Biology subjects

Moberg, M.

Publications and source records attributed to Moberg, M..

3 recordsLinked to original sources

bioRxiv2024

Endurance Exercise Elevates Plasma Mature Brain-Derived Neurotrophic Factor through Child- and Adulthood, with Amplified Effects in Adults

BackgroundBrain-derived neurotrophic factor (BDNF) is a neurotrophin that plays a central role in neuronal health. BDNF exists in two primary isoforms, the mature form (mBDNF) and its precursor (proBDNF), with opposing downstream effects on neuronal function. The positive effect of exercise on plasma levels of the BDNF-isoforms has been extensively studied in adults. However, equivalent investigations are lacking in children and youth. MethodsTwenty healthy children (9-12 years old), 19 adolescents (13-17 years old), and 39 adults (23-49 years old) donated venous blood before and after a 45-minute run. Platelet-poor plasma was analyzed for pro- and mBDNF using enzyme-linked immunosorbent assay. Maximal oxygen uptake and anthropometric data were assessed in all participants, while Tanner stage, circulating sex hormones, and accelerometry-based activity level were assessed in children and adolescents. ResultsWe found that children, adolescents, and adults have similar basal levels of pro-(337-543 pg x ml-1) and mBDNF (650-1111 pg x ml-1). For children and adolescents, basal levels of mBDNF correlated with average time spent in vigorous activity (r=0.5794, p=0.0015). In response to acute endurance exercise, mBDNF increased by 701 {+/-} 946, 1232 {+/-} 1105, and 1557 {+/-} 1168 pg x ml-1 in children, adolescents, and adults, respectively. The acute endurance exercise did not affect proBDNF levels (p>0.05). ConclusionOur results demonstrate that basal plasma pro- and mBDNF levels do not depend on age and maturity. Plasma mBDNF levels increase following endurance exercise in all age groups, but to a greater extent in adults. Highlights/ImpactO_LIWe show that in children and adolescents, regular vigorous physical activity is key to increased basal levels of plasma mBDNF, a factor linked to neuroplasticity and brain health. C_LIO_LIThe ability to elevate mBDNF through exercise is present across all age groups, with the greatest increase in adults. C_LIO_LIThe mBDNF response to physical exercise seems to be independent of underlying physical fitness. C_LIO_LIOur findings suggest that basal plasma mBDNF levels may reflect the cumulative effects of repeated exercise rather than an individuals overall physical fitness. C_LI

physiology↗

bioRxiv2024

Endurance exercise with reduced muscle glycogen content influences substrate utilization and attenuates acute mTORC1- and autophagic signaling in human type I and type II muscle fibers

BackgroundExercising with low muscle glycogen content can improve training adaptation, but the mechanisms underlying the muscular adaptation are still largely unknown. In this study, we measured substrate utilization and cell signaling in different muscle fiber types during exercise and investigated a possible link between these variables. MethodsFive subjects performed a single leg cycling exercise in the evening (day 1) with the purpose of reducing glycogen stores. The following morning (day 2), they performed two-legged cycling at [~]70% of VO2peak for 1h. Muscle biopsies were taken from both legs pre- and post-exercise for enzymatic analyses of glycogen, metabolite concentrations using LC-MS/MS-based quantification, and protein signaling using Western blot in pools of type I or type II fibers. ResultsGlycogen content was 60-65% lower for both fiber types (P<0.01) in the leg that exercised on day 1 (low leg) compared to the other leg with normal level of glycogen (normal leg) before the cycling exercise on day 2. Glycogen utilization during exercise was significantly less in both fiber types in the low compared to the normal leg (P<0.05). In the low leg, there was a 14- and 6-fold increase in long-chain fatty acids conjugated to carnitine in type I and type II fibers, respectively, post-exercise. This increase was 3-4 times larger than in the normal leg (P<0.05). Post-exercise, mTORSer2448 phosphorylation was increased in both fiber types in the normal leg (P<0.05) but remained unchanged in both fiber types in the low leg together with an increase in eEF2Thr56 phosphorylation in type I fibers (P<0.01). Exercise induced a reduction in the autophagy marker LC3B-II in both fiber types and legs, but the post-exercise level was higher in both fiber types in the low leg (P<0.05). Accordingly, the LC3B-II/I ratio decreased only in the normal leg (75% for type I and 87% for type II, P<0.01). ConclusionsStarting an endurance exercise session with low glycogen availability leads to profound changes in substrate utilization in both type I and type II fibers. This may reduce the mTORC1 signaling response, primarily in type I muscle fibers, and attenuate the normally observed reduction in autophagy.

physiology↗

bioRxiv2024

Anabolic sensitivity in healthy, lean, older men is associated with higher expression of amino acid sensors and mTORC1 activators

BackgroundSarcopenia is thought to be underlined by age-associated anabolic resistance and dysregulation of intracellular signalling pathways. However, it is unclear whether these phenomena are driven by ageing per se or other confounding factors. MethodsLean and healthy young (n=10, 22 {+/-} 3 yrs, BMI; 23.4 {+/-} 0.8 kg/m2) and old men (n=10, 70 {+/-} 3 yrs, BMI; 22.7 {+/-} 1.3 kg/m2) performed unilateral resistance exercise followed by intake of essential amino acids (EAA). Muscle biopsies were collected from the rested and the exercised leg before, immediately after, as well as 60 and 180 minutes after EAA intake. Muscle samples were analyzed for amino acid concentrations, muscle protein synthesis (MPS) and associated anabolic signaling. ResultsFollowing exercise, peak plasma levels of EAA and leucine were similar between groups, but the area under the curve was [~]11% and [~]28% lower in Young (p<0.01). Absolute levels of muscle EAA and leucine peaked 60 min after exercise, with [~]15 and [~]21 % higher concentrations in the exercising leg (p<0.01) but with no difference between groups. MPS increased in both the resting ([~] 0.035%{middle dot}h-1 to 0.056%{middle dot}h-1, p<0.05) and exercising leg ([~] 0.035%{middle dot}h-1 to 0.083%{middle dot}h-1, p<0.05) with no difference between groups. Phosphorylation of S6K1Thr389 increased to a similar extent in the exercising leg in both groups but was 2.8-fold higher in the resting leg of Old at the 60 min timepoint (p<0.001). Phosphorylation of 4E-BP1Ser65 increased following EAA intake and exercise, but differences between legs were statistically different only at 180 min (p<0.001). However, phosphorylation of this site was on average 78% greater across all timepoints in Old (p<0.01). Phosphorylation of eEF2Thr56 was reduced ([~] 66 and 39%) in the exercising leg at both timepoints after EAA intake and exercise, with no group differences (p<0.05). However, phosphorylation at this site was reduced by [~] 27% also in the resting leg at 60 min, an effect that was only seen in Old (p<0.01). Total levels of Rheb ([~] 45%), LAT1 ([~] 31%) and Rag B ([~] 31%) were higher in Old (p<0.001). ConclusionLean and healthy old men do not manifest AR as evidenced by potent increases in MPS and mTORC1 signalling following EAA intake and exercise. Maintained anabolic sensitivity with age appears to be a function of a compensatory increase in basal levels of proteins involved in anabolic signalling. Therefore, our results suggest that age per se does not appear to cause AR in human skeletal muscle.

physiology↗