Glucose Homeostasis

Glucose intolerance and decreased insulin sensitivity are independent risk factors for CVD (Hurley & Hagberg 1998). Abnormal glucose homeostasis is associated with worsened lipid lipoprotein profiles and an increased risk for the development of hypertension and type 2 diabetes (Hurley & Hagberg 1998; Warburton et al. 2001b2001a). It is well-established that habitual physical activity is an effective primary preventative strategy against insulin resistance and type 2 diabetes in the general population (Warburton et al. 2006). Although comparatively less information is available for SCI, it appears that exercise training programs are effective in improving glucose homeostasis (Hjeltnes et al. 1998; Chilibeck et al. 1999; de Groot et al. 2003; Phillips et al. 2004; Mahoney et al. 2005; Jeon et al. 2010). Key terms used when assessing glucose homeostasis are provided in Table 10.


The majority of the data is from experimental non-RCT trials. A search of the literature revealed eight investigations (n = 54). This included one RCT (de Groot et al. 2003) and seven experimental non-RCT (pre-post) trials (Hjeltnes et al. 1998; Chilibeck et al. 1999; Mohr et al. 2001; Jeon et al. 2002; Phillips et al. 2004; Mahoney et al. 2005; Jeon et al. 2010). The single RCT involved the randomization to two different forms of exercise, and, as such, an exercise condition served as the control (Table 11). The majority (six) of these trials examined the effectiveness of FES training.

Similar to other studies in the field of SCI research, this area of investigation is limited by the lack of quality RCTs. Moreover, the majority of the research relates to the effects of FES training. Limited work has been conducted using aerobic and/or resistance exercise training. As a whole, however, these studies are consistent and reveal several important findings. For instance, the improvements in glucose homeostasis may be the result of increased lean body mass (and associated changes in insulin sensitivity) and increased expression of GLUT-4, glycogen synthase, and hexokinase in exercised muscle.

Consistent with findings in able-bodied individuals (Warburton et al. 2001b2001a), the improvement in glucose homeostasis after exercise interventions (e.g., aerobic training or FES) does not appear to be related solely to decreases in body adiposity and/or increases in VO2max. This is due to the fact that significant improvements in glucose homeostasis can occur with minor changes in body composition (weight and fat to muscle ratios) and/or aerobic fitness.

It is also important to note that there appears to be a minimal volume of exercise required for improvements in glucose homeostasis. For instance, Mohr et al., (2001) revealed that beneficial changes in insulin sensitivity and GLUT-4 protein observed during a three days/week FES training program were not maintained when FES training was reduced.


There is level 1b evidence from 1 RCT (de Groot et al. 2003) and multiple level 4 studies (Chilibeck et al. 1999; Mohr et al. 2001; Jeon et al. 2002; Jeon et al. 2010) that both aerobic and FES training (approximately 20–30 min/day, three days/week for eight weeks or more) are effective in improving glucose homeostasis in persons with SCI.

There is level 4 evidence from multiple pre-post studies (Hjeltnes et al. 1998; Chilibeck et al. 1999; Mohr et al. 2001; Jeon et al. 2002; Phillips et al. 2004; Mahoney et al. 2005; Jeon et al. 2010) that the changes in glucose homeostasis after aerobic or FES training are clinically significant for the prevention and/or treatment of type 2 diabetes. (For a more detailed discussion on inter-relationship of diet and SCI, please refer to Nutrition chapter).