Shorter constant work rate cycling tests as proxies for longer tests in highly trained cyclists

Severe-intensity constant work rate (CWR) cycling tests are useful for monitoring training progression and adaptation as they impose significant physiological and psychological strain and thus simulate the high-intensity competition environment. However, fatiguing tests require substantial recovery and may disrupt athlete training or competition preparation. Therefore, the development of a brief, minimally fatiguing test providing comparable information is desirable. Purpose : To determine whether physiological variables measured during, and functional decline in maximal power output immediately after, a 2-min CWR test can act as a proxy for 4-min test outcomes. Methods : Physiological stress was monitored and pre-to-post-CWR changes in 10-s sprint power computed (to estimate performance fatigability) during 2- and 4-min CWR tests in high-level cyclists. Results : The 2-min CWR test evoked a smaller decline in sprint mechanical power (32% vs. 47%, p <0.001), however both the physiological variables and sprint mechanical power were independently and strongly correlated between 2- and 4-min tests. Differences in V?O 2peak and blood lactate concentration in both CWR tests were strongly associated with the decline in sprint mechanical power. Conclusion : Physiological variables measured during, and the loss in sprint mechanical power measured after, a severe-intensity 2-min CWR test were less than in the 4-min test. Yet strong correlations between 2- and 4-min test outcomes indicated that the 2-min test can be used as a proxy for the longer test. Because shorter tests are less strenuous, they should have less impact on training and competition preparation and may therefore be more practically applicable within the elite performance environment.

Similar time near VO2max regardless of work rate manipulation in cycling interval training

The current study aimed to compare time spent above 90% V̇O2max (tV̇O2max) during 3 work-matched interval training protocols comprising 8 x 60-second exercise efforts with decreasing, increasing, or constant work rate distribution within each exercise interval. Ten healthy male subjects (age: 27.6 ± 5.0 years; V̇O2max: 3.82 ± 0.52 L•min-1) performed an incremental test to determine V̇O2max and peak power output (Pmax). During visits 2, 3, and 4, three work-matched interval training sessions comprising 8 x 60 s efforts: 60 s active recovery with the power output held constant (100%Pmax; ITCON), decreasing (from 110 to 90%Pmax; ITDEC), or increasing (from 90 to 110%Pmax; ITINC) linearly throughout each work interval. Time sustained above 90% of V̇O2max (tV̇O2max) or HRmax (tHRmax), blood lactate concentrations (BLC) and rating of perceived exertion (RPE) were measured. The tV̇O2max (ITCON: 274 ± 132; ITDEC: 313 ± 102; ITINC: 310 ± 113 s, P = 0.37), tHRmax (ITCON: 396 ± 180; ITDEC: 441 ± 207; ITINC: 390 ± 212 s, P = 0.47), BLC (P = 0.73), and final RPE (P = 0.75) were similar among protocols. In conclusion, work-matched interval training induced similar time near V̇O2max and associated physiological responses regardless of work rate manipulation.

Effect of a day-trip to altitude (2500 m) on exercise performance in pulmonary hypertension: randomised crossover trial

Question addressed by the studyTo investigate exercise performance and hypoxia-related health effects in patients with pulmonary hypertension (PH) during a high-altitude sojourn.Patients and methodsIn a randomised crossover trial in stable (same therapy for >4 weeks) patients with pulmonary arterial hypertension (PAH) or chronic thromboembolic pulmonary hypertension (CTEPH) with resting arterial oxygen tension (PaO2) ≥7.3 kPa, we compared symptom-limited constant work-rate exercise test (CWRET) cycling time during a day-trip to 2500 m versus 470 m. Further outcomes were symptoms, oxygenation and echocardiography. For safety, patients with sustained hypoxaemia at altitude (peripheral oxygen saturation <80% for >30 min or <75% for >15 min) received oxygen therapy.Results28 PAH/CTEPH patients (n=15/n=13); 13 females; mean±sd age 63±15 years were included. After >3 h at 2500 m versus 470 m, CWRET-time was reduced to 17±11 versus 24±9 min (mean difference −6, 95% CI −10 to −3), corresponding to −27.6% (−41.1 to −14.1; p<0.001), but similar Borg dyspnoea scale. At altitude, PaO2 was significantly lower (7.3±0.8 versus 10.4±1.5 kPa; mean difference −3.2 kPa, 95% CI −3.6 to −2.8 kPa), whereas heart rate and tricuspid regurgitation pressure gradient (TRPG) were higher (86±18 versus 71±16 beats·min−1, mean difference 15 beats·min−1, 95% CI 7 to 23 beats·min−1) and 56±25 versus 40±15 mmHg (mean difference 17 mmHg, 95% CI 9 to 24 mmHg), respectively, and remained so until end-exercise (all p<0.001). The TRPG/cardiac output slope during exercise was similar at both altitudes. Overall, three (11%) out of 28 patients received oxygen at 2500 m due to hypoxaemia.ConclusionThis randomised crossover study showed that the majority of PH patients tolerate a day-trip to 2500 m well. At high versus low altitude, the mean exercise time was reduced, albeit with a high interindividual variability, and pulmonary artery pressure at rest and during exercise increased, but pressure–flow slope and dyspnoea were unchanged.

