Diaphragm muscle weakness/dysfunction is pervasive in many clinical populations, including chronic obstructive pulmonary disease (COPD), interstitial lung disease, heart failure, neuromuscular disease, critical illness and mechanical ventilation, and spinal cord injury (SCI; Baydur, 1991; Nishimura et al., 1994; Tantucci et al., 1994; Polkey et al., 1996; Baydur et al., 2001; Meyer et al., 2001; Laghi and Tobin, 2003; Brown et al., 2006; Kabitz et al., 2006, 2007; Petrof et al., 2010; West et al., 2012b). In these patient populations, diaphragm muscle weakness/dysfunction has been linked to increased breathlessness, impaired exercise tolerance, prolonged and difficult weaning from mechanical ventilation, and adverse health outcomes, including quality of life and death (Laghi and Tobin, 2003). It follows that non-disease specific interventions capable of increasing the pressure generating capacity of the diaphragm may have important clinical and pathophysiological implications. With the exception of inspiratory muscle training (Budweiser et al., 2006; Geddes et al., 2008; Moodie et al., 2011; Berlowitz and Tamplin, 2013; Smart et al., 2013; Martin-Valero et al., 2014) and the Ca²⁺ sensitizing agent, Levosimendan (van Hees et al., 2009; Doorduin et al., 2012), few generalized interventions exist to improve the force generating capacity of the human diaphragm.

Accumulating evidence from studies in health (Koulouris et al., 1989; West et al., 2012a) and SCI (Goldman et al., 1986; Hart et al., 2005; West et al., 2012a) suggest that elastic binding of the abdomen (AB) significantly increases maximal voluntary (e.g., sniff) and involuntary (e.g., twitch) pressure generating capacity of the diaphragm, presumably by reducing abdominal wall compliance, improving the operating length of the diaphragm due to its ascent to a more mechanically advantageous (cephalad) end-expiratory position, increasing intra-abdominal pressure, increasing the area of diaphragmatic apposition to the rib cage and/or increasing diaphragm-rib cage insertional forces (McCool et al., 1986; Koo et al., 2015). A series of studies by West et al. (2012a, 2014a,b) recently reported that AB sufficient to increase end-expiratory gastric pressure (Pga,ee) by an average of ~8 cmH₂O at rest in athletes with cervical SCI increased transdiaphragmatic twitch pressures by ~40% relative to the unbound control condition. In those studies, AB-induced improvements in diaphragmatic function were associated with concurrent improvements in static lung volumes and capacities; cardiac output at rest; the behavior of dynamic operating lung volumes during exercise; and selected measures of field-based exercise performance.

To our knowledge, only two studies have examined the impact of AB on exercise physiological responses in healthy adults (Vanmeenen et al., 1984; Hussain et al., 1985). Vanmeenen et al. (1984) examined the effects of decreasing vital capacity by ~30% through the application of an inelastic canvas corset around the abdomen (extending from the xyphoid process to the hips, thus encompassing the lower five ribs) on exercise physiological responses in 11 healthy men. In that study, AB impaired ventilatory and cardiovascular responses to exercise with attendant reductions in exercise performance, consistent with the established effects of external thoracic restriction on exercise physiological responses in healthy men (Harty et al., 1999; O'Donnell et al., 2000; Miller et al., 2002; Mendonca et al., 2014). A similar study by Hussain et al. (1985) found that applying an inelastic corset around the abdomen of five healthy men as tightly as possible while interfering minimally with ribcage movements, caused a “mild” restrictive lung deficit; significantly increased transdiaphragmatic pressure (Pdi) swings during exercise; and had no effect on exercise tolerance or an effect on ventilation (V˙_E), breathing pattern and diaphragmatic electromyography (EMGdi) responses to exercise. While the study by Hussain et al. (1985) suggested that AB has the potential to enhance neuromuscular efficiency of the human diaphragm during exercise (i.e., increase ratio of Pdi-to-EMGdi), the authors did not (1) control for the degree of abdominal compression applied; (2) account for the possibility that the “mild” restrictive lung deficit imposed by AB may have offset the potential benefits of enhanced neuromuscular efficiency of the diaphragm on exercise tolerance; and/or (3) examine the simultaneous effect of AB on cardiac, metabolic, dynamic operating lung volume, and breathlessness responses to exercise.

The purpose of this study was to examine the effect of AB sufficient to increase Pga,ee by 5–8 cmH₂O at rest on cardiac, metabolic, ventilatory, breathing pattern, dynamic operating lung volume, EMGdi, respiratory pressure, and breathlessness responses during high-intensity constant-load cycle endurance exercise testing in healthy men.

The main finding of this study was that AB sufficient to increase intra-abdominal pressure by an average of 6.6 cmH₂O at rest enhanced neuromuscular efficiency of the diaphragm during exercise, but had no effect on exercise endurance nor an effect on cardiac, metabolic, ventilatory, breathing pattern, dynamic operating lung volume, and perceptual responses to exercise in healthy young men.

