Detraining in Athletes and COVID-19: Comparison
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The COVID-19 pandemic has affected many people in general and athletes in particular. This has led to a series of restrictions, which from a pathophysiological point of view, may affect the athlete’s performance in the short and long term. The restrictions basically affect training and eating habits, disturbing physical condition, as well as psychological behavior and general health status. Several aspects of systemic alterations caused by the SARS-CoV-2 virus and the resultant COVID-19 disease have been currently explored in the general population. However, very little is known about these particular aspects in sportsmen and sportswomen. WeResearchers believe that the most important element to take into account is the neuromuscular aspect, due to the implications that this system entails in motion execution and coordination. In this context, deficient neuromuscular control when performing dynamic actions can be an important risk factor for injury. 

  • athletes
  • clinical consequences
  • COVID-19
  • physical activity
  • return to sport
  • SARS-CoV-2

1. Introduction

The COVID-19 pandemic has affected many people in general and athletes in particular. This has led to a series of restrictions, which from a pathophysiological point of view, may affect the athlete’s performance in the short and long term. The restrictions basically affect training and eating habits, disturbing physical condition, as well as psychological behavior and general health status [1,2,3,4,5][1][2][3][4][5].
The disease caused by SARS-CoV-2 infection, known as COVID-19, is accompanied by mild symptoms with fever, cough, myalgia, fatigue, mild dyspnoea, sore throat, and headache. Nevertheless, great variability of symptoms from one person to another has been reported. Since COVID-19 is an emerging infectious disease, an additional problem is that the long-term effects and sequelae of the disease are unknown, both for moderate and severe forms [6]. Moreover, the psychological component must be considered, because it can condition many biological responses. In this regard, i.e., in the context of disasters and traumatic events, significant increases in stress levels have been observed in the population [7,8][7][8]. The same results were obtained from the first countries affected by the SARS-CoV-2 virus, such as China and South Korea [9,10][9][10]. The state of stress resulting from the pandemic and restrictive measures has long-term health effects, with an increased risk of physical and mental illness affecting sportsmen and sportswomen as well [11,12,13,14,15][11][12][13][14][15]. Even in the absence of pandemic situations, chronic stress is a major public health concern [16]. Moreover, it should be kept in mind that SARS-CoV-2 infection not only affects the pulmonary and heart systems, but also other organs such as the liver and kidneys [17,18,19][17][18][19]. All these disturbances must have an impact on sports performance, particularly among professional sportsmen and sportswomen [20]. In this line, physical performance is a complex concept that takes into account many aspects, including [21]: (a) efficient energy production (aerobic and anaerobic); (b) neuromuscular dynamics (strength and technical skills); and (c) psychological features (motivation and strategies). The COVID-19 pandemic has disturbed this framework.

2. Respiratory Disturbances

It has been well established that reduction of physical activity impairs correct glycemic control and changes body composition, favoring the increase in fat mass (FM) and reducing muscle mass (MM), all with negative consequences on maximal oxygen uptake (VO2max) [31,32][22][23]. This situation could be aggravated in athletes that have undergone SARS-CoV-2 infection [33][24]. In addition to the metabolic changes and psychological impact due to inactivity, respiratory alterations have to be considered. Many athletes reported residual symptoms even months after the initial COVID infection, including a persistent cough, tachycardia, and fatigue. This situation makes it difficult to return to physical activity due to the sustained demand of the respiratory system for optimal sports performance, particularly in aerobic disciplines [23][25]. In addition, maintaining a relatively stable but at the same time adapted metabolism during exercise poses a major challenge to respiratory and circulatory functions [34][26]. Therefore, programmed physical activity is instrumental during post-infection recovery in order to improve oxygen uptake, healthy circulating metabolic parameters, energy balance, and metabolic control. However, safe recommendations under physician supervision and in base on the new evidence have to be updated for athletes who have suffered the disease when returning to competition. Altogether, COVID-19 has an impact on metabolic adaptation during exercise [35][27]. Therefore, athletes with COVID-19 disease display an increased risk of reduced maximal and submaximal performance as well as altered cardiovascular and muscle metabolic adaptations [36][28] (Figure 1).
