[1]
C. Lundby, D. Montero, and M. Joyner, ‘Biology of VO max: looking under the physiology lamp’, Acta Physiologica, vol. 220, no. 2, pp. 218–228, Jun. 2017, doi: 10.1111/apha.12827.
[2]
D. W. Ramey, How to Read a Scientific Paper, vol. 45. AAEP PROCEEDINGS, 1999, pp. 280–284 [Online]. Available: https://pdfs.semanticscholar.org/104b/3127547393d6b94a8641100e9c297d653f56.pdf
[3]
K. BAAR, ‘Training for Endurance and Strength’, Medicine & Science in Sports & Exercise, vol. 38, no. 11, pp. 1939–1944, Nov. 2006, doi: 10.1249/01.mss.0000233799.62153.19.
[4]
K. Baar and D. G. Hardie, ‘Small molecules can have big effects on endurance’, Nature Chemical Biology, vol. 4, no. 10, pp. 583–584, Oct. 2008, doi: 10.1038/nchembio1008-583.
[5]
R. Barrès et al., ‘Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle’, Cell Metabolism, vol. 15, no. 3, pp. 405–411, Mar. 2012, doi: 10.1016/j.cmet.2012.01.001.
[6]
A. Carè et al., ‘MicroRNA-133 controls cardiac hypertrophy’, Nature Medicine, vol. 13, no. 5, pp. 613–618, May 2007, doi: 10.1038/nm1582.
[7]
K. R. Chien, ‘Molecular medicine: MicroRNAs and the tell-tale heart’, Nature, vol. 447, no. 7143, pp. 389–390, May 2007, doi: 10.1038/447389a.
[8]
Y. Eto et al., ‘Calcineurin Is Activated in Rat Hearts With Physiological Left Ventricular Hypertrophy Induced by Voluntary Exercise Training’, Circulation, vol. 101, no. 18, pp. 2134–2137, May 2000, doi: 10.1161/01.CIR.101.18.2134.
[9]
T. Fernandes, V. G. Baraúna, C. E. Negrão, M. I. Phillips, and E. M. Oliveira, ‘Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs’, American Journal of Physiology-Heart and Circulatory Physiology, vol. 309, no. 4, pp. H543–H552, Aug. 2015, doi: 10.1152/ajpheart.00899.2014.
[10]
M. Iemitsu, S. Maeda, S. Jesmin, T. Otsuki, Y. Kasuya, and T. Miyauchi, ‘Activation pattern of MAPK signaling in the hearts of trained and untrained rats following a single bout of exercise’, Journal of Applied Physiology, vol. 101, no. 1, pp. 151–163, Jul. 2006, doi: 10.1152/japplphysiol.00392.2005.
[11]
M. Maillet, J. H. van Berlo, and J. D. Molkentin, ‘Molecular basis of physiological heart growth: fundamental concepts and new players’, Nature Reviews Molecular Cell Biology, vol. 14, no. 1, pp. 38–48, Jan. 2013, doi: 10.1038/nrm3495.
[12]
B. J. Wilkins et al., ‘Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy’, Circulation Research, vol. 94, no. 1, pp. 110–118, Jan. 2004, doi: 10.1161/01.RES.0000109415.17511.18.
[13]
M. O. Boluyt, J. L. Brevick, D. S. Rogers, M. J. Randall, A. F. Scalia, and Z. B. Li, ‘Changes in the rat heart proteome induced by exercise training: Increased abundance of heat shock protein hsp20’, PROTEOMICS, vol. 6, no. 10, pp. 3154–3169, May 2006, doi: 10.1002/pmic.200401356.
[14]
J. G. Burniston, ‘Changes in the rat skeletal muscle proteome induced by moderate-intensity endurance exercise’, Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics, vol. 1784, no. 7–8, pp. 1077–1086, Jul. 2008, doi: 10.1016/j.bbapap.2008.04.007.
[15]
J. G. Burniston, ‘Adaptation of the rat cardiac proteome in response to intensity-controlled endurance exercise’, PROTEOMICS, vol. 9, no. 1, pp. 106–115, Jan. 2009, doi: 10.1002/pmic.200800268.
