Introduction

SCI is one of the most debilitating chronic conditions that can affect people. When a SCI occurs at the cervical or high-thoracic spinal cord level it can immediately transition an active independent person to a dependent person with a significant burden of disability. Whilst the prevalence of SCI is relatively small (e.g., approx. 85,000 in Canada), the health care expenditures for individuals with chronic SCI are among the most expensive of any medical condition, largely due morbidity and premature mortality related to chronic secondary complications (Kreuger 2011; Krueger 2010). Cardiovascular disease is the leading cause of morbidity and mortality in individuals with chronic SCI (Garshick et al. 2005; Michael et al. 1999). In recent decades, there is a growing understanding that SCI also impacts metabolic function and population level data suggest that SCI increases the odds for metabolic disease, such as Type 2 diabetes, by several fold. Targeting the chronic cardiometabolic complications of SCI would dramatically improve the health and well-being of people with SCI, and positively impact health care costs. Importantly, targeting cardiometabolic complications post-SCI are ranked among the highest priorities among persons with SCI (Anderson, 2004).

The changes that occur in the cardiovascular system stem from multiple factors, but the effects of level/completeness of injury and physical deconditioning are arguably the most important. With respect to level of injury, when SCI occurs at or above the first thoracic level (T1) it immediately disrupts the sympathetic spinal pathways exiting the brainstem, which contains the cardiovascular control center that conveys signals to the heart and blood vessels. This loss of ‘normal neural control over the cardiovascular system’  impairs the cardiovascular response to exercise (Gee et al. 2021; Teasell et al. 2000), causes orthostatic hypotension (OH) (Claydon & Krassioukov 2006), autonomic dysreflexia, impairs macro- and micro-vessel function, and predisposes people with SCI to acute cardiac events (Collins et al. 2006; Wan & Krassioukov 2014). Conversely, when injury occurs at or below the T12 level then neural control of the cardiovascular system is essentially normal. With respect to injuries between the T1-T12 levels there can be a range of impairments to the cardiovascular system depending on the specific level and severity of injury. For a more comprehensive overview of the neuroanatomic implications that various levels/severities of SCI have for cardiovascular function several excellent reviews exist on this topic (Biering-Sørensen et al. 2018; Squair et al. 2015; Teasell et al. 2000).