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Figure 1. Scheme of the possible risks that can derive from the residual symptoms in respiratory function after SARS-CoV-2 infection. See the text for more details.

3. Muscular Repercussions

SARS-CoV-2 is capable of infecting multiple cell types with a preference for pulmonary epithelium and immune cells [37][29]. As a result, muscle pain (myalgia) and fatigue are usual initial symptoms of the disease, occurring in 35% of COVID-19 patients [38,39][30][31]. In general, these findings have been associated with critically ill myopathy and steroid myopathy associated with the clinical picture of COVID-19. This muscle deterioration could be explained through the activation of angiotensin-converting enzyme 2 (ACE2), a membrane-attached protein that mediates the entry of SARS-CoV-2. In this context, studies performed in animal models show that activation of ACE2 induces skeletal muscle alterations and reduces exercise capacity, with mitochondrial dysfunction and decreased oxidative fiber number, resulting in subsequent muscle atrophy [40][32].
Several factors may play a key role in muscle plasticity. One of them seems to be the degree of mechanical loading [41][33]. In this context, inactivity decreases the mass and size of muscle fibers and consequently leads to weakening [42][34]. Thus, it can be hypothesized that the acute inflammatory response to COVID-19 infection would consume the proteins that work as building blocks for muscle activity. As documented in other inflammatory processes, the synthesis of acute-phase proteins, such as C-reactive protein (CRP), ferritin, tumor necrosis factor-α (TNF-α), and the different interleukins (ILs), could appear concomitantly with albumin and muscle protein degradation. Nevertheless, this hypothesis needs to be investigated in future research.
Myalgia and fatigue are frequently observed in 44–70% of patients with COVID-19 [43][35], being the fifth most common symptom in patients with COVID-19 [38][30]. Several studies in patients infected with other coronaviruses have shown that myalgia increased serum CK concentrations [44][36] or produce rhabdomyolysis [45][37] in 1/3 of infected individuals. However, in the case of COVID-19, the circulating CK levels were close to baseline values (around 200 U/L), making it impossible to differentiate between a myogenic or neurogenic alteration [46,47][38][39]. It can be hypothesized that the “cytokine storm” induced by SARS-CoV-2 could be a possible mechanism underlying the persistent myalgia and fatigue [48][40], but this statement needs further research.
Under normal physiological conditions, intense and sustained exercise causes muscle damage with the release of muscle proteins leading to inflammation of myocytes and altered muscle integrity. This inflammatory response leads to increases in circulating muscle proteins, such as CK, lactate dehydrogenase (LDH), and myoglobin (Mb) as well as in pro-inflammatory cytokines, including TNF-α and IL-6 [49,50,51][41][42][43]. In the context of COVID-19, a similar inflammatory reaction occurs, together with high levels of acute phase reactants such as ferritin and CRP [52][44]. Increased pro-inflammatory cytokines are involved in the induction and effector phases of all immune and inflammatory responses [53][45]. In addition, the stress component that occurs in this situation enhances the synthesis of glucocorticoids. In this context, it exists a relationship between the immune system function, the inflammatory response, and the hypothalamic-pituitary-adrenal (HPA) system [54,55,56][46][47][48].
The muscle inflammatory process is associated with increased wasting, loss of strength, and functional damage [57][49]. One of the consequences is increased muscle fatigability. Fatigue is accompanied by the release of proteins and enzymes into the bloodstream: CK, Mb, and LDH. These proteins are indicators of muscle damage and muscle stress associated with intense exercise [58][50] (Figure 2). In the field of sport, it is known that exercise increases the activity of enzymes involved in glycolysis and glycogenolysis such as glycogen phosphorylase, phosphofructokinase, and LDH [59,60][51][52]. Therefore, an interesting hypothesis to check would be to investigate if the cumulative tiredness and metabolic demand that occurs during COVID-19 could be similar to the fatigue situation undergone after very intense exercise execution. Izquierdo et al. [61][53] observed that after a period of short-term strength training, exercise-induced loss of functional capacity occurred in athletes.
Figure 2. Scheme indicating that adequate physical activity results in positive muscle adaptations. The hypothesis to test (?) is if the inflammation associated with COVID-19 is responsible for myalgia and muscle fatigue. See the text for more details. Abbreviations used: ACE2, angiotensin-converting enzyme 2.