[16]
A. Bye et al., ‘Aerobic capacity-dependent differences in cardiac gene expression’, Physiological Genomics, vol. 33, no. 1, pp. 100–109, Mar. 2008, doi: 10.1152/physiolgenomics.00269.2007.
[17]
A. Bye et al., ‘Gene expression profiling of skeletal muscle in exercise-trained and sedentary rats with inborn high and low VO’, Physiological Genomics, vol. 35, no. 3, pp. 213–221, Nov. 2008, doi: 10.1152/physiolgenomics.90282.2008.
[18]
M. Iemitsu, S. Maeda, T. Miyauchi, M. Matsuda, and H. Tanaka, ‘Gene expression profiling of exercise-induced cardiac hypertrophy in rats’, Acta Physiologica Scandinavica, vol. 185, no. 4, pp. 259–270, Nov. 2005, doi: 10.1111/j.1365-201X.2005.01494.x.
[19]
S. W. Kong et al., ‘Genetic expression profiles during physiological and pathological cardiac hypertrophy and heart failure in rats’, Physiological Genomics, vol. 21, no. 1, pp. 34–42, Mar. 2005, doi: 10.1152/physiolgenomics.00226.2004.
[20]
G. M. Diffee, ‘Adaptation of Cardiac Myocyte Contractile Properties to Exercise Training’, Exercise and Sport Sciences Reviews, vol. 32, no. 3, pp. 112–119, Jul. 2004, doi: 10.1097/00003677-200407000-00007.
[21]
O. J. Kemi, P. M. Haram, U. Wisløff, and Ø. Ellingsen, ‘Aerobic Fitness Is Associated With Cardiomyocyte Contractile Capacity and Endothelial Function in Exercise Training and Detraining’, Circulation, vol. 109, no. 23, pp. 2897–2904, Jun. 2004, doi: 10.1161/01.CIR.0000129308.04757.72.
[22]
O. KEMI et al., ‘Moderate vs. high exercise intensity: Differential effects on aerobic fitness, cardiomyocyte contractility, and endothelial function’, Cardiovascular Research, vol. 67, no. 1, pp. 161–172, Jul. 2005, doi: 10.1016/j.cardiores.2005.03.010.
[23]
O. J. Kemi et al., ‘Aerobic interval training enhances cardiomyocyte contractility and Ca2+ cycling by phosphorylation of CaMKII and Thr-17 of phospholamban’, Journal of Molecular and Cellular Cardiology, vol. 43, no. 3, pp. 354–361, Sep. 2007, doi: 10.1016/j.yjmcc.2007.06.013.
[24]
O. J. Kemi et al., ‘Activation or inactivation of cardiac Akt/mTOR signaling diverges physiological from pathological hypertrophy’, Journal of Cellular Physiology, vol. 214, no. 2, pp. 316–321, Feb. 2008, doi: 10.1002/jcp.21197.
[25]
O. J. Kemi and U. Wisløff, ‘Mechanisms of exercise-induced improvements in the contractile apparatus of the mammalian myocardium’, Acta Physiologica, vol. 199, no. 4, pp. 425–439, Aug. 2010, doi: 10.1111/j.1748-1716.2010.02132.x.
[26]
C.-P. Hsu, C.-Y. Huang, J.-S. Wang, P.-C. Sun, and C.-C. Shih, ‘Extracellular Matrix Remodeling Attenuated After Experimental Postinfarct Left Ventricular Aneurysm Repair’, The Annals of Thoracic Surgery, vol. 86, no. 4, pp. 1243–1249, Oct. 2008, doi: 10.1016/j.athoracsur.2008.06.043.
[27]
B. Burstein and S. Nattel, ‘Atrial Fibrosis: Mechanisms and Clinical Relevance in Atrial Fibrillation’, Journal of the American College of Cardiology, vol. 51, no. 8, pp. 802–809, Feb. 2008, doi: 10.1016/j.jacc.2007.09.064.
[28]
V. KOVANEN, H. SUOMINEN, and E. HEIKKINEN, ‘Connective tissue of "fast” and "slow” skeletal muscle in rats…effects of endurance training’, Acta Physiologica Scandinavica, vol. 108, no. 2, pp. 173–180, Feb. 1980, doi: 10.1111/j.1748-1716.1980.tb06515.x.
