Krzysztof Duda

Oxygen uptake does not increase linearly at high power outputs during incremental exercise test in humans

Abstract A group of 12 healthy non-smoking men [mean age 22.3 (SD 1.1) years], performed an incremental exercise test. The test started at 30 W, followed by increases in power output (P) of 30 W every 3 min, until exhaustion. Blood samples were taken from an antecubital vein for determination of plasma concentration lactate [La−]pl and acid-base balance variables. Below the lactate threshold (LT) defined in this study as the highest P above which a sustained increase in [La−]pl was observed (at least 0.5 mmol · l−1 within 3 min), the pulmonary oxygen uptake (V˙O2) measured breath-by-breath, showed a linear relationship with P. However, at P above LT [in this study 135 (SD 30) W] there was an additional accumulating increase in V˙O2 above that expected from the increase in P alone. The magnitude of this effect was illustrated by the difference in the final P observed at maximal oxygen uptake (V˙O2max) during the incremental exercise test (Pmax,obs at V˙O2max) and the expected power output at V˙O2max(Pmax,exp at V˙O2max) predicted from the linear V˙O2-P relationship derived from the data collected below LT. The Pmax,obs at V˙O2max amounting to 270 (SD 19) W was 65.1 (SD 35) W (19%) lower (P<0.01) than the Pmax,exp at V˙O2max. The mean value of V˙O2max reached at Pmax,obs amounted to 3555 (SD 226) ml · min−1 which was 572 (SD 269) ml · min−1 higher (P<0.01) than the V˙O2 expected at this P, calculated from the linear relationship between V˙O2 and P derived from the data collected below LT. This fall in locomotory efficiency expressed by the additional increase in V˙O2, amounting to 572 (SD 269) ml O2 · min−1, was accompanied by a significant increase in [La−]pl amounting to 7.04 (SD 2.2) mmol · l−1, a significant increase in blood hydrogen ion concentration ([H+]b) to 7.4 (SD 3) nmol · l−1 and a significant fall in blood bicarbonate concentration to 5.78 (SD 1.7) mmol · l−1, in relation to the values measured at the P of the LT. We also correlated the individual values of the additional V˙O2 with the increases (Δ) in variables [La−]pl and Δ[H+]b. The Δ values for [La−]pl and Δ[H+]b were expressed as the differences between values reached at the Pmax,obs at V˙O2max and the values at LT. No significant correlations between the additional V˙O2 and Δ[La−]pl on [H+]b were found. In conclusion, when performing an incremental exercise test, exceeding P corresponding to LT was accompanied by a significant additional increase in V˙O2 above that expected from the linear relationship between V˙O2 and P occurring at lower P. However, the magnitude of the additional increase in V˙O2 did not correlate with the magnitude of the increases in [La−]pl and [H+]b reached in the final stages of the incremental test.

Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance

Abstract The purpose of this study was to develop a method to determine the power output at which oxygen uptake (V˙O2) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1 (SD 1.4) years, body mass 73.6 (SD 7.4) kg, height 179.4 (SD 7.5) cm, maximal oxygen uptake (V˙O2max) 3.726 (SD 0.363) l · min−1], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70 rev · min−1. The test started at a power output of 30 W, followed by increases amounting to 30 W every 3 min. At 5 min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1 ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]pl, partial pressure of O2 and CO2 and hydrogen ion concentration [H+]b. The lactate threshold (LT) in this study was defined as the highest power output above which [La−]pl showed a sustained increase of more than 0.5 mmol · l−1 · step−1. The V˙O2 was measured breath-by-breath. In the analysis of the change point (CP) of V˙O2 during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: Xi=ati+b+ɛi for i=1,2,…,T, and E(Xi)>ati+b for i =T+1,…,n, where X1, … , Xn are independent and ɛi∼N(0,σ2). In the first phase, a linear relationship between V˙O2 and power output was assumed, whereas in the second phase an additional increase in V˙O2 above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-V˙O2). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP-O2 as described in our model. The power output at CP-V˙O2 amounted to 136.8 (SD 31.3) W. It was only 11 W – non significantly – higher than the power output corresponding to LT. The V˙O2 at CP-V˙O2 amounted to 1.828 (SD 0.356) l · min−1 was [48.9 (SD 7.9)% V˙O2max]. The [La−]pl at CP-V˙O2, amounting to 2.57 (SD 0.69) mmol · l−1 was significantly elevated (P<0.01) above the resting level [1.85 (SD 0.46) mmol · l−1], however the [H+]b at CP-V˙O2 amounting to 45.1 (SD 3.0) nmol · l−1, was not significantly different from the values at rest which amounted to 44.14 (SD 2.79) nmol · l−1. An increase of power output of 30 W above CP-V˙O2 was accompanied by a significant increase in [H+]b above the resting level (P=0.03).

