thromb. Haemost. 2006; 4: 1017-1022
- The endothelium and thrombotic risk in heart failure.Thromb. Haemost. 2009; 102: 185-187
- Platelet mitochondrial function: from regulation of thrombosis to biomarker of disease.Biochem. Soc. Trans. 2013; 41: 118-123
- Anemic comorbidity reduces capacity of endogenous thrombin generation and is associated with consumptive coagulopathy in patients with heart failure.Int. J. Cardiol. 2013; 168: 4965-4967
- Regulation of carbohydrate metabolism in platelets. A review.Thromb. Haemost. 1978; 39: 712-724
- The bioenergetic health index: a new concept in mitochondrial translational research.Clin. Sci. 2014; 127: 367-373
- Bioenergetics and the oxidative burst: protocols for the isolation and evaluation of human leukocytes and platelets.J. Vis. Exp. 2014; 85e51301
- Dynamics of calcium spiking, mitochondrial collapse and phosphatidylserine exposure in platelet subpopulations during activation.J. Thromb. Haemost. 2016; 14: 1867-1881
- Acute versus habitual exercise, thrombogenesis and exercise intensity.Thromb. Haemost. 2004; 91: 416-419
- Exercise prescription and thrombogenesis.J. Biomed. Sci. 2006; 13: 753-761
- Dose-response issues concerning physical activity and health: an evidence-based symposium.Med. Sci. Sports Exerc. 2001; 33: S351-S358
- High-intensity interval training improves mitochondrial function and suppresses thrombin generation in platelets undergoing hypoxic stress.Sci. Rep. 2017; 7e4191
- Aerobic interval training improves oxygen uptake efficiency by enhancing cerebral and muscular hemodynamics in patients with heart failure.Int. J. Cardiol. 2013; 167: 41-50
- Effect of aerobic interval training on erythrocyte rheological and hemodynamic functions in heart failure patients with anemia.Int. J. Cardiol. 2013; 168: 1243-1250
- General principle of exercise prescription.in: Thompson W.R. Gordon N.F. Pescatello L.S. ACSM's Guidelines for Exercise Testing and Prescription. Lippincott Williams & Wilkins, Philadelphia2010: 152-182
- Ventilatory abnormalities during exercise in heart failure: a mini review.Curr. Respir. Med. Rev. 2007; 3: 179-187
- Oxygen uptake efficiency slope: an index of exercise performance and cardiopulmonary reserve requiring only submaximal exercise.J. Am. Coll. Cardiol. 2000; 36: 194-201
- Response of the oxygen uptake efficiency slope to exercise training in patients with chronic heart failure.Eur. J. Heart Fail. 2007; 9: 625-629
- Exercise training alleviates hypoxia-induced mitochondrial dysfunction in the lymphocytes of sedentary males.Sci. Rep. 2016; 6e35170
- Evaluation of 3 quality of life measurement tools in patients with chronic heart failure.Heart Lung. 2001; 30: 332-340
- Efficacy and safety of exercise training in patients with chronic heart failure: HF-ACTION randomized controlled trial.JAMA. 2009; 301: 1439-1450
- 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and Management of Heart Failure in adults: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation.Circulation. 2009; 119: e391-e479
- Mechanisms by which exercise training benefits patients with heart failure.Nat. Rev. Cardiol. 2009; 6: 292-300
- Aerobic exercise reduces cardiomyocyte hypertrophy and increases contractility, Ca2+ sensitivity and SERCA-2 in rat after myocardial infarction.Cardiovasc. Res. 2002; 54: 162-174
- Mitochondrial respiratory control and early defects of oxidative phosphorylation in the failing human heart.Int. J. Biochem. Cell Biol. 2011; 43: 1729-1738
- Bioenergetics of the failing heart.Biochim. Biophys. Acta. 1813; 2011: 1360-1372
- Oxidative stress in heart failure: the role of mitochondria.Intern. Med. 2001; 40: 1177-1182
- Mitochondrial redox status as a target for cardiovascular disease.Curr. Opin. Pharmacol. 2016; 27: 50-55
- Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.Nature. 2014; 515: 431-435
- Cardiovascular effects of exercise training: molecular mechanisms.Circulation. 2010; 122: 1221-1238
- Succinate: a metabolic signal in inflammation.Trends Cell Biol. 2014; 24: 313-320
- Mitochondria, muscle health, and exercise with advancing age.Physiology (Bethesda). 2015; 30: 208-223
- Generic and disease-specific quality of life as a predictor of long-term mortality in heart failure.Eur. J. Heart Fail. 2010; 12: 1372-1378
- Expert consensus document: mitochondrial function as a therapeutic target in heart failure.Nat. Rev. Cardiol. 2017; 14: 238-250
Article Info
Publication History
Published online: July 27, 2018
Accepted:
July 20,
2018
Received in revised form:
June 25,
2018
Received:
January 28,
2018
Identification
Copyright
© 2018 Elsevier B.V. All rights reserved.