4. Cardiac Consequences

It has been established that COVID-19 leads to cardiac and vascular complications. A possible link to the above-mentioned “cytokine storm” is hypothesized [65][54]. “Cytokine storm” occurs in the severe phase of COVID-19 and could lead to impaired cardiac function, presenting characteristics similar to those reported in classic forms of stress or catecholamine-induced cardiomyopathy [66][55]. As indicated, this is more noticeable in severe COVID-19 cases, particularly in subjects with comorbidities, such as hypertension, type 2 diabetes, and cardiovascular disorders [67][56]. In addition, it seems that SARS-CoV-2 may directly infect cardiomyocytes, causing myocarditis with acute and severe deterioration of cardiac function [67][56]. From the data reported so far by different media, many professional team sports players have been infected with SARS-CoV-2. According to some reports, athletes appear to be at a higher risk of developing myocarditis than the general population, although there is no evidence to support these claims. It is true that intense and sustained exercise may influence susceptibility to infection, depending on the intensity and duration of physical activity [49,50,68,69][41][42][57][58]. Myocarditis associated with COVID-19 has been reported in almost 1/5 of patients, with a 50% of survival rate [70][59]. Myocarditis has traditionally been considered the main cause of life-threatening ventricular arrhythmias in sportsmen [71,72,73][60][61][62]. Therefore, this incidence would support the hypothesis of the development of cardiomyopathies in athletes suffering from COVID-19. It is well established that after a long period of inactivity, aerobic capacity (according to VO2max) can decrease significantly, accompanied by an increase in heart rate [35,74][27][63]. These physiological changes lead to a decrease in muscle capillaries and a loss of sensitivity in the mechanisms that control body temperature [75,76][64][65]. As mentioned before, different outcomes have been reported by diverse aerobic training protocols during COVID-19 lockdown [5,63,64][5][66][67]. Taking into account the novelty and limited knowledge of COVID-19, the cardiomyopathy prevalence and clinical implications (acute and late) are largely unknown. Therefore, the incidence of myocardial affectation, which in many cases may be silent for a long period of time after the resolution of typical COVID-19 symptomatology, is also unknown.

References

  1. Demarie, S.; Galvani, C.; Billat, V.L. Horse-Riding Competitions Pre and Post COVID-19: Effect of Anxiety, sRPE and HR on Performance in Eventing. Int. J. Environ. Res. Public Health 2020, 17, 8648.
  2. Jimeno-Almazán, A.; Pallarés, J.G.; Buendía-Romero, Á.; Martínez-Cava, A.; Franco-López, F.; Sánchez-Alcaraz Martínez, B.J.; Bernal-Morel, E.; Courel-Ibáñez, J. Post-COVID-19 syndrome and the potential benefits of exercise. Int. J. Environ. Res. Public Health 2021, 18, 5329.
  3. Dauty, M.; Menu, P.; Fouasson-Chailloux, A. Effects of the COVID-19 confinement period on physical conditions in young elite soccer players. J. Sports Med. Phys. Fit. 2021, 61, 1252–1257.
  4. Spyrou, K.; Alcaraz, P.E.; Marín-Cascales, E.; Herrero-Carrasco, R.; Cohen, D.D.; Calleja-Gonzalez, J.; Pereira, L.A.; Loturco, I.; Freitas, T.T. Effects of the COVID-19 Lockdown on Neuromuscular Performance and Body Composition in Elite Futsal Players. J. Strength Cond. Res. 2021, 35, 2309–2315.
  5. Font, R.; Irurtia, A.; Gutierrez, J.; Salas, S.; Vila, E.; Carmona, G. The effects of COVID-19 lockdown on jumping performance and aerobic capacity in elite handball players. Biol. Sport 2021, 38, 753–759.
  6. Corsini, A.; Bisciotti, G.N.; Eirale, C.; Volpi, P. Football cannot restart soon during the COVID-19 emergency! A critical perspective from the Italian experience and a call for action. Br. J. Sports Med. 2020, 54, 1186–1187.
