The binding of high-mobility group box-1 (HMGB-1) to the membrane receptor for advanced glycation end-products (mRAGE) is a key early mediator of non-infectious inflammation and its triggers include ischaemia/hypoxia. The effects of acute hypoxia on soluble RAGE (sRAGE) are unknown. Fourteen healthy adults (50 % women; 26.6±3.8 years) were assessed at baseline normoxia (T0), followed by four time-points (T90, 95, 100 and 180 min) over three hours of continuous normobaric hypoxia (NH, 4,450 m equivalent) and again 60 min after return to normoxia (T240). A 5-min exercise step test was performed during NH at T90. Plasma concentrations of HMGB-1, sRAGE VCAM-1, ICAM-1, VEGF IL-8 and IL-13 were measured using venous blood. Arterial and tissue oxygen saturations were measured using pulse oximetry (SpO2) and near-infrared spectroscopy (StO2), respectively. NH led to a significant reduction in SpO2, StO2, sRAGE and VEGF, which was compounded by exercise, before increasing to baseline values with normoxic restoration (T240). NH-exercise led to a paired increase in HMGB-1. sRAGE inversely correlated with HMGB-1 (r=-0.32; p=0.006), heart rate (r=-0.43; p=0.004) but was not linked to SpO2 or StO2. In conclusion, short-term NH leads to a fall in sRAGE and VEGF concentrations with a transient rise post NH-exercise in HMGB-1.
Irisin is a myokine secreted during exercise. It has drawn the attention of researchers as it regulates several effects of exercise that are considered beneficial. It has also been proposed as a therapeutic tool to treat metabolic disorders. In recent years, the effect of different types of training on circulating irisin has been studied in large populations. An overall beneficial result has been shown, however, the outcome of the investigations has raised some controversy. Herein we evaluated the existing literature on the effects of different types of training on the circulating irisin levels in healthy subjects and in those displaying different metabolic condition. We conducted queries in the PubMed and Web of Science databases for literature published between January 2010 and January 2021. Thirty-seven original articles were retrieved and they were included in this review. Any letter to the editor, meta-analyses, reviews, and systematic review articles were excluded. From these 37 articles, 19 of them reported increased levels of circulating irisin. The interventions encompassed aerobic, resistance, combined, circuit, and interval training types. Such increase of circulating irisin was reported for healthy subjects and for those displaying different metabolic condition. A training that is steadily kept with a moderate to high intensity, including that characterized by brief highly intense intervals, were distinguishable from the rest. Nevertheless, the training effectiveness as evaluated by the increased circulating irisin levels depends on the subject’s metabolic condition and age.
Myostatin (MSTN), an important negative regulator of skeletal muscle, plays an important role in skeletal muscle health. In previous study, we found that the expression of MSTN was different during skeletal muscle injury repair. Therefore, we explored the expression changes of MSTN at different time points during skeletal muscle injury repair after eccentric exercise. In addition, MSTN is regulated by follistatin (FST) and decorin (DCN) in vivo, so our study examined the time-specific changes of FST, DCN and MSTN in the circulation and skeletal muscle during skeletal muscle injury repair after eccentric exercise, and to explore the reasons for the changes of MSTN in the process of exercise-induced muscle injury repair, to provide a basis for promoting muscle injury repair. The rats performed one-time eccentric exercise. Blood and skeletal muscle were collected at the corresponding time points, respectively immediate after exercise (D0), one day (D1), two days (D2), three days (D3), seven days (W1) and fourteen days (W2) after exercise (n=8). The levels of MSTN, FST, DCN in serum and mRNA and protein expression in muscle were detected. MSTN changes in the blood and changes in DCN and FST showed the opposite trend, except immediately after exercise. The change trends of mRNA and protein of gastrocnemius DCN and MSTN are inconsistent, there is post-transcriptional regulation of MSTN and DCN in gastrocnemius. Acute eccentric exercise might stimulate the secretion of DCN and FST into the circulation and inhibit MSTN. MSTN may be regulated by FST and DCN after acute eccentric exercise.
In this experiment we studied the effect of different pedalling rates during cycling at a constant power output (PO) 132±31 W (mean±S.D.), corresponding to 50 % V02 max, on the oxygen uptake and the magnitude of the slow component of V02 kinetics in humans. The PO corresponded to 50 % of V02 max, established during incremental cycling at a pedalling rate of 70 rev.min-1. Six healthy men aged 22.2 ±2.0 years with V02 max 3.89 ±0.92 l.min-1, performed on separate days constant PO cycling exercise lasting 6 min at pedalling rates 40, 60, 80, 100 and 120 rev.min-1, in random order. Antecubital blood samples for plasma lactate [La]pi and blood acid-base balance variables were taken at 1 min intervals. Oxygen uptake was determined breath-by-breath. The total net oxygen consumed throughout the 6 min cycling period at pedalling rates of 40, 60, 80, 100 and 120 rev.min-1 amounted to 7.727± 1.197, 7.705± 1.548, 8.679± 1.262, 9.945± 1.435 and 13.720± 1.862 1, respectively for each pedalling rate. The VO2 during the 6 min of cycling only rose slowly by increasing the pedalling rate in the range of 40-100 rev.min-1. This increase, was 0.142 1 per 20 rev.min-1 on the average. Plasma lactate concentration during the sixth minute of cycling changed little within this range of pedalling rates: the values were 1.83 ±0.70, 1.80 ± 0.48, 2.33 ±0.88 and 2.52 ±0.33 mmoLl-1. The values of [La]pi reached in the 6th minute of cycling were not significantly different from the pre-exercise levels. Blood pH was also not affected by the increase of pedalling rate in the range of 40-100 rev.min-1. However, an increase of pedalling rate from 100 to 120 rev.min-1 caused a sudden increase in the VO2 amounting to 0.747 1 per 20 rev.min-1, accompanied by a significant increase in [La]pj from 1.21 ±0.26 mmol.l-1 in pre-exercise conditions to 5.92±2.46 mmol.l-1 reached in the 6th minute of cycling (P<0.01). This was also accompanied by a significant drop of blood pH, from 7.355 ±0.039 in the pre-exercise period to 7.296 ± 0.060 in the 6th minute of cycling (P<0.01). The mechanical efficiency calculated on the basis of the net VO2 reached between the 4th and the 6th minute of cycling amounted to 26.6 ±2.7, 26.4±2.0, 23.4±3.4, 20.3 ±2.6 and 14.7±2.2 %, respectively for pedalling rates of 40, 60, 80,100 and 120 rev.min-1. No significant increase in the VO2 from the 3rd to the 6th min (representing the magnitude of the slow component of V02 kinetics) was observed at any of the pedalling rates (-0.022±0.056, -0.009±0.029, 0.012±0.073, 0.030±0.081 and 0.122±0.176 l.min-1 for pedalling rates of 40, 60, 80, 100 and 120 rev.min-1, respectively). Thus a significant increase in [La]pi and a decrease in blood pH do not play a major role in the mechanism(s) responsible for the slow component of VO2 kinetics in
humans.