Metabolic instability vs fibre recruitment contribution to the $${\dot{V}O_2}$$ slow component in different exercise intensity domains

This study focused on the steady-state phase of exercise to evaluate the relative contribution of metabolic instability (measured with NIRS and haematochemical markers) and muscle activation (measured with EMG) to the oxygen consumption ($${\dot{V}O_2}$$ V ˙ O 2 ) slow component ($${\dot{V}O_2}{_s}{_c}$$ V ˙ O 2 s c ) in different intensity domains. We hypothesized that (i) after the transient phase, $${\dot{V}O_2}$$ V ˙ O 2 , metabolic instability and muscle activation tend to increase differently over time depending on the relative exercise intensity and (ii) the increase in $${\dot{V}O_2}{_s}{_c}$$ V ˙ O 2 s c is explained by a combination of metabolic instability and muscle activation. Eight active men performed a constant work rate trial of 9 min in the moderate, heavy and severe intensity domains. $${\dot{V}O_2}$$ V ˙ O 2 , root mean square by EMG (RMS), deoxyhaemoglobin by NIRS ([HHb]) and haematic markers of metabolic stability (i.e. [La−], pH, HCO3−) were measured. The physiological responses in different intensity domains were compared by two-way RM-ANOVA. The relationships between the increases of [HHb] and RMS with $${\dot{V}O_2}$$ V ˙ O 2 after the third min were compared by simple and multiple linear regressions. We found domain-dependent dynamics over time of $${\dot{V}O_2}$$ V ˙ O 2 , [HHb], RMS and the haematic markers of metabolic instability. After the transient phase, the rises in [HHb] and RMS showed medium–high correlations with the rise in $${\dot{V}O_2}$$ V ˙ O 2 ([HHb] r = 0.68, p < 0.001; RMS r = 0.59, p = 0.002). Moreover, the multiple linear regression showed that both metabolic instability and muscle activation concurred to the $${\dot{V}O_2}{_s}{_c}$$ V ˙ O 2 s c (r = 0.75, [HHb] p = 0.005, RMS p = 0.042) with metabolic instability possibly having about threefold the relative weight compared to recruitment. Seventy-five percent of the dynamics of the $${\dot{V}O_2}{_s}{_c}$$ V ˙ O 2 s c was explained by [HHb] and RMS.

The Balance of Muscle Oxygen Supply and Demand Reveals Critical Metabolic Rate and Predicts Time to Exhaustion

We tested the hypothesis that during whole body exercise, the balance between muscle O2supply and metabolic demand may elucidate intensity domains, reveal a critical metabolic rate, and predict time to exhaustion. Seventeen active, healthy volunteers (12 male, 5 female; 32±2 years) participated in two distinct protocols. Study 1 (N=7) consisted of constant work rate cycling in the moderate, heavy, and severe exercise intensity domains with concurrent measures of pulmonary VO2and local %SmO2(via NIRS) on quadriceps and forearm sites. Average %SmO2at both sites displayed a domain dependent response (P<0.05). A negative %SmO2slope was evident during severe domain exercise but was positive during exercise below critical power (CP) at both muscle sites. In study 2 (N=10), quadriceps and forearm site %SmO2was measured during 3 continuous running trials to exhaustion and 3 intermittent intensity (ratio = 60s severe: 30s lower intensity) trials to exhaustion. Intensity dependent negative %SmO2slopes were observed for all trials (P<0.05), and predicted zero slope at critical velocity. %SmO2accurately predicted depletion and repletion of %D´ balance on a second-by-second basis (R2= 0.99, P<0.05; both sites). Time to exhaustion predictions during continuous and intermittent exercise were either not different or better with %SmO2(SEE < 20.52sec for quad, < 44.03sec for forearm) vs running velocity (SEE < 65.76sec). Muscle O2balance provides a dynamic physiological delineation between sustainable and unsustainable exercise (consistent with a 'critical metabolic rate'), and predicts real time depletion and repletion of finite work capacity and time to exhaustion.

