Effect of cadence on locomotor–respiratory coupling during upper-body exercise

Asynchronous arm-cranking performed at moderate-high cadences (70–90 rev min⁻¹) results in higher oxygen uptake (\( \dot{V}{\text{O}}_{ 2} \)) and minute ventilation (\( \dot{V}_{\text{E}} \)) at a given submaximal power output when compared to lower cadences (50–60 rev min⁻¹) (Price et al. 2007). These observations might be due to several mechanisms. First, at a given power output, low cadence arm-cranking extends the stroke duty cycle relative to high-cadence arm-cranking and, thus, requires greater force output from the exerciser to overcome the increased flywheel inertia. This might, in turn, predispose the exerciser to an earlier onset of local neuromuscular fatigue during low cadence ergometry (Smith et al. 2001). Second, the greater force output associated with low cadences likely results in the recruitment of aerobically meagre fast-twitch (type II) fibres which retard the O₂ response (Kushmerick et al. 1992). Third, the elevated \( \dot{V}{\text{O}}_{ 2} \) at high cadences has been attributed to greater isometric contractions of the postural muscles to stabilise the torso, in addition to a greater prevalence of locomotor–respiratory coupling (Price et al. 2007).

Locomotor–respiratory coupling (LRC), also termed entrainment, refers to the phase-locking of locomotor and respiratory frequencies during exercise (Perseqol et al. 1991; O’Halloran et al. 2011). The principal mechanism underpinning LRC is yet to be elucidated, but is associated with peripheral neurogenic drive from moving limbs (Iwamoto et al. 2010), perhaps, conferring an energetic or perceptual advantage (Stickford et al. 2015). Earlier studies in cycling exercise observed that the coupling of breathing and cycling rhythms resulted in a reduced oxygen uptake at a given workload (Garlando et al. 1985). However, LRC has not widely been studied during upper-body exercise, and it is not known how LRC is influenced by the extensive thoracic muscle loading that characterises this activity. Indeed, since most respiratory muscles attach to the ribs or associated structures, these muscles function to ventilate the lungs while simultaneously stiffening the spine (Hodges et al. 2005) and maintaining torso stabilisation and arm position (Celli et al. 1988). Furthermore, the abdominal muscles contract dynamically to flex and rotate the torso, and the diaphragm aids postural stability prior to sudden, voluntary movements of the upper-limbs (Hodges et al. 1997). As such, upper-body exercise places substantial demand on muscles of the thorax for simultaneous postural, locomotor, and ventilatory tasks. Since contractions of trunk musculature are initiated to counteract disturbances to spinal stability caused by limb movement (Hodges and Gandevia 2000), it is likely that rapid arm movements exhibited during high-cadence arm-cranking will exacerbate the essential reactive postural demands of the thoracic muscles, particularly at high exercise intensities. This may further increase O₂ consumption at high cadences. Because LRC may be initiated to facilitate airflow during periods of respiratory muscle antagonistic loading (Daley et al. 2013), it is possible that both postural loading and LRC would be exacerbated at high arm-crank cadences. As such, manipulating the arm-crank cadence provides an effective model with which to assess the relationship between cardiorespiratory function and LRC. Data to this effect will highlight the cadences that elicit optimal physiological responses and, therefore, might inform athletic training programmes that emphasise the upper-limbs. This data might also inform upper-body training or rehabilitation programmes for clinical populations.

Accordingly, the aim of the current study was to determine the acute effects of cadence and exercise intensity on cardiorespiratory function and prevalence of LRC during arm-cranking in healthy adults. We hypothesised that greater postural demand at high cadences would increase the reactive postural component, thereby increasing cardiorespiratory stress and necessitating an increased prevalence of LRC.

The aim of this study was to assess the acute influence of arm-crank cadence and work rate on locomotor-respiratory coupling and cardiorespiratory function. A novel finding was that participants more frequently synchronised their locomotor and respiratory rhythms when arm-cranking at moderate-high cadences (70–90 rev min⁻¹), compared to low cadences (50 rev min⁻¹). Furthermore, arm-cranking at 90 rev min⁻¹ significantly increased cardiorespiratory stress during moderate exercise when compared to either 50 or 70 rev min⁻¹, with correspondingly greater perceived intensity of dyspnoea. Collectively, these findings suggest that, for a given submaximal work rate, there may be a strong cadence-mediated influence on cardiorespiratory function, dyspnoea, and respiratory entrainment patterns, as per our original hypothesis.

Participants exhibited LRC more often at higher arm-crank cadences (70–90 rev min⁻¹) during both moderate and severe exercise. It has been suggested that participants engage in LRC to simplify the coordination of respiratory and postural tasks, particularly during dynamic exercise when loads on the torso exacerbate the mechanical demands of the respiratory muscles (Hodges et al. 2001). The greater prevalence of LRC, therefore, is likely associated with elevated thoracic postural demands imposed by the cadence rate.

