The magnitude of peripheral fatigue was attenuated by almost one-third when the inspiratory muscles were unloaded (−28% for CTRL versus−20% for PAV) and exacerbated to an even greater extent when the inspiratory muscles were loaded (−12% for CTRL-IRL versus−20% for IRL). The changes in contractile function were not due to reductions in action potential transmission because M-wave amplitudes were not different pre- versus postexercise. That muscle function began to recover rapidly after exercise and that the differences in fatigue between unloading/loading and control conditions were most pronounced immediately after exercise suggest a role for metabolic processes.
Respiratory muscle metaboreflex We propose, as originally hypothesised (see Introduction), that the increases and decreases in peripheral fatigue with respiratory muscle loading and unloading, respectively, reflect corresponding changes in limb blood flow and limb O2 transport. There are several findings that support this interpretation. First, our previous demonstration of a significant inverse relationship between the work of breathing and limb vascular conductance and blood flow during near maximum exercise would apply to the present findings, because the exercise intensities and the changes in the work of breathing achieved with loading and unloading were very comparable between studies (Harms et al. 1997). We note that the inspiratory muscle unloading increased but also reduced the total cardiac output, whereas inspiratory muscle loading reduced without an effect on cardiac output – probably because cardiac output was already at maximum achievable levels. Second, even though the effects on were only in the range of 5 to 7% with unloading and −9 to −10% with loading (Harms et al. 1997), it has been repeatedly demonstrated that even small changes in blood flow to the contracting limb have major effects on muscle force output (Barclay, 1986; Rabischong & Guiraud, 1993; Hogan et al. 1998; Cole & Brown, 2000). These effects of changing have been attributed to changes in O2 transport and/or to changes in the washout of local metabolites (Barclay, 1986; Frisbee et al. 1999). Third, we have recently shown that preventing even relatively small reductions in arterial O2 content (98 versus 91%S) and therefore in O2 transport during heavy-intensity endurance exercise also prevented about one-half the amount of exercise-induced peripheral fatigue, when comparisons were made at identical work rates and durations (Romer et al. 2006).
The mechanisms underlying the effects of respiratory muscle work on limb vascular conductance are believed to involve metaboreflex feedback from the fatiguing diaphragm and/or expiratory muscles, leading to increased sympathetically mediated vasoconstriction (Dempsey et al. 2002). This effect on muscle sympathetic nerve activity and limb vascular conductance has been demonstrated through the use of voluntary increases in inspiratory and expiratory muscle work to the point of task failure in the resting human (St Croix et al. 2000; Sheel et al. 2001; Derchak et al. 2002). Similar effects have been shown more specifically by the reduced vascular conductance induced by lactic acid infusions into the phrenic artery in the resting and exercising canine – an effect that was prevented via pharmacological sympathetic blockade (Rodman et al. 2003). Accordingly, since respiratory muscle unloading prevents the exercise-induced diaphragmatic fatigue that normally occurs during heavy exercise (Babcock et al. 2002), we may also expect suppression of the sympathetic vasoconstrictor outflow, and vice versa with greater than normal loading.
Is the magnitude of peripheral fatigue that is associated with the changes in respiratory muscle work biologically significant? Cycling exercise at ≥ 90% of to exhaustion caused a mean 28% (range 15–36%) reduction in maximum force output of the quadriceps in response to supramaximal stimulation and relieving 56% of the inspiratory muscle work prevented about one-third of this limb fatigue. This effect on peripheral fatigue is only a little more than one-half the effect we have recently found by preventing the 7–9% arterial O2 desaturation that can accompany heavy sustained exercise (Romer et al. 2006). Thus, this unloading effect, whilst consistent and statistically significant, appears to be relatively small. However, it is important to note that we reduced only slightly more than one-half the normal work of breathing so this effect probably represents an underestimation of what might be attributed to the total work of breathing of the inspiratory and expiratory muscles that occurs during heavy sustained exercise. An additional influence also not considered in our current study was the effect of relieving high expiratory pressures, which are often encountered in the face of expiratory flow limitation and hyperinflation during heavy exercise (Johnson et al. 1992) and which have a mechanical effect on reducing left ventricular stroke volume and cardiac output (Stark-Leyva et al. 2004).
The effect of artificially increasing inspiratory flow resistance on peripheral fatigue was much greater than unloading the inspiratory muscles. For example, 8 min of high intensity exercise caused an 18% reduction in limb force output, and superimposing an 80% increase in inspiratory muscle work caused a further 40% reduction in peripheral fatigue following exercise of equal duration and workload. Certainly part of this difference may be because the changes in the force output of the inspiratory muscles were not equal between unloading and loading (−50 versus+80%). However, another reason may be that increases in limb blood flow during unloading are typically less than the reductions in flow with loading (Harms et al. 1997), which is in part attributable to a reduction in total available cardiac output during unloading (Harms et al. 1998b).