Effects of active vs. passive recovery during Wingate-based training on the acute hormonal, metabolic and psychological response.
OBJECTIVE
The exercise-induced metabolic stress can be influenced by the mode of recovery and is associated with acute hormonal responses. Therefore, it is hypothesized that active recovery between high intensity intervals reduces the metabolic stimulus and therefore the hormonal response compared to passive recovery.


METHODS
12 male cyclist/triathletes performed four 30s all-out intervals, either with active (A) or passive (P) recovery between each bout. Human growth hormone (hGH), testosterone and cortisol, vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF) and macrophage migration inhibitory factor (MIF) were determined pre, 0', 30', 60' and 180' after both interventions. Metabolic stimuli and perturbations were characterized by lactate, blood gas (pH, BE, HCO3(-), PO2, PCO2), and spirometric analysis.


RESULTS
Both interventions caused a transient increase in circulating levels of cortisol, testosterone, testosterone/cortisol-ratio, hGH, VEGF and HGF. Transient differences between A- and P-recovery were found only for testosterone and HGF directly after exercise, despite significant differences in metabolic disturbances (lactate, acid base status).


CONCLUSIONS
Based on the data of testosterone, hGH and the testosterone/cortisol-ratio, as well as on the data of VEGF and HGF it appears that this kind of exercise protocol may promote anabolic processes and may lead to pro-angiogenic conditions independent of the mode of recovery. However transient differences between A- and P-recovery were shown for testosterone and HGF. In contrast, cortisol and hGH, which are known to be sensitive for metabolic perturbations (e.g. pH) showed no differences. Therefore, it is proposed that if a certain threshold for metabolic perturbations is exceeded, a hormonal response is induced, which does not differ between A- and P-recovery.
Institute of Training Science and Sport Informatics, German Sport University Cologne, Germany; Department of Molecular and Cellular Sport Medicine, Institute of Cardiovascular Research and Sport Medicine, German Sport University Cologne, Germany; Institute of Biochemistry, German Sport University Cologne, Germany. Electronic address: Wahl@dshs-koeln.de.
Patrick
P
Wahl
Sebastian
S
Mathes
Karsten
K
Köhler
Silvia
S
Achtzehn
Wilhelm
W
Bloch
Joachim
J
Mester
D000328:Adult; D015444:Exercise / Q000502:physiology*; D017228:Hepatocyte Growth Factor / Q000097:blood; D019382:Human Growth Hormone / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D019746:Intramolecular Oxidoreductases / Q000097:blood; D019344:Lactic Acid / Q000378:metabolism; D008263:Macrophage Migration-Inhibitory Factors / Q000097:blood; D008297:Male; D010101:Oxygen Consumption; D020127:Recovery of Function / Q000502:physiology*; D013312:Stress, Physiological; D013315:Stress, Psychological; D013739:Testosterone / Q000097:blood*; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D055815:Young Adult
D008263:Macrophage Migration-Inhibitory Factors; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D019382:Human Growth Hormone; D019344:Lactic Acid; D013739:Testosterone; D017228:Hepatocyte Growth Factor; D019746:Intramolecular Oxidoreductases; C515598:MIF protein, human; D006854:Hydrocortisone
Cortisol; HGF; MIF; Testosterone; VEGF; hGH