Abstract
The main aim of our study was to determinate whether a repeated bout (RB) (vs. first bout [FB]) of sprint interval cycling exercise (SIE) is sufficient to mitigate SIE-induced psychological and physiological biomarker kinetics within 48 h after the exercise. Ten physically active men (age, 22.6 ± 5.2 years; VO2max, 44.3 ± 5.7 ml/kg/min) performed the FB of SIE (12 repeats of 5 s each) on one day and the RB 2 weeks later. The following parameters were measured: motor performance (voluntary, electrically induced and isokinetic skeletal muscle contraction torque, and central activation ratio [CAR]); stress markers [brain-derived neurotrophic factor (BDNF), cortisol, norepinephrine, and epinephrine]; inflammatory markers (IL-6, IL-10, and TNF-α); metabolic markers (glucose and lactate); muscle and rectal temperature; cycling power output; and psychological perceptions. The average cycling power output and neuromuscular fatigue after exercise did not differ between the FB and RB. There were significant decreases in cortisol and BDNF concentration at 12 h (P < 0.05) and 24 h (P < 0.001) after the FB, respectively. The decrease in cortisol concentration observed 12 h after exercise was significantly greater after the RB (P < 0.05) than after the FB. The immune-metabolic response to the RB (vs. FB) SIE was suppressed and accompanied by lower psychological exertion. Most of the changes in psychological and physiological biomarkers in the FB and RB were closely related to the response kinetics of changes in BDNF concentration.
Highlights
Sprint interval exercise (SIE) is being used increasingly as a form of exercise training
It has been speculated that skeletal muscle cells might be involved in mediating changes in brain-derived neurotrophic factor (BDNF), and that skeletal muscle contractions during high-intensity exercise might be a possible trigger of a biochemical pathway linking an exercise-induced secreted factor from skeletal muscle to BDNF gene expression in the brain (Wrann et al, 2013)
We found that the preexercise BDNF concentration and kinetics of the change in BDNF concentration after both the first bout (FB) and repeated bout (RB) correlated significantly with indicators of prolonged neuromuscular fatigue, including central motor fatigue
Summary
Sprint interval exercise (SIE) is being used increasingly as a form of exercise training. Sprint interval exercise is a type of exercise that should not cause skeletal muscle damage, but should cause fatigue because of metabolic stress to muscle fibers (Place et al, 2015). Alterations of cortisol and IL-6 levels can regulate the availability of substrate during the exercise, and these alterations are modified by the type, intensity, and duration of the exercise (Petersen and Pedersen, 2005). It has been speculated that skeletal muscle cells might be involved in mediating changes in BDNF, and that skeletal muscle contractions during high-intensity exercise might be a possible trigger of a biochemical pathway linking an exercise-induced secreted factor from skeletal muscle to BDNF gene expression in the brain (Wrann et al, 2013). Exposure to corticosterone decreases BDNF expression in the brain; this suggests a negative relationship between cortisol and BDNF (Smith et al, 1995), which alters mood and may cause depression (Brunoni et al, 2008; Stein et al, 2008; Hashimoto, 2010; Polyakova et al, 2015)
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