Background 300 million people worldwide suffer from depression. A poorly understood stress-related pathophysiology is compounded by frequent treatment-resistance.
Undertaking regular exercise has consistently shown to prevent, protect and increase resilience against the development of aberrant stress-related responses seen in depression, whereas sedentary behaviour tends to heighten symptoms. Despite the promise shown by exercise its clinical use is undermined by poor understanding of how beneficial effects are produced.
Stress exposure can dysregulate important physiological pathways such as the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. Disruption of tryptophan metabolism, including increased metabolism along the kynurenine pathway, is a neurobiological hallmark of depressed patients. Recent studies have shown that the beneficial impact of exercise for mood and cognition may be linked to reduced kynurenine production.
The aim was to examine the benefits of a 12-week exercise programme in healthy sedentary adults across mood, stress, anxiety and depression were mediated by the regulation of tryptophan metabolism in a dose dependent manner.
Methods 32 healthy sedentary adults participated (16 females). To establish a baseline profile each participant undertook a battery of psychometric assessments, cognitive assessments and a cycle ergometer-based incremental fitness assessment. Measures of oxygen uptake and capillary blood lactate levels were taken at the end of each stage during the fitness assessment.
After the baseline assessment, participants were randomised into one of four groups (high, moderate, low dose exercise, or the sedentary control group). Exercise was administered over 3 sessions/week based on individual fitness and group. Monthly fitness and psychometric assessments were performed throughout to monitor change across the 12-week exercise programme. Data analyses were performed using SPSS.
Results As expect, participants showed a positive increase in fitness and performance with an increase in maximal oxygen uptake (F(1,28)=14.62, p=0.001, ηp2=0.343) after 12-weeks exercise training, accompanied by an increased relative peak power output (rPPO) (F(1,28)=16.93, p=0.000, ηp2=0.377) and an increased time to exhaustion (T2Ex) (F(1,28)=31.07, p=0.000, ηp2=0.526). Post hoc paired T-tests revealed that the most pronounced effects on rPPO and T2Ex occurred in the moderate or high intensity groups There was a reduction in scores on the Beck Depression Inventory (BDI) (F(1,28)=6.50, p=0.017, ηp2=0.189) and the Perceived Stress Scale (PSS) (F(1,28)=4.09, p=0.053, ηp2=0.127) scores after 12 weeks of exercise.
Conclusion In summary, these results confirm that exercise training beneficially influences measures of stress and depression. Further work is required to understand the role of exercise-induced alterations in tryptophan metabolism in mediating these effects.
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