Independent thesis Basic level (degree of Bachelor), 15 credits / 22,5 HE credits
Exercise is known to affect vitamin D bioavailability and its mobilization from muscle and fat stores. Still, the molecular mechanisms underlying these effects, including potential changes in gene expression, remains yet to be fully understood. This study investigates how short-term high-intensity training (HIT) affects vitamin D metabolism through changes in body composition, with a focus on serum vitamin D levels and vitamin D receptor (VDR) expression. It also examines how these changes relate to blood and cardiovascular biomarkers of metabolic health. The hypotheses are: (1) exercise-induced changes in body compositions improve vitamin D status and modulate VDR expression (VDR and PDIA3) and (2) improved vitamin D metabolism is associated with favourable changes in haematological and cardiovascular biomarkers. Four healthy adult females participated in a structured bodyweight-based training program. Pre- and post-intervention assessments included bioelectrical impedance analysis, blood tests for vitamin D levels, blood and heart biomarker profiling, and qPCR analysis of VDR and PDIA3 from peripheral blood cells. Analysing the data, statistically significant gains were observed in haematocrit (p-value=0.046), increase in HDL cholesterol, moderate reductions in body fat and higher muscle mass. Moreover, vitamin D levels showed a moderate increase of 2.95% following the intervention, although it was not significant. Additionally, qPCR analysis revealed modest, non-significant downregulation in VDR (fold change -1.41) and PDIA3 (fold change -1.37), suggesting early molecular adaptations to exercise. These findings highlight the capacity of short-term HIT exercise to beneficially modulate cardiovascular and haematological markers, while also promoting subtle changes in vitamin D bioavailability.
Popular scientific summary
Most people understand that regular exercise and sufficient vitamin D levels are important for maintaining good health. But could exercise itself help increase our vitamin D levels, without the need for supplements? And could these two factors work together in ways that influence not just our muscles and heart, but also our genes? This study looked at the relationship of short-term, high-intensity exercise could influence the availability of vitamin D stored in the body, and how this might be linked to changes in body composition, cardiovascular health and on a more experimental level, gene expression linked to vitamin D.
To explore this, four healthy females between the ages of 23 and 33 participated in a four week, high-intensity, bodyweight dependent exercise program. The workouts, which included exercises like squats, lunges, push-ups, and burpees, were performed five days a week and was designed for the participants to reach their maximum heart rates. Throughout the study, participants were informed to maintain their usual diet and sunlight exposure to identify the effects of exercise alone.
Both before and after the intervention, a set of health indicators were measured. These included body weight, muscle and fat mass, and various blood biomarkers linked to cardiovascular and blood function. The study also investigated the activity of two genes related to vitamin D namely, VDR (Vitamin D Receptor) and PDIA3 to explore how the body uses vitamin D and manages cellular stress.
Even though the study involved only a small number of participants, several positive trends were observed. Lean muscle mass increased slightly, while body fat percentage decreased, even without any changes to diet. In the blood, markers like haematocrit (which reflects red blood cell concentration) it showed statistically significant improvement, indicating better oxygen carrying capacity. HDL cholesterol, which is often referred to as “good” cholesterol, also increased after the exercise sessions, which is an encouraging sign of improved heart health.
Interestingly, when looking at gene expression, both the genes VDR and PDIA3 showed a modest decrease in activity after the exercise program. While these changes were not statistically significant, they may reflect early-stage adaptations at the molecular level due to the exercise intervention. One possible explanation is that exercise may have mobilized vitamin D from fat and muscle into the bloodstream. Therefore, the body might not need as much local VDR or PDIA3 activity in cells at that moment.
In summary, this analysis provides early indications that even a short period of consistent, HIT intervention can produce beneficial changes in body composition, blood and cardiovascular markers. These findings support the concept that exercise, and vitamin D pathways may interact in meaningful ways which could eventually be applied to improve health in populations at risk of cardiovascular or metabolic diseases. Perhaps most importantly, the study shows that it doesn’t take long to start seeing results, within just four weeks, the body and even the genes may begin to respond to the power of movement.
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