Five days of tart cherry supplementation improves exercise performance in normobaric hypoxia

Previous studies have shown tart cherry (TC) to improve exercise performance in normoxia. The effect of TC on hypoxic exercise performance is unknown. This study investigated the effects of 5 days of tart cherry (TC) or placebo (PL) supplementation on hypoxic exercise performance. Thirteen healthy participants completed an incremental cycle exercise test to exhaustion (TTE) under two conditions: (i) hypoxia (13% O2) with PL and (ii) hypoxia with TC (200 mg anthocyanin per day for 4 days and 100 mg on day 5). Pulmonary gas exchange variables, peripheral arterial oxygen saturation (SpO2), deoxygenated hemoglobin (HHb), and tissue oxygen saturation (StO2) assessed by near-infrared spectroscopy in the vastus lateralis muscle were measured at rest and during exercise. Urinary 8-hydro-2′ deoxyguanosine (8-OHdG) excretion was evaluated pre-exercise and 1 and 5 h post-exercise. The TTE after TC (940 ± 84 s, mean ± standard deviation) was longer than after PL (912 ± 63 s, p 2 and SpO2 were higher after TC than PL. Moreover, a significant interaction (supplements × time) in urinary 8-OHdG excretion was found (p 2 in the working muscles during submaximal exercise

Measuring the Energy of Ventilation and Circulation during Human Walking using Induced Hypoxia

Energy expenditure (EE) during walking includes energy costs to move and support the body and for respiration and circulation. We measured EE during walking under three different oxygen concentrations. Eleven healthy, young, male lowlanders walked on a treadmill at seven gait speeds (0.67–1.83 m s−1) on a level gradient under normobaric normoxia (room air, 21% O2), moderate hypoxia (15% O2), and severe hypoxia (11% O2). By comparing the hypoxia-induced elevation in heart rate (HR [bpm]), ventilation (VE [L min−1]) with the change in energy expenditure (EE [W]) at each speed, we were able to determine circulatory and respiratory costs. In a multivariate model combining HR and VE, respiratory costs were 0.44 ± 0.15 W per each L min−1 increase in VE, and circulatory costs were 0.24 ± 0.05 W per each bpm increase in HR (model adjusted r2 = 0.97, p \u3c 0.001). These VE costs were substantially lower than previous studies that ignored the contribution of HR to cardiopulmonary work. Estimated HR costs were consistent with, although somewhat higher than, measures derived from catheterization studies. Cardiopulmonary costs accounted for 23% of resting EE, but less than 5% of net walking costs (i.e., with resting EE subtracted)

Exercise hyperpnea and hypercapnic ventilatory responses in women

SummaryWe studied the relationship between exercise hyperpnea (i.e., ventilatory dynamics) at the onset of exercise and hypercapnic ventilatory response (HCVR), and their differences between the follicular (FP) and luteal (LP) phases of the menstrual cycle in six healthy females. HCVR was tested under three O2 conditions: hyperoxia (FiO2=1.0), normoxia (0.21), and hypoxia (0.12). HCVR was defined as the relationship between the end-tidal PCO2 and minute ventilation (V˙E) using the regression line of the CO2 slope and a mimetically apneic threshold of CO2. HCVR provocation and measurements were conducted using an inspired CO2 concentration of up to approximately 8mmHg higher than the end-tidal PCO2 level of basal isocapnic the end-tidal PCO2 at each menstrual both the slope and threshold in HCVR showed no statistically significant difference between LP and FP under any inspired FiO2 conditions. In the case of exercise hyperpnea during the onset of submaximal exercise, the mean response time (MRT) in V˙E dynamics showed no significant difference between LP and FP. Consequently, MRT in V˙E response was not related to the slope in HCVR. During steady-state exercise, even though the V˙E/V˙CO2 showed no significance between LP and FP, V˙E/V˙CO2 was significantly related to the slope in HCVR (r=0.59, P<0.05). Exercise ventilation (i.e., V˙E/V˙CO2) would partly be adjusted by the enhancement of the chemoreflex drive to CO2 only during the steady-state exercise

Influence of Age on Cardiorespiratory Kinetics During Sinusoidal Walking in Humans

We sought to determine the influence of age on cardiorespiratory kinetics during sinusoidal walking in two groups: 13 healthy young subjects (YG; 7 men and 6 women, age 21 ± 2 years) and 15 healthy elderly subjects (ELD; 9 men and 6 women, age 67 ± 5 years). A treadmill’s speed was sinusoidally changed between 3 and 6 km h-1 in the YG and between 3 and 5 km h-1 in the ELD during periods of 1, 2, 5, and 10 min, and in a stepwise manner. We compared the groups’ heart rate (HR), ventilation (V˙E), and gas exchange (CO2 output (V˙CO2) and O2 uptake (V˙O2)) responses. We determined the phase shift (PS) and the normalized amplitude (Amp) ratio of these kinetics in relation to the sinusoidal change in walking speed in response to the magnitude from the maximum to minimum speeds as revealed by a Fourier analysis in all cardiorespiratory variables. Both the Amp ratio and PS in the V˙E, V˙CO2, and V˙O2 responses were very similar between the ELD and YG, and being independent of the periods of sinusoidal oscillations. In marked contrast, the PS of the HR kinetics was significantly slowed in the ELD compared to the YG. The Amp ratio of HR was not related to the covariance variation of HR (CVHR) at standing rest in the ELD. The HR kinetics during sinusoidal walking may not be attributable to parasympathetic nerve activity into the heart in the ELD. The slope of the Amp of V˙E related to the Amp of V˙CO2 (V˙E/V˙CO2 slope) was steeper in the ELD (0.0258) compared to the YG (0.0132), suggesting that exercise hyperpnea could be greatly induced during walking in the ELD. These findings suggest that aging influences the alterations of autonomic nervous system-dependent slower HR kinetics and exercise hyperpnea during walking in the ELD