[29]
A. Daniels, M. van Bilsen, R. Goldschmeding, G. J. van der Vusse, and F. A. van Nieuwenhoven, ‘Connective tissue growth factor and cardiac fibrosis’, Acta Physiologica, vol. 195, no. 3, pp. 321–338, Mar. 2009, doi: 10.1111/j.1748-1716.2008.01936.x.
[30]
E. E. J. M. Creemers et al., ‘Deficiency of TIMP-1 exacerbates LV remodeling after myocardial infarction in mice’, American Journal of Physiology-Heart and Circulatory Physiology, vol. 284, no. 1, pp. H364–H371, Jan. 2003, doi: 10.1152/ajpheart.00511.2002.
[31]
P. E. Williams and G. Goldspink, ‘Connective tissue changes in immobilised muscle’, vol. 138, no. 2, pp. 343–350 [Online]. Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1164074/
[32]
G. MURPHY and H. NAGASE, ‘Progress in matrix metalloproteinase research’, Molecular Aspects of Medicine, vol. 29, no. 5, pp. 290–308, Oct. 2008, doi: 10.1016/j.mam.2008.05.002.
[33]
V. Di Biase and C. Franzini-Armstrong, ‘Evolution of skeletal type e–c coupling’, The Journal of Cell Biology, vol. 171, no. 4, pp. 695–704, Nov. 2005, doi: 10.1083/jcb.200503077.
[34]
R. Meeusen, M. F. Piacentini, B. Busschaert, L. Buyse, G. De Schutter, and J. Stray-Gundersen, ‘Hormonal responses in athletes: the use of a two bout exercise protocol to detect subtle differences in (over)training status’, European Journal of Applied Physiology, vol. 91, no. 2–3, pp. 140–146, Mar. 2004, doi: 10.1007/s00421-003-0940-1.
[35]
F. W. BOOTH, B. S. TSENG, M. FLUCK, and J. A. CARSON, ‘Molecular and cellular adaptation of muscle in response to physical training’, Acta Physiologica Scandinavica, vol. 162, no. 3, pp. 343–350, Feb. 1998, doi: 10.1046/j.1365-201X.1998.0326e.x.
[36]
M. Hill, A. Wernig, and G. Goldspink, ‘Muscle satellite (stem) cell activation during local tissue injury and repair’, Journal of Anatomy, vol. 203, no. 1, pp. 89–99, Jul. 2003, doi: 10.1046/j.1469-7580.2003.00195.x.
[37]
M. B. Reid, ‘Response of the ubiquitin-proteasome pathway to changes in muscle activity’, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, vol. 288, no. 6, pp. R1423–R1431, Jun. 2005, doi: 10.1152/ajpregu.00545.2004.
[38]
R. Hambrecht et al., ‘Regular Physical Activity Improves Endothelial Function in Patients With Coronary Artery Disease by Increasing Phosphorylation of Endothelial Nitric Oxide Synthase’, Circulation, vol. 107, no. 25, pp. 3152–3158, Jul. 2003, doi: 10.1161/01.CIR.0000074229.93804.5C.
[39]
P. M. Haram et al., ‘Time-course of endothelial adaptation following acute and regular exercise’, European Journal of Cardiovascular Prevention & Rehabilitation, vol. 13, no. 4, pp. 585–591, Aug. 2006, doi: 10.1097/01.hjr.0000198920.57685.76.
[40]
P. M. Haram, O. J. Kemi, and U. Wisloff, ‘Adaptation of endothelium to exercise training: Insights from experimental studies’, vol. 13, pp. 336–346, 1AD [Online]. Available: https://www.bioscience.org/2008/v13/af/2683/fulltext.htm
[41]
A. Linke, S. Erbs, and R. Hambrecht, ‘Effects of exercise training upon endothelial function in patients with cardiovascular disease’, vol. 13, pp. 424–432, 1AD [Online]. Available: https://www.bioscience.org/2008/v13/af/2689/fulltext.htm
[42]
M. Miyachi, M. Iemitsu, M. Okutsu, and S. Onodera, ‘Effects of endurance training on the size and blood flow of the arterial conductance vessels in humans’, Acta Physiologica Scandinavica, vol. 163, no. 1, pp. 13–16, May 1998, doi: 10.1046/j.1365-201x.1998.0337f.x.
