Mechanical Work and Physiological Responses to Simulated Flat Water Slalom Kayaking

The purpose of this study was to assess the physical work demand in relation to metrics of force and subsequent physiological response to a simulated flatwater slalom competition. Eight New Zealand team members completed a standard incremental step-test to ascertain power:oxygen consumption relationship. This was followed by a simulated race run where breath-by-breath analysis along with force and power data logged at 50 Hz to determine stroke length, impulse, peak force, time to peak force, and rate of peak force per stroke. Physiological response to negotiating a flatwater slalom course was greater than straight-line paddling (36.89 ± 2.01 vs. 32.17 ± 1.97 ml⋅kg-1⋅min-1, p = 0.0065) at the same power output. Mean power output for the duration of the simulated race (91.63 ± 7.19 s) was 203.8 ± 45.0 W, incurring an oxygen deficit of 1.386 ± 0.541 L⋅min-1 translating to an overall anaerobic contribution of 32 ± 18% and aerobic contribution of 68 ± 18%. Moderate to strong relationships between time duration and stroke peak force (R2 = 0.354, R2 = 0.485) and rate of peak force development (R2 = 0.345, R2 = 0.426) but not for stroke length (R2 = 0.022, R2 = 0.012), impulse (R2 = 0.088, R2 = 0.097) or time to peak force (R2 = 0.001, R2 = 0.0001) for left and right strokes, respectively. The number of propulsive (<0.6 s) strokes outweighed turning/driving (>0.6 s) strokes with a ratio of 94:6%. Longer stroke duration was significantly correlated to greater impulse (R2 = 0.507, p < 0.0001) and time to peak force (R2 = 0.851, p < 0.0001), but a lower rate of force development (R2 = 0.107, p < 0.0001). The results show that a flatwater slalom under simulated race conditions entails initial supra-maximal (anaerobic) work rate with a subsequent transition to one associated with maximal aerobic capacity. Inability to sustain work done and the subsequent decline in peak force and force profile per stroke requires further research regarding strategies to enhance performance

Nicotine Supplementation Does Not Influence Performance of a 1h Cycling Time-Trial in Trained Males

The use of nicotine amongst professional and elite athletes is high, with anecdotal evidence indicating increased prevalence amongst cycling sports. However, previous investigations into its effects on performance have not used high-validity or -reliability protocols nor trained cyclists. Therefore, the present study determined whether nicotine administration proved ergogenic during a ∼1 h self-paced cycling time-trial (TT). Ten well-trained male cyclists (34 ± 9 years; 71 ± 8 kg; O2max: 71 ± 6 ml ⋅ kg−1 ⋅ min−1) completed three work-dependent TT following ∼30 min administration of 2 mg nicotine gum (GUM), ∼10 h administration of 7 mg ⋅ 24 h−1 nicotine patch (PAT) or color- and flavor-matched placebos (PLA) in a randomized, crossover, and double blind design. Measures of nicotine’s primary metabolite (cotinine), core body temperature, heart rate, blood biochemistry (pH, HCO3−, La−) and Borg’s rating of perceived exertion (RPE) accompanied performance measures of time and power output. Plasma concentrations of cotinine were highest for PAT, followed by GUM, then PLA, respectively (p < 0.01). GUM and PAT resulted in no significant improvement in performance time compared to PLA (62.9 ± 4.1 min, 62.6 ± 4.5 min, and 63.3 ± 4.1 min, respectively; p = 0.73), with mean power outputs of 264 ± 31, 265 ± 32, and 263 ± 33 W, respectively (p = 0.74). Core body temperature was similar between trials (p = 0.33) whilst HR averaged 170 ± 10, 170 ± 11, and 171 ± 11 beats ⋅ min−1 (p = 0.60) for GUM, PAT, and PLA, respectively. There were no differences between trials for any blood biochemistry (all p > 0.46) or RPE with mean values of 16.7 ± 0.9, 16.8 ± 0.7, and 16.8 ± 0.8 (p = 0.89) for GUM, PAT, and PLA, respectively. In conclusion: (i) nicotine administration, whether via gum or transdermal patch, did not exert an ergogenic or ergolytic effect on self-paced cycling performance of ∼1 h; (ii) systemic delivery of nicotine was greatest when using a transdermal patch; and (iii) nicotine administration did not alter any of the psycho-physiological measures observed

The Efficacy of Ingesting Water on Thermoregulatory Responses and Running Performance in a Warm-Humid Condition

