Objective. The objective of this study was to correlate metabolic and hormonal parameters before and after 8, 16, and 24 weeks (wk) of moderate aerobic training in individuals with chronic primary insomnia. Method. Four male and sixteen female volunteers (adults, sedentary, and healthy) performed exercise training for 24 weeks. Blood and Pittsburgh Sleep Quality Index (PSQI) was obtained at baseline, 8, 16, and 24?wk of training. Results. PSQI scores decreased after 8, 16, and 24?wk of training regarding baseline values. Indeed, total sleep time (TST) increased after 16 and 24?wk of exercise training regarding baseline values. The correlations were analyzed using the delta ( ) values ( ?wk less baseline; ?wk less baseline; ?wk less baseline). We have observed a negative correlation for between TST and cortisol, a positive correlation for between TST and growth hormone, a negative correlation for between TST and VLDL, a negative correlation for between TST and triacylglycerols, and a negative correlation for and between TST and thyroid-stimulating hormone. Conclusion. The exercise training improved the sleep quality of patients with chronic primary insomnia. 1. Introduction In modern society, sleep disorders are increasing every day around the world. Recently, a study with 4957 American adults determined that 40% of the participants had at least one sleep disorder [1]. In S?o Paulo, Brazil, a study observed that 33% of the society presented insomnia characteristics, and a higher incidence of insomnia was detected in women (40%) [2]. Chronic primary insomnia is a sleep disorder that is characterized by long-term difficulties with initiating and maintaining sleep, waking up too early, nonrestorative sleep, and daytime impairment, including fatigue, poor mood, impaired concentration, and poor quality of life [3–6]. Budhiraja et al. 2011 [7] have shown that medical disorders such as hypertension and diabetes are associated with a higher prevalence of insomnia. The prevalence of insomnia increased as the number of medical disorders increased, suggesting an additive adverse effect of these medical conditions on insomnia [7]. Other studies have concluded that few hours of sleep are associated with overweight, obesity, metabolic alterations (insulin resistance, dyslipidemia, and increased activity of the HPA axis), and inflammatory diseases [8–11]. Physical exercise is used as a nonpharmacological treatment in many different diseases, including sleep disorders [12–15]. Recently, our group demonstrated that acute and chronic aerobic exercise improves subjective
References
[1]
S. M. W. Rajaratnam, L. K. Barger, S. W. Lockley et al., “Sleep disorders, health, and safety in police officers,” Journal of the American Medical Association, vol. 306, no. 23, pp. 2567–2578, 2011.
[2]
L. R. A. Bittencourt, R. Santos-Silva, J. A. Taddei, M. L. Andersen, M. T. de Mello, and S. Tufik, “Sleep complaints in the adult Brazilian population: a national survey based on screening questions,” Journal of Clinical Sleep Medicine, vol. 5, no. 5, pp. 459–463, 2009.
[3]
A. P. Association, Diagnostic and Statistical of Mental Disorders (DSM-IV), American Psychiatric Press, Washington, DC, USA, 1994.
[4]
Medicine AAoS, The International Classification of Sleep Disorders (ICSD): Diagnostic and Coding Manual, Diagnopstic Classification Steering Committee, Westchester, Ill, USA, 2005.
[5]
G. E. Simon and M. Vonkorff, “Prevalence, burden, and treatment of insomnia in primary care,” The American Journal of Psychiatry, vol. 154, no. 10, pp. 1417–1423, 1997.
[6]
M. O. Summers, M. I. Crisostomo, and E. J. Stepanski, “Recent development in the classification, evaluation, and treatment of insomnia,” Chest, vol. 130, no. 1, pp. 276–286, 2006.
[7]
R. Budhiraja, T. Roth, D. W. Hudgel, P. Budhiraja, and C. L. Drake, “Prevalence and polysomnographic correlates of insomnia comorbid with medical disorders,” Sleep, vol. 34, no. 7, pp. 859–867, 2011.
[8]
H. R. Colten and B. M. Altevogt, Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem, 2006.
[9]
M. R. Irwin, M. Wang, D. Ribeiro et al., “Sleep loss activates cellular inflammatory signaling,” Biological Psychiatry, vol. 64, no. 6, pp. 538–540, 2008.
[10]
A. N. Vgontzas, E. O. Bixler, H.-M. Lin et al., “Chronic insomnia is associated with nyctohemeral activation of the hypothalamic-pituitary-adrenal axis: clinical implications,” Journal of Clinical Endocrinology and Metabolism, vol. 86, no. 8, pp. 3787–3794, 2001.
[11]
A. N. Vgontzas, D. A. Papanicolaou, E. O. Bixler et al., “Circadian interleukin-6 secretion and quantity and depth of sleep,” Journal of Clinical Endocrinology and Metabolism, vol. 84, no. 8, pp. 2603–2607, 1999.
[12]
E. S. Alves, F. S. Lira, R. V. T. Santos, S. Tufik, and M. T. de Mello, “Obesity, diabetes and OSAS induce of sleep disorders: exercise as therapy,” Lipids in Health and Disease, vol. 10, article 148, 2011.