[43]
A. L. Spence, H. H. Carter, L. H. Naylor, and D. J. Green, ‘A prospective randomized longitudinal study involving 6 months of endurance or resistance exercise. Conduit artery adaptation in humans’, The Journal of Physiology, vol. 591, no. 5, pp. 1265–1275, Mar. 2013, doi: 10.1113/jphysiol.2012.247387.
[44]
G. C. Bogdanis, M. E. Nevill, L. H. Boobis, H. K. Lakomy, and A. M. Nevill, ‘Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man.’, The Journal of Physiology, vol. 482, no. 2, pp. 467–480, Jan. 1995, doi: 10.1113/jphysiol.1995.sp020533.
[45]
A. Casey, D. Constantin-Teodosiu, S. Howell, E. Hultman, and P. L. Greenhaff, ‘Creatine ingestion favorably affects performance and muscle metabolism during maximal exercise in humans’, American Journal of Physiology-Endocrinology and Metabolism, vol. 271, no. 1, pp. E31–E37, Jul. 1996, doi: 10.1152/ajpendo.1996.271.1.E31.
[46]
S. B. Jørgensen, E. A. Richter, and J. F. P. Wojtaszewski, ‘Role of AMPK in skeletal muscle metabolic regulation and adaptation in relation to exercise’, The Journal of Physiology, vol. 574, no. 1, pp. 17–31, Jul. 2006, doi: 10.1113/jphysiol.2006.109942.
[47]
B. Kiens and E. A. Richter, ‘Utilization of skeletal muscle triacylglycerol during postexercise recovery in humans’, American Journal of Physiology-Endocrinology and Metabolism, vol. 275, no. 2, pp. E332–E337, Aug. 1998, doi: 10.1152/ajpendo.1998.275.2.E332.
[48]
O. K. Tsintzas, C. Williams, L. Boobis, and P. Greenhaff, ‘Carbohydrate ingestion and single muscle fiber glycogen metabolism during prolonged running in men’, Journal of Applied Physiology, vol. 81, no. 2, pp. 801–809, Aug. 1996, doi: 10.1152/jappl.1996.81.2.801.
[49]
G. Walter, K. Vandenborne, K. K. McCully, and J. S. Leigh, ‘Noninvasive measurement of phosphocreatine recovery kinetics in single human muscles’, American Journal of Physiology-Cell Physiology, vol. 272, no. 2, pp. C525–C534, Feb. 1997, doi: 10.1152/ajpcell.1997.272.2.C525.
[50]
O. KEMI et al., ‘Exercise training restores aerobic capacity and energy transfer systems in heart failure treated with losartan’, Cardiovascular Research, vol. 76, no. 1, pp. 91–99, Oct. 2007, doi: 10.1016/j.cardiores.2007.06.008.
[51]
U. Wisløff, ‘Aerobic exercise reduces cardiomyocyte hypertrophy and increases contractility, Ca2+ sensitivity and SERCA-2 in rat after myocardial infarction’, Cardiovascular Research, vol. 54, no. 1, pp. 162–174, Apr. 2002, doi: 10.1016/S0008-6363(01)00565-X.
[52]
U. Wisløff et al., ‘Superior Cardiovascular Effect of Aerobic Interval Training Versus Moderate Continuous Training in Heart Failure Patients’, Circulation, vol. 115, no. 24, pp. 3086–3094, Jun. 2007, doi: 10.1161/CIRCULATIONAHA.106.675041.
[53]
J. A. Hawley, M. Hargreaves, M. J. Joyner, and J. R. Zierath, ‘Integrative Biology of Exercise’, Cell, vol. 159, no. 4, pp. 738–749, Nov. 2014, doi: 10.1016/j.cell.2014.10.029.
[54]
G. C. Rowe, A. Safdar, and Z. Arany, ‘Running Forward’, Circulation, vol. 129, no. 7, pp. 798–810, Feb. 2014, doi: 10.1161/CIRCULATIONAHA.113.001590.