Impact of ambient temperature on energy cost and economical speed during level walking in healthy young males

We measured oxygen consumption and carbon dioxide output during walking [per unit distance (Cw) values] for 14 healthy young human males at seven speeds from 0.67 to 1.67 m s−1 (4 min per stage) in thermoneutral (23°C), cool (13°C), and hot (33°C) environments. The Cw at faster gait speeds in the 33°C trial was slightly higher compared to those in the 23°C and 13°C trials. We found the speed at which the young males walked had a significant effect on the Cw values (P0.05). Economical speed (ES) which can minimize the Cw in each individual was calculated from a U-shaped relationship. We found a significantly slower ES at 33°C [1.265 (0.060) m s−1 mean (s.d.)] compared to 23°C [1.349 (0.077) m s−1] and 13°C [1.356 (0.078) m s−1, P0.05). Heart rate and mean skin temperature responses in the 33°C condition increased throughout the walking trial compared to 23°C and 13°C (all P<0.05). These results suggest that an acutely hot environment slowed the ES by ∼7%, but an acutely cool environment did not affect the Cw and ES

Energy cost and lower leg muscle activities during erect bipedal locomotion under hyperoxia

Abstract Background Energy cost of transport per unit distance (CoT) against speed shows U-shaped fashion in walking and linear fashion in running, indicating that there exists a specific walking speed minimizing the CoT, being defined as economical speed (ES). Another specific gait speed is the intersection speed between both fashions, being called energetically optimal transition speed (EOTS). We measured the ES, EOTS, and muscle activities during walking and running at the EOTS under hyperoxia (40% fraction of inspired oxygen) on the level and uphill gradients (+ 5%). Methods Oxygen consumption V̇O2 $$\left(\dot{V}{\mathrm{O}}_2\right)$$ and carbon dioxide output V̇CO2 $$\left(\dot{V}{\mathrm{CO}}_2\right)$$ were measured to calculate the CoT values at eight walking speeds (2.4–7.3 km h−1) and four running speeds (7.3–9.4 km h− 1) in 17 young males. Electromyography was recorded from gastrocnemius medialis, gastrocnemius lateralis (GL), and tibialis anterior (TA) to evaluate muscle activities. Mean power frequency (MPF) was obtained to compare motor unit recruitment patterns between walking and running. Results V̇O2 $$\dot{V}{\mathrm{O}}_2$$, V̇CO2 $$\dot{V}{\mathrm{CO}}_2$$, and CoT values were lower under hyperoxia than normoxia at faster walking speeds and any running speeds. A faster ES on the uphill gradient and slower EOTS on both gradients were observed under hyperoxia than normoxia. GL and TA activities became lower when switching from walking to running at the EOTS under both FiO2 conditions on both gradients, so did the MPF in the TA. Conclusions ES and EOTS were influenced by reduced metabolic demands induced by hyperoxia. GL and TA activities in association with a lower shift of motor unit recruitment patterns in the TA would be related to the gait selection when walking or running at the EOTS. Trial registration UMIN000017690 (R000020501). Registered May 26, 2015, before the first trial

Walking economy at simulated high altitude in human healthy young male lowlanders

We measured oxygen consumption during walking per unit distance (Cw) values for 12 human healthy young males at six speeds from 0.667 to 1.639 m s−1 (four min per stage) on a level gradient under normobaric normoxia, moderate hypoxia (15% O2), and severe hypoxia (11% O2). Muscle deoxygenation (HHb) was measured at the vastus lateralis muscle using near-infrared spectroscopy. Economical speed which can minimize the Cw in each individual was calculated from a U-shaped relationship. We found a significantly slower economical speed (ES) under severe hypoxia [1.237 (0.056) m s−1; mean (s.d.)] compared to normoxia [1.334 (0.070) m s−1] and moderate hypoxia [1.314 (0.070) m s−1, P0.05). HHb gradually increased with increasing speed under severe hypoxia, while it did not increase under normoxia and moderate hypoxia. Changes in HHb between standing baseline and the final minute at faster gait speeds were significantly related to individual ES (r=0.393 at 1.250 m s−1, r=0.376 at 1.444 m s−1, and r=0.409 at 1.639 m s−1, P<0.05, respectively). These results suggested that acute severe hypoxia slowed ES by ∼8%, but moderate hypoxia left ES unchanged