1.5.1. Defining HRV
HRV refers to the variation in instantaneous HR or the intervals between heartbeats, also known as RR intervals or IBIs (Malik and Camm 1995; Task Force 1996; von Borell et al.
2007; Kamath et al. 2012). HRV was first recognised as a promising marker of autonomic function in the 1960s and has since been incorporated into a wide array of clinical research examining various physical, psychological, and pathological conditions (Malik and Camm 1995;
Task Force 1996; von Borell et al. 2007; Kamath et al. 2012). HRV has also been applied extensively within veterinary and animal research, where it has been well established as a reliable indicator of both acute and chronic stress (von Borell et al. 2007).
1.5.2. Regulation of cardiac activity: HRV as an indicator of sympathovagal balance
Cardiac activity is largely under control of the ANS (Task Force 1996). The sino-atrial (SA) node, the primary regulator of HR, is innervated by both sympathetic and parasympathetic branches of the ANS (Task Force 1996; Berntson et al. 1997; von Borell et al. 2007).
Parasympathetic influence, which decelerates HR, is mediated by acetylcholine secreted from the vagus nerve. Conversely, sympathetic influence, which accelerates HR, is mediated predominantly by adrenaline and noradrenaline secreted from the sympathetic nerve terminals – but also circulatory catecholamines secreted from the adrenal medulla (Task Force 1996;
Charmandari et al. 2005; von Borell et al. 2007). HR represents the net effect of parasympathetic and sympathetic activity (Malik and Camm 1995; von Borell et al. 2007).
Although the parasympathetic nervous system (PNS) and SNS are mutually exclusive (i.e.
simultaneous relaxation and arousal cannot occur) they do not function on a continuum (Malik and Camm 1995; von Borell et al. 2007; Schmidt-Nielsen 2007). Increasing activity in one branch does not result in decreasing activity in the other (Berntson et al. 1997; Malik and Camm 1995; von Borell et al. 2007). Instead, both branches may function synchronously or independently of one another (Berntson et al. 1997; Malik and Camm 1995; von Borell et al.
2007). For example, the PNS can either assist or antagonise sympathetic activity by withdrawing or increasing parasympathetic input (Sapolsky et al. 2000; Tsigos and Chrousos 2002; Charmandari et al. 2005). An increase in HR is typically caused by an increase in sympathetic activity, but may also result from reduced parasympathetic activity or a combination
of both (Malik and Camm 1995; von Borell et al. 2007). Thus, HR alone cannot be used to accurately assess either parasympathetic or sympathetic activity (von Borell et al. 2007).
HRV measures the fluctuations in parasympathetic and sympathetic activity (i.e.
sympathovagal balance) at the SA node (Malik and Camm 1995; Task Force 1996; von Borell et al. 2007). Consequently, it can be used to measure the balance of autonomic control, both
under baseline conditions and following exposure to an acute stressor (von Borell et al. 2007).
At rest, both sympathetic and parasympathetic branches are tonically active, though parasympathetic activity is dominant (Malik and Camm 1995; Task Force 1996; von Borell et al.
2007). Cardiac activity is maintained within a homeostatic range, which is regulated by various control and feedback mechanisms (Malik and Camm 1995; von Borell et al. 2007). Fluctuations in these regulatory components result in fluctuations in cardiac activity. As a result, the time intervals between consecutive heartbeats are highly variable and irregular at rest (Malik and Camm 1995; von Borell et al. 2007). HRV under baseline conditions can be used as an indicator for stress vulnerability (Johnson et al. 1992; Porges 1995). High vagal tone (i.e. high parasympathetic activity/reactivity as indicated by high basal HRV) has been associated with increased responsiveness to stressors and/or environmental challenges (Johnson et al. 1992;
Porges 1995). Conversely, low vagal tone (i.e. low parasympathetic activity/reactivity as indicated by low basal HRV) has been associated with increased susceptibility to stressors (Johnson et al. 1992; Porges 1995). Physical activity or stressors, both physiological and psychological, are capable of shifting sympathovagal balance (Task Force 1996; von Borell et al. 2007). Generally speaking, a decrease in HRV (and a concurrent increase in HR) indicates
reduced parasympathetic activity (and increased sympathetic activity) – and vice versa (Malik and Camm 1995; Task Force 1996; von Borell et al. 2007).
1.5.3. HRV as an indicator of coping styles
HRV has been applied primarily within stress research to improve animal welfare, veterinary research as an indicator of various pathologies, and biomedical research using animal models of human disease (von Borell et al. 2007). Almost all animal research studies using HRV have been conducted on laboratory or domesticated animals such as rats, chickens, Japanese quail, pigs, goats (Capra aegagrus hircus), sheep (Ovis aries), cattle, and horses. A handful of studies have examined HRV using non-laboratory or non-domesticated species, such
as European starlings (Sturnus vulgaris), northern elephant seals, and harbour seals (Phoca vitulina). HRV in wild-caught European starlings have been used to investigate how transport
into captivity alters basal sympathetic tone and sympathetic reactivity in response to acute stressors (Dickens and Romero 2009), cardiovascular responses to acute and chronic stress (Cyr et al. 2009), and cardiovascular responses to chronic stress during different life-history stages (e.g. moult) (Kostelanetz et al. 2009). HRV in pinnipeds has been used to estimate breathing frequencies of wild juvenile northern elephant seals (Andrews et al. 2000) and to investigate the development of diving bradycardia in wild (Greaves et al. 2004) and rehabilitated (Fonfara and Casamian-Sorrosal 2014) harbour seal pups. Overall, however, few studies within animal research have focused on inter-individual variation in HRV.
To date, only four studies have used HRV concurrently with catecholamines to infer coping styles. Sgoifo et al. (1998, 2005) demonstrated that aggressive and non-aggressive rats show differences in HRV following exposure to acute stressors that are concomitant with differences in HR and plasma catecholamine concentrations. When challenged with restraint or social defeat, aggressive rats show comparatively greater plasma catecholamine concentrations, higher HR, and lower HRV that persists for longer – suggesting greater sympathetic reactivity and reduced parasympathetic rebound following sympathetic activation.
Similar cardiac and catecholamine responses to restraint have been documented in HFP and LFP hens (Korte et al. 1997, 1999).
Accordingly, HR and HRV can be used to distinguish underlying differences in autonomic function between coping styles (Table 1.2). Proactive individuals are characterised by greater sympathetic reactivity and reduced parasympathetic reactivity compared to reactive coping styles (Korte et al. 1997, 1999; Sgoifo et al. 1998, 2005; Koolhaas et al. 1999). Greater sympathetic reactivity manifests as higher HR and lower HRV following exposure to an acute stressor, whereas reduced parasympathetic activity manifests as longer latency for HR and HRV to return to baseline values.