  7. Brackbill, R.M.; Thorpe, L.E.; DiGrande, L.; Perrin, M.; Sapp, J.H.; Wu, D.; Campolucci, S.; Walker, D.J.; Cone, J.; Pulliam, P.; et al. Surveillance for World Trade Center Disaster Health Effects Among Survivors of Collapsed and Damaged Buildings. MMWR Surveill. Summ. 2006, 55, 1–18.
  8. Mills, M.A.; Edmondson, D.; Park, C.L. Trauma and Stress Response Among Hurricane Katrina Evacuees. Am. J. Public Health 2007, 97, S116–S123.
  9. Wang, C.; Pan, R.; Wan, X.; Tan, Y.; Xu, L.; Ho, C.S.; Ho, R.C. Immediate Psychological Responses and Associated Factors during the Initial Stage of the 2019 Coronavirus Disease (COVID-19) Epidemic among the General Population in China. Int. J. Environ. Res. Public Health 2020, 17, 1729.
  10. Park, S.-C.; Park, Y.C. Mental Health Care Measures in Response to the 2019 Novel Coronavirus Outbreak in Korea. Psychiatry Investig. 2020, 17, 85–86.
  11. Martínez-Patiño, M.J.; Blas Lopez, F.J.; Dubois, M.; Vilain, E.; Fuentes-García, J.P. Effects of COVID-19 Home Confinement on Behavior, Perception of Threat, Stress and Training Patterns of Olympic and Paralympic Athletes. Int. J. Environ. Res. Public Health 2021, 18, 12780.
  12. Şenışık, S.; Denerel, N.; Köyağasıoğlu, O.; Tunç, S. The effect of isolation on athletes’ mental health during the COVID-19 pandemic. Phys. Sportsmed. 2021, 49, 187–193.
  13. Uroh, C.C.; Adewunmi, C.M. Psychological Impact of the COVID-19 Pandemic on Athletes. Front. Sports Act. Living 2021, 3, 603415.
  14. Melnyk, Y.B.; Stadnik, A.V.; Pypenko, I.S.; Kostina, V.V.; Yevtushenko, D.O. Impact of COVID-19 on the social and psychological state of athletes. J. Sports Med. Phys. Fit. 2022, 62, 297–299.
  15. Lima, Y.; Denerel, N.; Öz, N.D.; Senisik, S. The psychological impact of COVID-19 infection on athletes: Example of professional male football players. Sci. Med. Footb. 2021, 5, 53–61.
  16. Garfin, D.R.; Thompson, R.R.; Holman, E.A. Acute stress and subsequent health outcomes: A systematic review. J. Psychosom. Res. 2018, 112, 107–113.
  17. Kirwan, R.; McCullough, D.; Butler, T.; de Heredia, F.P.; Davies, I.G.; Stewart, C. Sarcopenia during COVID-19 lockdown restrictions: Long-term health effects of short-term muscle loss. Geroscience 2020, 42, 1547–1578.
  18. Palmer, K.; Monaco, A.; Kivipelto, M.; Onder, G.; Maggi, S.; Michel, J.-P.; Prieto, R.; Sykara, G.; Donde, S. The potential long-term impact of the COVID-19 outbreak on patients with non-communicable diseases in Europe: Consequences for healthy ageing. Aging Clin. Exp. Res. 2020, 32, 1189–1194.
  19. Magdy, D.M.; Metwally, A.; Tawab, D.A.; Hassan, S.A.; Makboul, M.; Farghaly, S. Long-term COVID-19 effects on pulmonary function, exercise capacity, and health status. Ann. Thorac. Med. 2022, 17, 28–36.
  20. Fabre, J.-B.; Grelot, L.; Vanbiervielt, W.; Mazerie, J.; Manca, R.; Martin, V. Managing the combined consequences of COVID-19 infection and lock-down policies on athletes: Narrative review and guidelines proposal for a safe return to sport. BMJ Open Sport Exerc. Med. 2020, 6, e000849.
  21. Córdova, A. Fisiología Deportiva; Síntesis: Madrid, Spain, 2013.
  22. Olsen, R.H.; Krogh-Madsen, R.; Thomsen, C.; Booth, F.W.; Pedersen, B.K. Metabolic Responses to Reduced Daily Steps in Healthy Nonexercising Men. JAMA 2008, 299, 1261–1263.