Endurance training decreases the non-linearity in the oxygen uptake–power output relationship in humans

In this study, we hypothesized that 5 weeks of cycling endurance training can decrease the magnitude of the non‐proportional increase in oxygen uptake ( ) to power output relationship ( ‘excess’) at exercise intensities exceeding the lactate threshold (LT). Ten untrained, physically active men performed a bout of incremental cycling exercise until exhaustion before and after training. The mitochondrial DNA copy number, myosin heavy chain composition and content of uncoupling protein 3 and sarcoplasmic reticulum Ca2+‐ATPases (SERCAs) were analysed in muscle biopsies taken from vastus lateralis before and after training. The training resulted in an enhancement of the power‐generating capabilities at maximal oxygen uptake ( ) by ∼7% (P= 0.002) despite there being no changes in (P= 0.49). This effect was due to a considerable reduction in the magnitude of the ‘excess’ (P < 0.05) above the LT. A decrease in plasma ammonia concentration was found during exercise after training (P < 0.05). A downregulation of SERCA2 in vastus lateralis (P= 0.006) was observed after training. No changes in myosin heavy chain composition, selected electron transport chain proteins, uncoupling protein 3 or the mitochondrial DNA copy number (P > 0.05) were found after training. We conclude that the training‐induced increase in power‐generating capabilities at was due to attenuation of the ‘excess’ above the LT. This adaptive response seems to be related to the improvement of muscle metabolic stability, as judged by a lowering of plasma ammonia concentration. The enhancement of muscle metabolic stability after training could be caused by a decrease in ATP usage at a given power output owing to downregulation of SERCA2 pumps.

Endurance training increases exercise-induced prostacyclin release in young, healthy men – relationship with VO2max

In the present study, we evaluated the effect of 5 weeks of moderate-intensity endurance training on the basal and exercise-induced systemic release of prostacyclin (PGI(2)), as assessed by plasma 6-keto-PGF(1 alpha) concentration. Twelve physically active young men with the following characteristics participated in this study (the mean +/- SD): age, 22.7 +/- 2.0 years; body mass, 76.8 +/- 8.9 kg; BMI, 23.48 +/- 2.17 kg x m(-2); and maximal oxygen uptake (VO(2 max)), 46.1 +/- 4.0 ml x kg(-1) x min(-1). Plasma 6-keto-PGF(1 alpha) concentrations were measured in venous blood samples taken prior to the exercise and at exhaustion (at VO(2 max)) before and after completing the training protocol. On average, the training resulted in a significant increase in VO(2 max) (p = 0.03), power output at VO(2 max) (p = 0.001) and a significant increase (p = 0.05) in the net-exercise-induced increase in plasma 6-keto-PGF(1 alpha) concentration (Delta 6-keto-PGF(1 alpha) i.e., the difference between the end-exercise and pre-exercise 6-keto-PGF(1 alpha) concentrations). No effect of training on the basal PGI(2) concentration was found. Interestingly, within the study sample (n = 12), two subgroups could be defined with a differential pattern of response with respect to Delta 6-keto-PGF(1 alpha) concentrations. In one subgroup (n = 7), a significant increase in Delta 6-keto-PGF(1 alpha) concentration after training was found (p < 0.02) (responders). This enhancement in the exercise-induced PGI(2) release was accompanied by a significant (p < 0.05) increase in VO(2 max) after training. In contrast, in another subgroup (n = 5), there was no observed effect of training on the Delta 6-keto-PGF(1 alpha) concentration and the VO(2 max) after training (non-responders). In both of these subgroups, training did not influence the basal PGI(2) concentration. In conclusion, the endurance training resulted in the adaptive augmentation of the systemic release of PGI(2) in response to exercise, which plays a role in the training-induced increase in VO(2 max) in young, healthy men. The impairment of the training-induced augmentation of PGI(2) release in response to exercise demonstrated in the non-responders subgroup may predispose them to increased cardiovascular risk during vigorous exercise.