In addition to changes in cardiovascular function and control, SCI also impacts metabolic function. People with SCI experience accelerated risk for accumulating adipose tissue (Buchholz & Bugaresti 2005; Chen et al. 2006; Cirnigliaro et al. 2015; Farkas et al. 2019; Gorgey & Dudley 2007; Gorgey et al. 2018; Gorgey & Gater 2011b, 2011c; Gorgey et al. 2011; Groah et al. 2009; Liang et al. 2007; Spungen et al. 2003; Spungen et al. 2000; Wen et al. 2019) and developing lipid (Brenes et al. 1986; Ellenbroek et al. 2014; Emmons et al. 2010; Karlsson et al. 1995a; La Fountaine et al. 2018; La Fountaine et al. 2017; Maki et al. 1995; McGlinchey-Berroth et al. 1995; Nash et al. 2005; Zlotolow et al. 1992) and glucose (Aksnes et al. 1996; Battram et al. 2007a; Bauman et al. 1999; Chilibeck et al. 1999b; Duckworth et al. 1983a; Duckworth et al. 1980; Elder et al. 2004; Gorgey & Gater 2011a; Jeon et al. 2002; Karlsson et al. 1995b; Lewis et al. 2010; Palmer et al. 1976; Segal et al. 2007; Wang et al. 2009; Yarar-Fisher et al. 2013b) metabolic disorders. The disease outcomes of these, and other, metabolic changes can be categorized as cardiometabolic disease (CMD). The Consortium for Spinal Cord Medicine (CSCM) recently released Clinical Practice Guidelines for CMD in SCI (Nash et al. 2019a). These guidelines are the first to establish SCI-specific diagnostic criteria for the cluster of risk factors that coalesce as CMD, as well as population-specific management strategies. Obesity is the most prevalent CMD risk factor in the SCI population (Libin et al. 2013; Nash et al. 2019b), with a CMD body mass index (BMI) cut-off ≥22 kg/m². The SCI-specific BMI cut-off (≥22 kg/m² vs 30 kg/m²) is required due to dysregulation of muscle (Crameri et al. 2002; Ditor et al. 2004; Duffell et al. 2008; Gorgey et al. 2020; Grimby et al. 1976; Shields 1995; Stewart et al. 2004a; Talmadge, Castro et al. 2002; Talmadge, Roy et al. 2002), bone (Carpenter et al. 2020; Gorgey et al. 2013; Minaire et al. 1984; Zleik et al. 2019), and adipose (Buchholz & Bugaresti 2005; Chen et al. 2006; Cirnigliaro et al. 2015; Farkas et al. 2019; Gorgey & Dudley 2007; Gorgey et al. 2018; Gorgey & Gater 2011b, 2011c; Gorgey et al. 2011; Groah et al. 2009; Liang et al. 2007; Spungen et al. 2003; Spungen et al. 2000; Wen et al. 2019) tissue that results in greater adiposity per unit mass. For example, a recent study of seventy-two participants with chronic motor complete SCI showed that a BMI of 27.3 kg/m² corresponded with a body fat percentage of 42 % (Gater et al. 2021), a much higher body fat percentage than would be expected for a person without SCI and a BMI <30 kg/m². Insulin resistance, or diabetes, uses a cut-off of fasting blood glucose ≥100 mg/dL, the same value as used in persons without SCI. However, it should be noted that laboratory tests for insulin resistance (Aksnes et al. 1996; Duckworth et al. 1980; Jeon et al. 2002; Karlsson et al. 1995b; Palmer et al. 1976) and oral glucose tolerance (Aksnes et al. 1996; Battram et al. 2007b; Bauman et al. 1999; Chilibeck et al. 1999a; Duckworth et al. 1983b; Duckworth et al. 1980; Elder et al. 2004; Gorgey & Gater 2011a; Jeon et al. 2002; Karlsson et al. 1995b; Lewis et al. 2010; Segal et al. 2007; Wang et al. 2009; Yarar-Fisher et al. 2013a) have routinely found that persons with SCI who have “normal” fasting blood glucose (<100 mg/dL) are likely to have impaired glycemic regulation (Aksnes et al. 1996; Bauman et al. 1999; Gorgey & Gater 2011a; Lewis et al. 2010; Segal et al. 2007; Wang et al. 2009). Dyslipidemia has two cut-off criteria: (1) blood triglyceride (TG) concentration ≥ 150 mg/dL, and (2) blood high density lipoprotein cholesterol (HDL-C) concentration of ≤ 40 and ≤ 50 mg/dL for men and women, respectively. The TG concentration cut-off is similar to CMD cut-offs used for people without SCI, but the HDL-C cut-off is population-specific due to the highly reproducible finding of low HDL-C in SCI (Bauman et al. 1992; Gilbert et al. 2014; Krum et al. 1992; La Fountaine et al. 2018; Liang et al. 2007; Lieberman et al. 2014; Washburn & Figoni 1999). Finally, a hypertension cut-off for blood pressure is also similar to that of the general population (≥ 130 and 85 mmHg for systolic and diastolic blood pressure, respectively). However, as mentioned above, especially in high-level SCI blood pressure can be low for neurogenic reasons that confounds the use of this outcome to reflect cardiovascular disease risk.

Whilst changes in neural control following injury are extremely hard to alter, physical activity and/or exercise can act as a powerful disease modifying intervention. Evidence-based guidelines have established the use of physical activity to increase cardiorespiratory fitness and muscular strength in persons with SCI (Martin Ginis et al. 2011). More recently, the CSCM CMD guidelines recommend physical exercise as a primary treatment strategy for the management of CMD in SCI. Furthermore, AGREE II evidence-based activity guidelines (Martin Ginis et al. 2011) were recently updated (Martin Ginis et al. 2018) and state with moderate to high confidence that exercise benefits CMD in persons with SCI (Martin Ginis et al. 2018). Yet despite this, individuals with SCI continually self-report some of the lowest levels of activity among any population in society. In the present chapter we review the effect various forms of exercise and/or physical activity have on cardiovascular and metabolic function in individuals with chronic SCI. In reviewing each exercise/physical activity modality/intervention we critically evaluate the strength of the evidence underlying the findings. Although we will use physical activity and/or exercise interchangeably throughout this chapter it is important to note that physical activity is any form of movement that elicits an increase in energy expenditure, whereas exercise is a program of planned and specific physical activity that specifically targets a desired outcome. It is also important to note that “exercise” is used in a separate context from the type of “rehabilitation exercises” commonly employed by allied-health therapists in a rehabilitation context (where the goal is to augment specific neuromotor function). The vast majority of studies in the field of SCI have investigated the effect of exercise on cardiometabolic function.