  23. Mikus, C.R.; Oberlin, D.J.; Libla, J.L.; Taylor, A.M.; Booth, F.W.; Thyfault, J.P. Lowering Physical Activity Impairs Glycemic Control in Healthy Volunteers. Med. Sci. Sports Exerc. 2012, 44, 225–231.
  24. Martinez-Ferran, M.; De La Guía-Galipienso, F.; Sanchis-Gomar, F.; Pareja-Galeano, H. Metabolic Impacts of Confinement during the COVID-19 Pandemic Due to Modified Diet and Physical Activity Habits. Nutrients 2020, 12, 1549.
  25. Wilson, M.G.; Hull, J.H.; Rogers, J.; Pollock, N.; Dodd, M.; Haines, J.; Harris, S.; Loosemore, M.; Malhotra, A.; Pieles, G.; et al. Cardiorespiratory considerations for return-to-play in elite athletes after COVID-19 infection: A practical guide for sport and exercise medicine physicians. Br. J. Sports Med. 2020, 54, 1157–1161.
  26. Astrand, P.O. Quantification of exercise capability and evaluation of physical capacity in man. Prog. Cardiovasc. Dis. 1976, 19, 51–67.
  27. Yu, C.; Li, A.M.; So, R.C.H.; McManus, A.; Ng, P.C.; Chu, W.; Chan, D.; Cheng, F.; Chiu, W.K.; Leung, C.W.; et al. Longer term follow up of aerobic capacity in children affected by severe acute respiratory syndrome (SARS). Thorax 2006, 61, 240–246.
  28. Narici, M.; De Vito, G.; Franchi, M.; Paoli, A.; Moro, T.; Marcolin, G.; Grassi, B.; Baldassarre, G.; Zuccarelli, L.; Biolo, G.; et al. Impact of sedentarism due to the COVID-19 home confinement on neuromuscular, cardiovascular and metabolic health: Physiological and pathophysiological implications and recommendations for physical and nutritional countermeasures. Eur. J. Sport Sci. 2021, 21, 614–635.
  29. Gu, J.; Gong, E.; Zhang, B.; Zheng, J.; Gao, Z.; Zhong, Y.; Zou, W.; Zhan, J.; Wang, S.; Xie, Z.; et al. Multiple organ infection and the pathogenesis of SARS. J. Exp. Med. 2005, 202, 415–424.
  30. Zhu, J.; Ji, P.; Pang, J.; Zhong, Z.; Li, H.; He, C.; Zhang, J.; Zhao, C. Clinical characteristics of 3062 COVID-19 patients: A meta analysis. J. Med. Virol. 2020, 92, 1902–1914.
  31. Cao, Y.; Liu, X.; Xiong, L.; Cai, K. Imaging and clinical features of patients with 2019 novel coronavirus SARS-CoV-2: A systematic review and meta-analysis. J. Med. Virol. 2020, 92, 1449–1459.
  32. Kadoguchi, T.; Kinugawa, S.; Takada, S.; Fukushima, A.; Furihata, T.; Homma, T.; Masaki, Y.; Mizushima, W.; Nishikawa, M.; Takahashi, M.; et al. Angiotensin II can directly induce mitochondrial dysfunction, decrease oxidative fibre number and induce atrophy in mouse hindlimb skeletal muscle. Exp. Physiol. 2015, 100, 312–322.
  33. Kim, J.-H.; Thompson, L.V. Inactivity, age, and exercise: Single-muscle fiber power generation. J. Appl. Physiol. 2013, 114, 90–98.
  34. Jee, H.; Kim, J.-H. A mini-overview of single muscle fibre mechanics: The effects of age, inactivity and exercise in animals and humans. Swiss. Med. Wkly. 2017, 147, w14488.
  35. Rehman, T.; Josephson, G.; Sunbuli, M.; Chadaga, A.R. Spontaneous Pneumothorax in an Elderly Patient with Coronavirus Disease (COVID-19) Pneumonia. Ochsner J. 2020, 20, 343–345.
