We examined the effects of hypoxia severity on peripheral versus central determinants of exercise performance. Eight cyclists performed constant-load exercise to exhaustion at various fractions of inspired O 2 fraction (F IO 2 0.21/0.15/0.10). At task failure (pedal frequency < 70% target) arterial hypoxaemia was surreptitiously reversed via acute O 2 supplementation (F IO 2 = 0.30) and subjects were encouraged to continue exercising. Peripheral fatigue was assessed via changes in potentiated quadriceps twitch force (ΔQ tw,pot ) as measured pre-versus post-exercise in response to supramaximal femoral nerve stimulation. At task failure in normoxia (haemoglobin saturation (S pO 2 ) ∼94%, 656 ± 82 s) and moderate hypoxia (S pO 2 ∼82%, 278 ± 16 s), hyperoxygenation had no significant effect on prolonging endurance time. However, following task failure in severe hypoxia (S pO 2 ∼67%; 125 ± 6 s), hyperoxygenation elicited a significant prolongation of time to exhaustion (171 ± 61%). The magnitude of ΔQ tw,pot at exhaustion was not different among the three trials (−35% to −36%, P = 0.8). Furthermore, quadriceps integrated EMG, blood lactate, heart rate, and effort perceptions all rose significantly throughout exercise, and to a similar extent at exhaustion following hyperoxygenation at all levels of arterial oxygenation. Since hyperoxygenation prolonged exercise time only in severe hypoxia, we repeated this trial and assessed peripheral fatigue following task failure prior to hyperoxygenation (125 ± 6 s). Although Q tw,pot was reduced from pre-exercise baseline (−23%; P < 0.01), peripheral fatigue was substantially less (P < 0.01) than that observed at task failure in normoxia and moderate hypoxia. We conclude that across the range of normoxia to severe hypoxia, the major determinants of central motor output and exercise performance switches from a predominantly peripheral origin of fatigue to a hypoxia-sensitive central component of fatigue, probably involving brain hypoxic effects on effort perception.
We evaluated the effects of specific inspiratory muscle training on simulated time-trial performance in trained cyclists. Using a double-blind, placebo-controlled design, 16 male cyclists (VO2max = 64 +/- 2 ml x kg(-1) x min(-1); mean +/- s(x)) were assigned at random to either an experimental (pressure-threshold inspiratory muscle training) or sham-training control (placebo) group. Pulmonary function, maximum dynamic inspiratory muscle function and the physiological and perceptual responses to maximal incremental cycling were assessed. Simulated time-trial performance (20 and 40 km) was quantified as the time to complete pre-set amounts of work. Pulmonary function was unchanged after the intervention, but dynamic inspiratory muscle function improved in the inspiratory muscle training group (P < or = 0.05). After the intervention, the inspiratory muscle training group experienced a reduction in the perception of respiratory and peripheral effort (Borg CR10: 16 +/- 4% and 18 +/- 4% respectively; compared with placebo, P < or = 0.01) and completed the simulated 20 and 40 km time-trials faster than the placebo group [66 +/- 30 and 115 +/- 38 s (3.8 +/- 1.7% and 4.6 +/- 1.9%) faster respectively; P = 0.025 and 0.009]. These results support evidence that specific inspiratory muscle training attenuates the perceptual response to maximal incremental exercise. Furthermore, they provide evidence of performance enhancements in competitive cyclists after inspiratory muscle training.
Romer LM, Polkey MI. Exercise-induced respiratory muscle fatigue: implications for performance. J Appl Physiol 104: 879 -888, 2008. First published December 20, 2007 doi:10.1152/japplphysiol.01157.2007.-It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O 2 and CO2 transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exerciseinduced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles. respiratory muscles; exercise; diaphragm; abdominals; magnetic stimulation; metaboreflex THE PURPOSE OF THIS MINIREVIEW is to address the question of whether the respiratory demands of exercise contribute significantly toward exercise limitation, either directly through limitations of the respiratory muscle pump or indirectly through effects on limb blood flow and locomotor muscle fatigue. We describe the mechanical and metabolic costs of meeting the ventilatory requirements of exercise. We then ask whether the respiratory muscles fatigue with exercise, what factors contribute to any such fatigue, and what the implications of these factors are for exercise tolerance. Finally, we deal with the potential mechanisms by which respiratory muscle fatigue could compromise exercise tolerance and whether it is possible to overcome this potential respiratory limitation. Our review focuses on the healthy young adult exercising near sea level. However, we also consider special circumstances that determine the balance between metabolic demand and respiratory system capacity in the highly trained endurance ...
Neuromuscular fatigue compromises exercise performance and is determined by central and peripheral mechanisms. Interactions between the two components of fatigue can occur via neural pathways, including feedback and feedforward processes. This brief review discusses the influence of feedback and feedforward mechanisms on exercise limitation. In terms of feedback mechanisms, particular attention is given to group III/IV sensory neurons which link limb muscle with the central nervous system. Central corollary discharge, a copy of the neural drive from the brain to the working muscles, provides a signal from the motor system to sensory systems and is considered a feedforward mechanism that might influence fatigue and consequently exercise performance. We highlight recent findings from studies focusing on fatigue-related feedback and feedforward mechanisms and discuss their relevance for the previously proposed hypotheses that a ‘critical threshold of peripheral fatigue’ and/or a ‘sensory tolerance limit’ may regulate neuromuscular fatigue and ultimately exercise performance. The concept of a ‘critical threshold of peripheral fatigue’ is based on the idea that a negative feedback loop operates to protect the exercising limb muscle from severe threats to muscle homeostasis during whole-body exercise. The concept of a ‘sensory tolerance limit’ can be viewed as a more global negative feedback loop suggesting that the sum of all feedback and feedforward signals is processed within the central nervous system which ultimately regulates the intensity of exercise to ensure that voluntary activity remains tolerable.
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