Abstract
At the beginning, the survival of humans was strictly related to their physical capacity. There was the need to resist predators and to provide food and water for life. Achieving these goals required a prompt and efficient energy system capable of sustaining either high intensity or maintaining prolonged physical activity. Energy for skeletal muscle contraction is supplied by anaerobic and aerobic metabolic pathways. The former can allow short bursts of intense physical activity (60-90 sec) and utilizes as energetic source the phosphocreatine shuttle and anaerobic glycolysis. The aerobic system is the most efficient ATP source for skeletal muscle. The oxidative phosporylation of carbohydrates, fats and, to a minor extent, proteins, can sustain physical activity for many hours. Carbohydrates are the most efficient fuel for working muscle and their contribution to total fuel oxidation is positively related to the intensity of exercise. The first metabolic pathways of carbohydrate metabolism to be involved are skeletal muscle glycogenolysis and glycolysis. Later circulating glucose, formed through activated gluconeogenesis, becomes an important energetic source. Among glucose metabolites, lactate plays a primary role as either direct or indirect (gluconeogenesis) energy source for contracting skeletal muscle. Fat oxidation plays a primary role during either low-moderate intensity exercise or protracted physical activity (over 90-120 min). Severe muscle glycogen depletion results in increased rates of muscle proteolysis and branched chain amino acid oxidation. Endurance training ameliorates physical performance by improving cardiopulmonary efficiency and optimizing skeletal muscle supply and oxidation of substrates. 2003, Editrice Kurtis
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References
Stryer L. Biochemistry. New York: WH Freeman and Co. 1995, 441–682.
Brooks GA. Mammalian fuel utilization during sustained exercise. Comp Biochem Physiol 1998, 120: 89–107.
Christensen EH, Hansen O. Arbeitsfahigkeit und ehrna-hrung. Sand Arch Physiol 1939, 81: 160–3.
O’Brien MJ, Viguie CA, Mazzeo RS, et al. Carbohydrate dependence during marathon running. Med Sci Sports Exerc 1993, 25: 1009–17.
Williams C. Physiological responses to exercise. In: Burr B Nagi D eds. Exercise and Sport in Diabetes. Chichester: John Wiley & Sons. 1999, 1.
Davies KJA, Packer L, Brooks GA. Biochemical adaptation of mitochondria, muscle and whole animal respiration to endurance training. Arch Biochem Biophys 1981, 209: 539–54.
O’Doherty RM, Bracy DP, Granner DK, et al. Transcription of the rat skeletal muscle hexokinase II gene is increased by acute exercise. J Appl Physiol 1996, 81: 789–93.
Dudley G.A., Tullson P.C., Terjung R.L. Influence of mitochondrial content on the sensitivity of respiratory control. J. Biol. Chem. 1987, 262: 9109–9114.
Friedlander AL, Casazza GA, Huie MJ, et al. Endurance training alters glucose kinetics in response to the same absolute, but not the same relative workload. J Appl Physiol 1997, 82: 1360–9.
Philips SM, Green HJ, Tarnopolsky MA, et al. Effects of training duration on substrate turnover and oxidation during exercise. J Appl Physiol 1996, 81: 2182–8.
Hamdy O, Goodyear LJ, Horton ES. Diet and exercise in type 2 diabetes mellitus. Endocrinol Metab Clin North Am 2001, 30: 883–907.
Merrill GF, Kurth EJ, Hardie DG, et al. AICA riboside increases AMP-activated protein kinase, fatty acid oxidation, and glucose uptake in rat muscle. Am J Physiol 1997, 273: E1107–12.
Balon T, Nadler J. Evidence that nitric oxide increases glucose transport in skeletal muscle. J Appl Physiol 1997, 82: 359–63.
Roberts C, Barnard R, Scheck S, et al. Exercise stimulated glucose transport in skeletal muscle is nitric oxide dependent. Am J Physiol 1997, 273: E220–5.
Hill AV, Long CHN, Lupton H. Muscular exercise, lactic acid and the supply and utilization of oxygen. I-III Proc R Soc London (Biol) 1924, 97: 84–176.
Jsöbsis FF, Stainsby WN. Oxidation of NADH during contractions of circulated skeletal muscle. Resp Physiol 1968, 4: 292–300.
Connett RJ, Gayeski TEJ, Honig CR. Lactate accumulation in fully aerobic, working, dog gracilis muscle. Am J Physiol 1984, 246: H120–8.
Welch HG, Stainsby WN. Oxygen debt in contracting dog skeletal muscle in situ. Resp Physiol 1967, 3: 229–42.
Brooks GA, Butterfield GE, Wolfer RR, et al. Decreased reiance on lactate during exercise after acclimatization to 4300 m. J Appl Phsiol 1991, 71: 333–41.
Depocas F, Minaire Y, Chatonnet T. Rates of formation and oxidation of lactic acid in dogs at rest and during moderate exercise. Can J Physiol Pharmacol 1969, 47: 603–10.
Roth DA, Brooks GA. Lactate transport is mediated by a membrane-borne carrier in rat skeletal muscle sarcolemma vesicles. Arch Biochem Biophys 1990, 279: 377–85.
Kline ES, Brandt RB, Laux JE, et al. Localization of L-lactate dehydrogenase in mitochondria. Arch Biochem Biophys 1986, 246: 673–80.
Laughlin MR, Taylor J, Chensnick AS, et al. Pyruvate and actate metabolism in the in vivo dog heart. Am J Physiol 1993, 264: H2068–79.
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De Feo, P., Di Loreto, C., Lucidi, P. et al. Metabolic response to exercise. J Endocrinol Invest 26, 851–854 (2003). https://doi.org/10.1007/BF03345235
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DOI: https://doi.org/10.1007/BF03345235