Eccentric exercise-induced muscle damage dissociates the lactate and gas exchange thresholds

Abstract

We tested the hypothesis that exercise-induced muscle damage would increase the ventilatory (V(E)) response to incremental/ramp cycle exercise (lower the gas exchange threshold) without altering the blood lactate profile, thereby dissociating the gas exchange and lactate thresholds. Ten physically active men completed maximal incremental cycle tests before (pre) and 48 h after (post) performing eccentric exercise comprising 100 squats. Pulmonary gas exchange was measured breath-by-breath and fingertip blood sampled at 1-min intervals for determination of blood lactate concentration. The gas exchange threshold occurred at a lower work rate (pre: 136 ± 27 W; post: 105 ± 19 W; P < 0.05) and oxygen uptake (VO(2)) (pre: 1.58 ± 0.26 litres · min(-1); post: 1.41 ± 0.14 litres · min(-1); P < 0.05) after eccentric exercise. However, the lactate threshold occurred at a similar work rate (pre: 161 ± 19 W; post: 158 ± 22 W; P > 0.05) and VO(2) (pre: 1.90 ± 0.20 litres · min(-1); post: 1.88 ± 0.15 litres · min(-1); P > 0.05) after eccentric exercise. These findings demonstrate that exercise-induced muscle damage dissociates the V(E) response to incremental/ramp exercise from the blood lactate response, indicating that V(E) may be controlled by additional or altered neurogenic stimuli following eccentric exercise. Thus, due consideration of prior eccentric exercise should be made when using the gas exchange threshold to provide a non-invasive estimation of the lactate threshold.

Time-course of recovery of peak oxygen uptake after exercise-induced muscle damage

“…Our findings that participants were unable to reach similar heart rates at exercise cessation combined with similar reductions in strength and V˙ O 2 peak (∼10%) suggest reduced strength and/or motivational factors rather than direct impairments of cardiorespiratory or mitochondrial function may be at play. Consistent with this idea, EIMD leads to heightened ratings of perceived exertion (RPE) (Black and Dobson, 2013;Burt et al, 2012Burt et al, , 2013Davies et al, 2009Davies et al, , 2011bGleeson et al, 1995;Twist and Eston, 2009) and heightened ratings of muscle pain (Black and Dobson, 2013) in humans during exercise.…”

Mechanism and implications of hyperpnea exaggeration at the onset of exercise in mechanical hyperalgesia after eccentric exercise

“…2, 1-[1]) 20,21) . As a result, effort sense during the same exercise increases after ECC compared with that before conducting ECC [11][12][13]15,35) . Since Williamson et al 36) suggested that effort sense is closely related to central command, central command might be augmented as a result of the loss of muscle strength after ECC (Fig.…”

“…On the other hand, in comparable concentric contractions yielding a similar metabolic response, hyperventilation has been observed during ECC 10) , though the slope of the relationship between ventilation and arterial blood CO2 partial pressure in concentric exercise and that in ECC are almost the same 9) . Regarding the effect of a prior bout of ECC on ventilatory response to exercise, some investigators reported that the response at phases II and III during constant load or incremental exercise a few days after ECC was exaggerated [11][12][13][14][15] . Gleeson et al 13) and Schneider et al 14) suggested that this phenomenon is due to ventilatory compensation for greater blood lactacidosis after ECC.…”

“…Gleeson et al 13) and Schneider et al 14) also presumed that increased afferent discharges from pain receptors or metaboreceptors and sensation of muscle pain or soreness affected ventilatory response to exercise after ECC. Davis et al 12,15) proposed that the augmentation of ventilatory response and reduction in the gas exchange threshold, at least during incremental exercise after ECC, are most likely evoked by increased activation of thin muscle afferents (without using the terms "pain receptor" and "pain sensation") stimulated via mechanical disruption of muscle fibers and local microvasculature, and are not the result of altered blood lactate. Furthermore, Gleeson et al 13) conjectured that central neural effects contributed to the increased ventilatory response.…”

A Reduction in Maximal Incremental Exercise Test Duration 48 h Post Downhill Run Is Associated with Muscle Damage Derived Exercise Induced Pain

“…Furthermore, this muscle fiber disruption can also increases noxious (e.g., bradykinin, prostaglandin, hydrogen ions) stimuli (Clarkson and Hubal, 2002), which could stimulate group III/IV metabo-sensitive afferent fibers responsible for feedback to the brain (Amann et al, 2010) and explain EIMD derived pain (i.e., delayed onset muscle soreness). This muscle soreness could be associated with an increased sense of effort during MIE exercise (Davies et al, 2011) as a result of an increase in motor unit recruitment following EIMD (Eston et al, 2000). Damage to selective fibers may require additional motor units to be recruited in order to achieve the same force output, which could increase an individual's perception of effort (Braun and Dutto, 2003).…”