## 1 Introduction  
Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease that may affect any system of the body including the peripheral and central nervous system, skin, joints, blood, kidneys and serous membranes [1; 2]. Chronic inflammation is the background for the various systemic manifestations. There is also prolonged endothelial damage, which impairs blood flow and causes cardiovascular events, which leads to increased mortality in patients who have had the disease long-term. The burden of the illness and its morbidity have being increasingly studied, since mortality has decreased in the past decades [3]. The treatment of individuals with lupus involves the suppression of disease activity [4], as well as the prevention of irreversible organ damage and related mobidities. For that purpose, several medications are employed but glucocorticoids (GCs) are still the cornerstone of treatment and multiple dosings of GCs over a lifespan is common [3]. Along with the inflammatory background, the chronic use of glucocorticoids directly impairs bone and muscle health through different mechanisms, including endocrine effects on calcium metabolism. GCs may cause hypocalcemia and affect parathormone (PTH) levels [5]. Prolonged glucocorticoidoid use reduces intestinal calcium absorption. Lower circulating levels of calcidiol may stimulate PTH secretion secondary to decreased calcium absorption or increased urinary calcium excretion, thus affecting bone remodeling [6]. There is also a reduction of osteoblast activity through decreases of their functional indices and useful time of action, especially on the pro-peptide of type I N-terminal (P1 NP), pro-peptide of type I C-terminal (P1 CP) and osteoclastin. There is decreased bone formation through inhibition of Dickkopf 1 protein (DKK-1) and sclerostin [5]. GC may also reduce osteocl activity, with increased production of receptor activator of nuclear factor kappa B ligand (RANK-L) and reduction of osteoprotegerin (OPG) [7; 8]. Loss of bone mass might occur with GC use [9; 10; 11], and in contrast to the observations in postmenopausal osteoporosis (OP), fractures in glucocorticoidoid induced osteoporosis (GIOP) occur even at higher scores of bone mass [8]. With only 6 months use, there is already a reduction of bone mass in more than 25% of patients [7]. Vertebral and non-vertebral fractures are common, ranging from 30% to 50% in people who use GC for more than three months [10]. GC chronic use causes muscular catabolism and atrophy determined by a decrease in protein synthesis and proteolysis [12]. Thus, loss of muscular tissue, OP and fragility fractures should be prevented in all individuals who will initiate or who are already using these steroids [13]. Physical activities (PA) and exercises along with appropriate diet are reliable strategies to amend theseorbidities [10]. In lupus, however, several questions related to optimal type of exercise to improve fracture risk parameters (muscle strength and bone density) are not yet answered [14]. Therapeutic exercise interventions to SLE patients appear to be safe, and not induce disease activity. Improvements on scores of fatigue, depression, and physical conditioning following exercise-based programs, such as stretching, resistance training, or aerobic exercise have been described [15]. It is known that not all exercises are equally effective in terms of improving musculoskeletal condition as well as consequences of GIOP, but no randomized controlled trials have shown a significant positive effect on bone mass and/or a reduction in fracture occurrence in individuals with SLE [11]. In fact, most publications involving exercise benefits in lupus, evaluated benefits on cardiovascular events and fatigue [15]. Since the disease may also cause pain, arthritis, damage to circulatory and nervous systems, and propensity to falls, along with a strong recommendation to avoid sun exposure, the safety when prescribing the exercise must also be considered [16].