In keeping with the results of earlier AB studies in health (Hussain et al., 1985) and SCI (Hart et al., 2005; West et al., 2012a, 2014a,b), the increased Pdi,tidal, Pdi,inspir, and Pdi,IC responses observed at rest and during exercise with vs. without AB were mechanistically linked to increased intra-abdominal pressures (i.e., Pga,ee and Pga,expir). The increased intra-abdominal pressures associated with AB effectively shift the abdominal contents toward the diaphragm (cephalad), thereby increasing both insertional and appositional forces of the diaphragm on the lower rib cage (Wilson and De Troyer, 2013; Koo et al., 2015). By shifting the diaphragm cephalad, AB also lengthens diaphragm muscle fibers and optimizes its length-tension relationship (Koo et al., 2015). As a result, the diaphragm initiates its inspiratory contraction at a longer length, thus generating a greater pressure at any given level of muscle activation, reflecting enhanced diaphragmatic contractility (De Troyer, 1983). Abdominal binding may further enhance pressure-generating capacity of the diaphragm by improving (reducing) abdominal compliance, thus impeding diaphragmatic descent at the costal fibers during inspiration and minimizing muscle fiber shortening, i.e., maintaining the muscle length on a more favorable region of the length-tension curve (De Troyer, 1983; Hart et al., 2005; Koo et al., 2015). Finally, by increasing intra-abdominal pressures and decreasing abdominal compliance, AB may increase the inflationary action of the diaphragm on the lower rib cage by increasing the zone of apposition and improving the diaphragm's ability to lift and expand the lower rib cage (De Troyer, 1983; Koo et al., 2015). The combination of these mechanically advantageous changes to the shape and configuration of the diaphragm are most likely responsible for the 85–95% increase in neuromuscular efficiency of the diaphragm observed during exercise with vs. without AB.

Although AB increased diaphragmatic contractility/pressure-generating capacity, it had no demonstrable effect on EMGdi,rms, Pes, V˙_E, breathing pattern, and dynamic operating lung volume responses to exercise. These findings are similar to those of earlier AB studies by Hussain et al. (1985) in health and by West et al. (2014b) in SCI, and presumably reflect the fact that AB had no untoward effect on expiratory flow generation during exercise (as evidenced by relative preservation of the relationship between exercise-induced increases in peak tidal expiratory Pes and peak expiratory flow) or an effect on exercise-induced increases the rate of CO₂ production, which is the proximate source of increased ventilatory requirements during exercise. It could be argued that the increased intra-abdominal pressures associated with AB may have hindered descent of the diaphragm into the abdomen at rest and particularly during exercise when ventilatory requirements were ~13-fold higher than at rest. If this was true, then maximal voluntary EMGdi,rms as well as the magnitude of exercise-induced increases in EMGdi,rms should have been consistently higher under AB vs. CTRL conditions. However, this is not what we observed in our study nor what Hussain et al. (1985) reported in their AB study of five healthy men.

In the setting of a relatively preserved EMGdi,rms, V˙_E, breathing pattern and dynamic operating lung volume response to exercise with vs. without AB, we speculate that the disparate effect of AB on Pdi and Pes responses to exercise reflected “off-loading” of the inspiratory action(s) of the rib cage muscles. In other words, by increasing Pdi,inspir and thus Pdi,tidal responses to exercise, AB effectively decreased the rib cage muscles' relative contribution to any given level of negative intrathoracic pressure development throughout inspiration during exercise. Additional research with simultaneous measures of accessory inspiratory muscle EMG activity is needed to confirm this postulate.

In the absence of changes in EMGdi,rms, V˙_E, breathing pattern, expiratory flow generation, and dynamic operating lung volume responses to exercise, isolated and acute improvements in neuromuscular efficiency of the diaphragm during exercise with vs. without AB had no effect on exercise endurance and/or exertional breathlessness. These findings support the view that, in healthy young adults: (1) respiratory mechanical/muscular factors do not likely contribute to the limits of exercise tolerance; and (2) progressive neuromuscular uncoupling of the diaphragm is not likely a proximate source of exertional breathlessness. Nevertheless, the results of our study provide a physiological rationale for future examination of AB as a potentially effective non-pharmacological means of improving exercise tolerance in pathophysiological disease states where neuromuscular uncoupling of the diaphragm has been mechanistically linked to a heightened perception of exertional breathlessness, most notably in patients with COPD (Laghi et al., 1998). Interestingly, a case report by Celli et al. (1985) found that AB sufficient to increase Pga,ee from 4 to 12 cmH₂O was associated with objective and potentially clinically meaningful improvements in diaphragmatic function, exercise tolerance, and breathlessness in a symptomatic patient with severe COPD and a large midline hernia of the anterior abdominal wall.

The collective results of studies by Vivier et al. (2006), Aliverti et al. (2009, 2010), and Uva et al. (2015) suggest that AB, by increasing intra-abdominal pressure and/or the abdominal circulatory pump action of the diaphragm and abdominal muscles, has the potential to improve cardiac function at rest and during exercise by increasing central venous return from the splanchnic venous circulation. In our study, however, AB had no demonstrable effect on impedance cardiograph-derived estimates of CO and SV at rest and during exercise, which is in agreement with West et al. (2012a) who reported no effect of AB on echocardiography-derived measures of cardiac function at rest (e.g., CO, SV, end-diastolic volume, end-systolic volume, ejection fraction) in eight healthy adults. We speculate that AB-induced increases in intra-abdominal pressure and/or the abdominal circulatory pump action of the diaphragm and abdominal muscles were of insufficient magnitude(s) to shift large enough quantities of blood from the splanchnic to central venous circulation to enhance cardiac function at rest and during exercise in our participants.

In summary, the increased intra-abdominal pressures associated with AB enhanced neuromuscular efficiency of the diaphragm by 85–95% during high-intensity constant-load cycle endurance exercise testing in healthy men. Additional research is recommended to examine potential benefits of AB on exertional symptoms in clinical populations where diaphragmatic weakness/dysfunction has been implicated as a source of physical activity-related breathlessness and exercise intolerance.

SA, DC, RG, and DJ contributed to the conception of the study as well as to data collection, analysis, and interpretation. CM contributed to data collection and analysis. SA and DJ wrote the manuscript, with critical input from all other authors. All authors read and approved the final version of the manuscript.