The understanding that fluid ingestion attenuates thermoregulatory and circulatory stress during exercise in the heat was based on studies conducted in relatively dry (∼50% RH) environments. It remains undetermined whether similar effects occur during exercise in a warm and more humid environment, where evaporative capacity is reduced. Nine well-trained, unacclimatised male runners were randomly assigned to perform four experimental trials where they ran for 60 min at an intensity of 70% VO2max followed by an incremental exercise test until volitional exhaustion. The four trials consisted of non-fluid ingestion (NF) and fluid ingestion (FI) in a warm-dry (WD) and warm-humid condition (WH). Time to exhaustion (TTE), body temperature (Tb), whole body sweat rate, partitional calorimetry measures, heart rate and plasma volume were recorded during exercise. There was no significant difference in Tb following 60 min of exercise in FI and NF trial within both WD (37.3°C ± 0.4 vs. 37.4°C ± 0.3; p > 0.05) and WH conditions (38.0°C ± 0.4 vs. 38.1°C ± 0.4; p > 0.05). The TTE was similar between FI and NF trials in both WH and WD, whereas exercise capacity was significantly shorter in WH than WD (9.1 ± 2.8 min vs. 12.7 ± 2.4 min, respectively; p = 0.01). Fluid ingestion failed to provide any ergogenic benefit in attenuating thermoregulatory and circulatory stress during exercise in the WH and WD conditions. Consequently, exercise performance was not enhanced with fluid ingestion in the warm-humid condition, although the humid environment detrimentally affected exercise endurance

Indirect measures of substrate utilisation following exercise-induced muscle damage

This study investigated whether exercise-induced muscle damage (EIMD) resulted in changes to whole-body substrate utilisation during exercise performed during the subsequent 48 hours. Eight males (31 ± 6 years) performed 30 minutes of bench-stepping exercise. One leg performed eccentric contractions (Ecc) by lowering the body whilst the control leg performed concentric contractions (Con) by raising the body. On the two days following bench-stepping exercise participants performed measures of muscle function on an isokinetic dynamometer and undertook a bout of one leg cycling exercise, at two differing workloads, with the first workload (WL1) at 1.5 ± 0.25 W/kg and the second workload (WL2) at 1.8 ± 0.25 W/kg with each leg. Expired respiratory gases were collected during cycling to estimate whole body substrate utilisation. There were significant decrements in measures of muscular performance (isometric force, concentric and eccentric torque) and increased perception of soreness in Ecc compared with Con (P < 0.05). The effect of the Ecc treatment on substrate utilisation during one-legged cycling revealed a significant trial × time interaction with higher rates of CHO oxidation in the Ecc condition compared with Con that were further increased 48 hours later (P = 0.02). A significant treatment × time × effort interaction (P < 0.01) indicated the effect of the treatment altered as workload increased with higher rates of CHO oxidation occurring in WL2. This is consistent with greater reliance upon muscle glycogen. Suggesting that in EIMD, reductions in strength and increased feelings of soreness can be associated with greater reliance upon intramuscular CHO oxidation, than lipid, during subsequent concentric work

VEGF-A isoforms differentially regulate ATF-2-dependent VCAM-1 gene expression and endothelial-leukocyte interactions

Vascular endothelial growth factor A (VEGF-A) regulates many aspects of vascular physiology. VEGF-A stimulates signal transduction pathways that modulate endothelial outputs such as cell migration, proliferation, tubulogenesis, and cell-cell interactions. Multiple VEGF-A isoforms exist, but the biological significance of this is unclear. Here we analyzed VEGF-A isoform-specific stimulation of VCAM-1 gene expression, which controls endothelial-leukocyte interactions, and show that this is dependent on both ERK1/2 and activating transcription factor-2 (ATF-2). VEGF-A isoforms showed differential ERK1/2 and p38 MAPK phosphorylation kinetics. A key feature of VEGF-A isoform-specific ERK1/2 activation and nuclear translocation was increased phosphorylation of ATF-2 on threonine residue 71 (T71). Using reverse genetics, we showed ATF-2 to be functionally required for VEGF-A-stimulated endothelial VCAM-1 gene expression. ATF-2 knockdown blocked VEGF-A-stimulated VCAM-1 expression and endothelial-leukocyte interactions. ATF-2 was also required for other endothelial cell outputs, such as cell migration and tubulogenesis. In contrast, VCAM-1 was essential only for promoting endothelial-leukocyte interactions. This work presents a new paradigm for understanding how soluble growth factor isoforms program complex cellular outputs and responses by modulating signal transduction pathways

Acute whole-body vibration elicits post-activation potentiation

Whole-body vibration (WBV) leads to a rapid increase in intra-muscular temperature and enhances muscle power. The power-enhancing eVects by WBV can, at least in part, be explained by intra-muscular temperature. However, this does not exclude possible neural eVects of WBV occurring at the spinal level. The aim of this study was to examine if muscle twitch and patellar reXex properties were simultaneously potentiated from an acute bout of WBV in a static squat position. Six male and six female athletes performed three interventions for 5 min, static squat with WBV (WBV+, 26 Hz), static squat without WBV (WBV¡) and stationary cycling (CYCL, 70 W). Transcutaneous muscle stimulation consisting of a single 200 s pulse and three patellar tendon taps were administered prior to and then 90 s, 5, 10 min post-intervention. Ninety-seconds after WBV+ muscle twitch peak force (PF) and rate of force development (RFD) were signiWcantly higher (P < 0.01) compared to WBV¡ and CYCL. However the patellar tendon reXex was not potentiated. An acute continuous bout of WBV caused a post-activation potentiation (PAP) of muscle twitch potentiation (TP) compared to WBV¡ and CYCL indicating that a greater myogenic response was evident compared to a neural-mediated eVect of a reXex potentiation (RP)