Coronary and muscle blood flow during physical exercise in humans; heterogenic alliance

In this review, we present the relation between power generation capabilities and pulmonary oxygen uptake during incremental cycling exercise in humans and the effect of exercise intensity on the oxygen cost of work. We also discuss the importance of oxygen delivery to the working muscles as a factor determining maximal oxygen uptake in humans. Subsequently, we outline the importance of coronary blood flow, myocardial oxygen uptake and myocardial metabolic stability for exercise tolerance. Finally, we describe mechanisms of endothelium-dependent regulation of coronary and skeletal muscle blood flow, dysregulation of which may impair exercise capacity and increase the cardiovascular risk of exercise.

Moderate‐intensity endurance training improves endothelial glycocalyx layer integrity in healthy young men

What is the central question of this study? The main aim of the present study was to determine the effect of prolonged moderate‐intensity endurance training on the endothelial glycocalyx layer integrity in relationship to the training‐induced changes in oxidative stress and antioxidant defence in humans. What is the main finding and its importance? We have shown, for the first time, a protective effect of prolonged moderate‐intensity endurance training on endothelial glycocalyx layer integrity, as judged by significantly lower basal and end‐exercise serum concentrations of glycocalyx damage markers, i.e. syndecan‐1 and heparan sulfate, accompanied by attenuation of oxidative stress and enhancement of antioxidant defence after training in previously untrained healthy young men.

Endurance training-induced changes in the GH-IGF-I axis influence maximal muscle strength in previously untrained men

OBJECTIVE In this study we have determined the effects of 20weeks of endurance running training on the GH-IGF-I axis changes in the context of the skeletal muscle performance and physical capacity level. DESIGN Before and after the endurance training program a maximal incremental exercise tests, a 1500m race and a muscle strength measurements were performed and the blood samples were taken to determine both resting as well as end-exercise serum growth hormone (GH), insulin-like growth hormone-I (IGF-I), insulin-like growth hormone binding protein-3 (IGFBP-3) and plasma interleukin-6 (IL-6) concentrations. RESULTS 20weeks of endurance running training improved power output generated at the end of the maximal incremental test by 24% (P<0.012), 1500m running time by 13% (P<0.012) and maximal muscle strength by 9% (P<0.02). End-exercise IGF-I/IGFBP-3 ratio was decreased by 22% after the training (P<0.04) and the magnitude of IGF-I/IGFBP-3 ratio decrease (ΔIGF-I/IGFBP-3ex) was 2.3 times higher after the training (P<0.04). The magnitude of the exercise-induced changes in IGFBP-3 concentration was also significantly higher (P<0.04) and there was a trend toward lower end-exercise IGF-I concentration (P=0.08) after the training. These changes were accompanied by a significantly higher (30%) end-exercise IL-6 concentration (P<0.01) as well as by a 3.4 times higher magnitude of IL-6 increase (P<0.02) after the training. Moreover, there were strong positive correlations between changes in resting serum IGF-I concentration (ΔIGF-Ires) and IGF-I/IGFBP-3 ratio (ΔIGF-I/IGFBP-3res) and changes in muscle strength (ΔMVC) (r=0.95, P=0.0003 and r=0.90, P=0.002, respectively). CONCLUSIONS The training-induced changes in the components of the GH-IGF-I axis may have additive effects on skeletal muscle performance and physical capacity improvement.

Horner syndrome after unsuccessful venous port implantation by cannulation of the right internal jugular vein

BACKGROUND Horner syndrome is a rare but likely underdiagnosed complication of internal jugular vein cannulation. CASE REPORT We present a case of a young woman undergoing chemotherapy for gestational trophoblastic disease for whom venous port implantation was attempted due to poor peripheral vein access. Despite ultrasound guidance, the procedure was unsuccessful and complicated by a local haematoma, causing compression of the sympathetic nerves with Horner syndrome. The symptoms subsided within 3 weeks without treatment. The possible pathomechanisms of Horner syndrome after central venous cannulation are presented with suggested diagnostic and therapeutic approaches. Special emphasis must be placed on excluding carotid artery dissection because it carries the risk of subsequent cerebral vascular incidents. In the event of a carotid dissection, a multidisciplinary team must choose a pharmacological (antiplatelet drugs/anticoagulation) or interventional approach. CONCLUSION Even with ultrasonography, central venous cannulation is not free of serious risks. In case of anisocoria following an uneventful procedure, diagnostic imaging of the vascular structures in the neck is mandatory for the exclusion of potentially serious complications, such as carotid dissection or venous thrombosis.