The Effect of Long-Acting Dual Bronchodilator Therapy on Exercise Tolerance, Dynamic Hyperinflation and Dead Space during Constant Work Rate Exercise in COPD

Purpose: We investigated whether dual bronchodilator therapy (glycopyrrolate/formoterol fumarate; GFF; Bevespi Aerosphere®) would increase exercise tolerance during a high-intensity constant work rate exercise test (CWRET) and the relative contributions of dead space ventilation (VD/VT) and dynamic hyperinflation (change in inspiratory capacity) to exercise limitation in COPD. Methods: 48 COPD patients (62.9±7.6yrs; 33 male; GOLD spirometry stage 1/2/3/4, n=2/35/11/0) performed a randomized, double blind, placebo (PL) controlled, two period crossover, single-center trial. Gas exchange and inspiratory capacity (IC) were assessed during cycle ergometry at 80% incremental exercise peak work rate. Transcutaneous PCO2(TcPCO2) measurement was used for VD/VTestimation. Results: Baseline post-albuterol FEV1was 1.86±0.58L (63.6%±13.9 predicted). GFF increased FEV1by 0.18±0.21L relative to PL (P<0.001). CWRET endurance time was greater after GFF vs. PL (383±184s vs 328±115s; difference 55±125s; P=0.013; C.I. 20-90s), a 17% increase. IC on GFF was above placebo IC at all time points and fell less with GFF vs. PL (P≤0.0001). Isotime tidal volume (1.54±0.50 vs. 1.47±0.45L; P=0.022) and ventilation (52.9±19.9 vs. 51.0±18.9 L/min; P=0.011) were greater, and respiratory rate was unchanged (34.9±9.2 vs. 35.1±8.0 br/min, P=0.865). Isotime VD/VTdid not differ between groups (GFF 0.28±0.08 vs. PL 0.27±0.09; P=0.926). Conclusions: GFF increased exercise tolerance in COPD patients and the increase was accompanied by attenuated dynamic hyperinflation without altering VD/VT. ClinicalTrials.Gov Identifier: NCT03081156

Dynamic exercise changes in venous pressure and liver stiffness in Fontan patients: effects of Treprostinil

Background: Systemic venous hypertension and low cardiac output are believed to be important mediators of liver injury after the Fontan procedure. Pulmonary vasodilators have the potential to improve such haemodynamics. The aim of this study was to assess the acute effects of exercise on liver stiffness and venous pressures and to assess the impact of inhaled Treprostinil on this response. Methods: In this prospective, double-blind, placebo-controlled, crossover trial, 14 patients with a Fontan circulation were randomised to inhalation of placebo and Treprostinil. Incremental and constant work rate exercise tests were performed to assess the effect of Treprostinil on exercise tolerance. Venous pressures were measured throughout and liver stiffness at rest and immediately after peak exercise. Results: Mean age was 27.8 ± 7.9 years and 66% were females. Exercise acutely increased liver stiffness by 30% (mean shear wave speed: 2.38 ± 0.71 versus 2.89 ± 0.51 ms, p = 0.02). Peripheral venous pressures increased acutely during both incremental (12.1 ± 2.4 versus 22.6 ± 8.0 mmHg, p < 0.001) and constant work rate exercise (12.5 ± 2.5 versus 23.4 ± 5.2 mmHg, p < 0.001). Overall, Treprostinil failed to attenuate exercise-induced increases in liver stiffness. Compared with placebo, Treprostinil did not significantly impact venous pressure responses, VO2peak, nor exercise endurance times. Conclusions: Peripheral venous pressure increased acutely during exercise by an average of 88% above baseline and was not altered by administration of inhaled Treprostinil. Liver stiffness measured immediately post-exercise increased acutely by an average of 30%, with no attenuation following Treprostinil inhalation.