  36. Wang, J.-T.; Sheng, W.-H.; Fang, C.-T.; Chen, Y.-C.; Wang, J.-L.; Yu, C.-J.; Chang, S.-C.; Yang, P.-C. Clinical Manifestations, Laboratory Findings, and Treatment Outcomes of SARS Patients. Emerg. Infect. Dis. 2004, 10, 818–824.
  37. Chen, L.-L.; Hsu, C.-W.; Tian, Y.-C.; Fang, J.-T. Rhabdomyolysis associated with acute renal failure in patients with severe acute respiratory syndrome. Int. J. Clin. Pract. 2005, 59, 1162–1166.
  38. Mao, L.; Jin, H.; Wang, M.; Hu, Y.; Chen, S.; He, Q.; Chang, J.; Hong, C.; Zhou, Y.; Wang, D.; et al. Neurologic Manifestations of Hospitalized Patients with Coronavirus Disease 2019 in Wuhan, China. JAMA Neurol. 2020, 77, 683–690.
  39. Kley, R.A.; Schmidt-Wilcke, T.; Vorgerd, M. Differential Diagnosis of HyperCKemia. Neurol. Int. Open 2018, 2, E72–E83.
  40. Mangalmurti, N.; Hunter, C.A. Cytokine Storms: Understanding COVID-19. Immunity 2020, 53, 19–25.
  41. Córdova, A.; Martin, J.F.; Reyes, E.; Alvarez-Mon, M. Protection against muscle damage in competitive sports players: The effect of the immunomodulator AM3. J. Sports Sci. 2004, 22, 827–833.
  42. Cordova, A.; Monserrat, J.; Villa, G.; Reyes, E.; Soto, M.A.-M. Effects of AM3 (Inmunoferon) on increased serum concentrations of interleukin-6 and tumour necrosis factor receptors I and II in cyclists. J. Sports Sci. 2006, 24, 565–573.
  43. Córdova-Martínez, A.; Martorell-Pons, M.; Sureda-Gomila, A.; Tur-Marí, J.A.; Pons-Biescas, A. Changes in circulating cytokines and markers of muscle damage in elite cyclists during a multi-stage competition. Clin. Physiol. Funct. Imaging 2015, 35, 351–358.
  44. Wang, D.; Hu, B.; Hu, C.; Zhu, F.; Liu, X.; Zhang, J.; Wang, B.; Xiang, H.; Cheng, Z.; Xiong, Y.; et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus—Infected Pneumonia in Wuhan, China. JAMA 2020, 323, 1061–1069.
  45. Lee, D.W.; Gardner, R.; Porter, D.L.; Louis, C.U.; Ahmed, N.; Jensen, M.C.; Grupp, S.A.; Mackall, C.L. Current concepts in the diagnosis and management of cytokine release syndrome. Blood 2014, 124, 188–195.
  46. Cordova, A. Fisiología Dinámica; Ed Elsevier-Masson: Barcelona, Spain, 2003.
  47. Majano, P.; Roda-Navarro, P.; Alonso-Lebrero, J.L.; Brieva, A.; Casal, C.; Pivel, J.P.; López-Cabrera, M.; Moreno-Otero, R. AM3 inhibits HBV replication through activation of peripheral blood mononuclear cells. Int. Immunopharmacol. 2004, 4, 921–927.
  48. Prompetchara, E.; Ketloy, C.; Palaga, T. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac. J. Allergy Immunol. 2020, 38, 1–9.
  49. Draganidis, D.; Karagounis, L.G.; Athanailiidis, I.; Chatzinikolaou, A.; Jamurtas, A.Z.; Fatouros, I.G. Inflammaging and Skeletal Muscle: Can Protein Intake Make a Difference? J. Nutr. 2016, 146, 1940–1952.
  50. Banfi, G.; Colombini, A.; Lombardi, G.; Lubkowska, A. Metabolic markers in sports medicine. Adv. Clin. Chem. 2012, 56, 1–54.
  51. Linossier, M.-T.; Dormois, D.; Perier, C.; Frey, J.; Geyssant, A.; Denis, C. Enzyme adaptations of human skeletal muscle during bicycle short-sprint training and detraining. Acta Physiol. Scand. 1997, 161, 439–445.