[13]
A. M. Esteves, M. T. de Mello, M. Pradella-Hallinan, and S. Tufik, “Effect of acute and chronic physical exercise on patients with periodic leg movements,” Medicine and Science in Sports and Exercise, vol. 41, no. 1, pp. 237–242, 2009.
[14]
G. S. Passos, D. Poyares, M. G. Santana et al., “Effects of moderate aerobic exercise training on chronic primary insomnia,” Sleep Medicine, vol. 12, no. 10, pp. 1018–1027, 2011.
[15]
G. S. Passos, D. Poyares, M. G. Santana, S. A. Garbuio, S. Tufik, and M. T. de Mello, “Effect of acute physical exercise on patients with chronic primary insomnia,” Journal of Clinical Sleep Medicine, vol. 6, no. 3, pp. 270–275, 2010.
[16]
A. T. Beck, C. H. Ward, M. Mendelson, J. Mock, and J. Erbaugh, “An inventory for measuring depression,” Archives of General Psychiatry, vol. 4, pp. 561–571, 1961.
[17]
W. L. Beaver, K. Wasserman, and B. J. Whipp, “A new method for detecting anaerobic threshold by gas exchange,” Journal of Applied Physiology, vol. 60, no. 6, pp. 2020–2027, 1986.
[18]
L. Goldberg, D. L. Elliot, and K. S. Kuehl, “Assessment of exercise intensity formulas by use of ventilatory threshold,” Chest, vol. 94, no. 1, pp. 95–98, 1988.
[19]
D. J. Buysse, C. F. Reynolds III, T. H. Monk, S. R. Berman, and D. J. Kupfer, “The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research,” Psychiatry Research, vol. 28, no. 2, pp. 193–213, 1989.
[20]
W. T. Friedewald, R. I. Levy, and D. S. Fredrickson, “Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge,” Clinical Chemistry, vol. 18, no. 6, pp. 499–502, 1972.
[21]
K. J. Reid, K. G. Baron, B. Lu, E. Naylor, L. Wolfe, and P. C. Zee, “Aerobic exercise improves self-reported sleep and quality of life in older adults with insomnia,” Sleep Medicine, vol. 11, no. 9, pp. 934–940, 2010.
[22]
P. D. Nowell and D. J. Buysse, “Treatment of insomnia in patients with mood disorders,” Depression and Anxiety, vol. 14, no. 1, pp. 7–18, 2001.
[23]
American College of Sports Medicine Position Stand, “The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness, and flexibility in healthy adults,” Medicine & Science in Sports & Exercise, vol. 30, pp. 975–991, 1998.
[24]
A. N. Vgontzas, G. Mastorakos, E. O. Bixler, A. Kales, P. W. Gold, and G. P. Chrousos, “Sleep deprivation effects on the activity of the hypothalamic- pituitary-adrenal and growth axes: potential clinical implications,” Clinical Endocrinology, vol. 51, no. 2, pp. 205–215, 1999.
[25]
E. Spath-Schwalbe, M. Gofferje, W. Kern, J. Born, and H. L. Fehm, “Sleep disruption alters nocturnal ACTH and cortisol secretory patterns,” Biological Psychiatry, vol. 29, no. 6, pp. 575–584, 1991.
[26]
M. Duclos, M. Guinot, and Y. L. Bouc, “Cortisol and GH: odd and controversial ideas,” Applied Physiology, Nutrition and Metabolism, vol. 32, no. 5, pp. 895–903, 2007.
[27]
E. van Cauter, F. Latta, A. Nedeltcheva et al., “Reciprocal interactions between the GH axis and sleep,” Growth Hormone and IGF Research, vol. 14, supplement A, pp. S10–S17, 2004.
[28]
L. Klingenberg, A. Sj?din, U. Holmb?ck, A. Astrup, and J.-P. Chaput, “Short sleep duration and its association with energy metabolism,” Obesity Reviews, vol. 13, pp. 565–577, 2012.
[29]
L. Kessler, A. Nedeltcheva, J. Imperial, and P. D. Penev, “Changes in serum TSH and free T4 during human sleep restriction,” Sleep, vol. 33, no. 8, pp. 1115–1118, 2010.
[30]
M. L. Andersen and S. Tufik, “Is thyroid screening of sleep clinic patients essential?” Sleep Medicine, vol. 13, no. 10, pp. 1215–1216, 2012.
[31]
C. Sabanayagam and A. Shankar, “Sleep duration and hypercholesterolaemia: results from the National Health Interview Survey 2008,” Sleep Medicine, vol. 13, no. 2, pp. 145–150, 2012.
[32]
I. Soreca, M. L. Wallace, E. Frank, B. P. Hasler, J. C. Levenson, and D. J. Kupfer, “Sleep duration is associated with dyslipidemia in patients with bipolar disorder in clinical remission,” Journal of Affective Disorders, vol. 141, pp. 484–487, 2012.
[33]
F. S. Lira, G. D. Pimentel, R. V. T. Santos et al., “Exercise training improves sleep pattern and metabolic profile in elderly people in a time-dependent manner,” Lipids in Health and Disease, vol. 10, article 113, pp. 1–6, 2011.