Cardiorespiratory, hormonal and haematological responses to submaximal cycling performed 2 days after eccentric or concentric exercise bouts

Abstract

Eccentric muscle actions are known to induce delayed-onset muscle soreness (DOMS) and muscle weakness (reduced static strength and dynamic peak power output) that may persist for several days. The aim of the present study was to determine whether DOMS-inducing exercise affects physiological responses to subsequent submaximal dynamic exercise. Physiological and metabolic responses to a standardized exercise task were measured 2 days after the performance of an eccentric or concentric exercise bout. Six healthy, untrained male subjects aged 30 +/- 7 years (mean +/- S.D.) performed repeated eccentric contractions during 30 min of bench stepping (47-cm step, 15 steps min-1). On another occasion, they performed concentric contractions by walking uphill (8% incline) for 30 min at 5 km h-1, which elicited a similar heart rate response to bench stepping. Two days after the eccentric or concentric exercise, the subjects cycled for 15 min on an electrically braked cycle ergometer at a work rate (172 +/- 37 W) equivalent to 80% VO2 max. The order of the preceding treatments was randomized and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of serum creatine kinase activity (P < 0.01) and plasma cortisol concentration (P < 0.05). After uphill walking, the subjects were not sore and serum creatine kinase activity was unchanged. Minute volume, breathing frequency, respiratory exchange ratio, heart rate, rating of perceived exertion, venous blood lactate concentration and plasma cortisol concentration were all higher (P < 0.05) during cycling after eccentric exercise compared with after uphill walking. Increases in plasma catecholamine concentrations and numbers of circulating leucocytes after cycling at 80% VO2 max for 15 min were similar under both experimental conditions, but the delayed leucocytosis (at 150 min post-exercise) was significantly greater (P < 0.01) for the post-eccentric exercise condition. We conclude that dynamic submaximal exercise performed 2 days following exercise with a large eccentric component produces physiological responses that are indicative of a higher relative exercise stress. It is likely that such effects will significantly limit the level and duration of exercise that can be achieved in subsequent training bouts over several days.

Desmistificando a Ação Do Lactato Nos Eventos De Dor Muscular Tardia Induzida Pelo Exercício Físico: Proposta De Uma Aula Prática

“…Como conseqüência, haveria a caracterização dos seguintes sintomas: DMT [18][19][20], decréscimo na produção de força muscular [1,6], alterações na amplitude de movimento [22,23] e liberação enzimática no meio extracelular [24,25].…”

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

“…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.…”

“…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.…”

“…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.…”