  52. Dawson, B.; Fitzsimons, M.; Green, S.; Goodman, C.; Carey, M.; Cole, K. Changes in performance, muscle metabolites, enzymes and fibre types after short sprint training. Eur. J. Appl. Physiol. Occup. Physiol. 1998, 78, 163–169.
  53. Izquierdo, M.; Ibañez, J.; Calbet, J.A.L.; González-Izal, M.; Navarro-Amézqueta, I.; Granados, C.; Malanda, A.; Idoate, F.; González-Badillo, J.J.; Häkkinen, K.; et al. Neuromuscular Fatigue after Resistance Training. Int. J. Sports Med. 2009, 30, 614–623.
  54. Hu, B.; Huang, S.; Yin, L. The cytokine storm and COVID-19. J. Med. Virol. 2021, 93, 250–256.
  55. Clerkin, K.J.; Fried, J.A.; Raikhelkar, J.; Sayer, G.; Griffin, J.M.; Masoumi, A.; Jain, S.S.; Burkhoff, D.; Kumaraiah, D.; Rabbani, L.R.; et al. COVID-19 and Cardiovascular Disease. Circulation 2020, 141, 1648–1655.
  56. Paul, J.-F.; Charles, P.; Richaud, C.; Caussin, C.; Diakov, C. Myocarditis revealing COVID-19 infection in a young patient. Eur. Heart. J. Cardiovasc. Imaging 2020, 21, 776.
  57. Nieman, D.C. Is infection risk linked to exercise workload? Med. Sci. Sports Exerc. 2000, 32, S406–S411.
  58. Simpson, R.J.; Campbell, J.P.; Gleeson, M.; Krüger, K.; Nieman, D.C.; Pyne, D.B.; Turner, J.E.; Walsh, N.P. Can exercise affect immune function to increase susceptibility to infection? Exerc. Immunol. Rev. 2020, 26, 8–22.
  59. Doyen, D.; Moceri, P.; Ducreux, D.; Dellamonica, J. Myocarditis in a patient with COVID-19: A cause of raised troponin and ECG changes. Lancet 2020, 395, 1516.
  60. Boraita-Pérez, A.; Serratosa-Fernández, L. Sudden death (IV). Sudden death in the athlete. The minimal requirements before performing a competitive sport. Rev. Esp. Cardiol. 1999, 52, 1139–1145.
  61. Emery, M.S.; Kovacs, R.J. Sudden Cardiac Death in Athletes. JACC Heart Fail. 2018, 6, 30–40.
  62. Corrado, D.; Zorzi, A. Sudden death in athletes. Int. J. Cardiol. 2017, 237, 67–70.
  63. Muñoz-Martínez, F.A.; Rubio-Arias, J.Á.; Ramos-Campo, D.J.; Alcaraz, P.E. Effectiveness of Resistance Circuit-Based Training for Maximum Oxygen Uptake and Upper-Body One-Repetition Maximum Improvements: A Systematic Review and Meta-Analysis. Sports Med. 2017, 47, 2553–2568.
  64. Costill, D.L.; Fink, W.J.; Hargreaves, M.; King, D.S.; Thomas, R.; Fielding, R. Metabolic characteristics of skeletal muscle during detraining from competitive swimming. Med. Sci. Sports Exerc. 1985, 17, 339–343.
  65. Neufer, P.D.; Costill, D.L.; Fielding, R.A.; Flynn, M.G.; Kirwan, J.P. Effect of reduced training on muscular strength and endurance in competitive swimmers. Med. Sci. Sports Exerc. 1987, 19, 486–490.
  66. Demarie, S.; Chirico, E.; Galvani, C. Prediction and Analysis of Tokyo Olympic Games Swimming Results: Impact of the COVID-19 Pandemic on Swimmers’ Performance. Int. J. Environ. Res. Public Health 2022, 19, 2110.
  67. Rampinini, E.; Donghi, F.; Martin, M.; Bosio, A.; Riggio, M.; Maffiuletti, N.A. Impact of COVID-19 Lockdown on Serie a Soccer Players’ Physical Qualities. Int. J. Sports Med. 2021, 42, 917–923.
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