Our observations reflect that of the previous research which has also observed LRC to occur with a prevalence of ~25% during arm-cranking performed at 90 rev min⁻¹, as well as a magnitude of LRC (~25%) that appears to be independent of work rate (Paterson et al. 1986). Early studies of LRC that used cross correlation to detect relationships between trains of respiratory and locomotor impulses also observed an increased tendency to entrain when exercising at faster cadences, although such measurements were made during lower-limb cycle ergometry (Bechbache and Duffin 1977).

Phase-locking of locomotor and respiratory patterns reduces the mechanical interactions between locomotion and ventilation, and might, therefore, minimise the conflict between muscles that contribute to both (Deban and Carrier 2002). As such, LRC occurs most frequently during periods of heightened respiratory muscle conflict to reduce the energy cost of breathing (Daley et al. 2013). Since the primary mechanical factors controlling LRC are thoracic loading and inertial displacement of soft body tissues (Bramble and Carrier 1983; Bramble and Jenkins 1993), it is likely that the fast, rhythmical rotations of the arms and shoulders during arm-cranking exacerbated the mechanical interactions between locomotor and ventilatory muscular contractions. The present observation that LRC is more prevalent at 90 rev min⁻¹ during severe exercise is indirect evidence that such conditions result in additional mechanical demands on the thoracic complex.

The present findings suggest a causal relationship between the greater prevalence of LRC and the higher cadence rate. We found that moderate exercise at 90 rev min⁻¹ resulted in greater mean inspiratory flow compared to either 70 or 50 rev min⁻¹ (1.28 ± 0.16 vs. 1.23 ± 0.21 vs. 1.12 ± 0.15 L s⁻¹). Similar patterns were noted for T _I and T _TOT at both intensities, in that there were shorter respiratory duty cycles at 90 rev min⁻¹, indicative of faster inspiration to expiration transitions. Others have found that when engaged in LRC, healthy participants tend to initiate the inspiration to expiration transition at mechanically compatible (assistive) phases of the locomotor cycle to facilitate, rather than impede, pulmonary airflow; resulting in faster inspiration to expiration transitions (Daley et al. 2013). Since we observed no differences in respiratory frequency across cadences at either work rate, it appears that our participants entrained more frequently at higher cadences to facilitate lung expansion via significant increases in expiratory and inspiratory flow. This is in contrast with earlier suggestions that greater LRC at faster cadences may result in greater respiratory frequency (Price et al. 2007). Collectively, these observations are consistent with the hypothesis that LRC results from heightened respiratory muscle conflict to facilitate respiratory flow. Since isometric contractions elicit the same \( \dot{V}{\text{O}}_{ 2} \) per unit of muscle mass as dynamic muscle contractions (Elder et al. 2006), faster cadence arm ergometry may have resulted in postural muscle contractions that elevated \( \dot{V}{\text{O}}_{ 2} \) without directly contributing to force output or propulsion of the crank shaft. Such responses have been reported to reduce gross and net mechanical efficiency (Powers et al. 1984).

In an effort to quantify the combined ventilatory and reactive postural contractions of the respiratory muscles, we measured neural drive to the diaphragm during exercise. Since the diaphragm has both inspiratory and static postural functions (Hodges et al. 1997; Hodges and Gandevia 2000), it was expected that greater postural disturbances at high cadences would manifest in greater neural drive to the diaphragm, and yet, the present data do not support this hypothesis. Although diaphragm EMG may increase during static postural contractions (Hodges et al. 1997; Hodges and Gandevia 2000), isometric rotational tasks do not elicit significant increases in diaphragm EMG (Hudson et al. 2010). Furthermore, when ventilation increases during dynamic exercise, neural input to the diaphragm is altered to prioritise its ventilatory functions (Hodges et al. 2001), resulting in diminished postural drive. Although we were currently unable to assess phrenic postural input, it appears that the role of the diaphragm in postural support at high cadences may be minimal, as suggested by the present data. Since inspiratory drive is distributed differently across various inspiratory muscles, possibly according to their mechanical effectiveness (Butler 2007), it may be that other trunk muscles—those with a less dominant role in pulmonary ventilation—make a more functional contribution to isometric postural support during high-cadence arm-cranking. Further assessment of the accessory respiratory muscles, deep muscles of the abdomen, and superficial muscles of the lower back may yield additional insight into their respective postural contributions during dynamic upper-body exercise.

The influence of cadence on cardiorespiratory function was reduced during severe exercise, as also noted in the previous studies on arm-cranking (Powers et al. 1984). This attenuated response at high intensities may relate to the greater work rate of severe compared to moderate exercise (77 ± 18 vs. 40 ± 13% W _peak). It has been suggested that unloaded arm-cranking at high cadences elicits a greater energy cost of moving the exercising limbs compared to low cadences (Price et al. 2007). As the power output (and subsequent energy demand) increases, however, the energy cost associated with unloaded arm-cranking becomes an increasingly smaller contributor to total energy expenditure. Moreover, generating a high absolute external power output during severe exercise likely requires a greater volume of active muscle mass, at both high and low cadences, to revolve the flywheel. Cardiorespiratory function, therefore, is ultimately dictated by the greater volume of muscle mass recruited during high-intensity arm-cranking, thus minimising the cadence influence on \( \dot{V}{\text{O}}_{ 2} \) at this work rate.