Development of new Kanoe ergometer with Virtual technology

科学研究費助成事業(学術研究助成基金助成金)研究成果報告書：挑戦的萌芽研究2011-2012課題番号：2365038

Effects of work-matched moderate- and high-intensity warm-up on power output during 2-min supramaximal cycling

We tested the hypothesis that compared with a moderate-intensity warm-up, a work-matched high-intensity warm-up improves final-sprint power output during the last 30 s of a 120-s supramaximal exercise that mimics the final sprint during events such as the 800-m run, 1,500-m speed skate, or Keirin (cycling race). Nine active young males performed a 120-s supramaximal cycling exercise consisting of 90 s of constantworkload cycling at a workload that corresponds to 110% peak oxygen uptake (VO2peak) followed by 30 s ofmaximal cycling. This exercise was preceded by 1) no warm-up (control), 2) a 10-min cycling warm-up at a workload of 40% VO2peak (moderate-intensity), or 3) a 5-min cycling warm-up at a workload of 80% VO2peak (high-intensity). Total work was matched between the two warm-up conditions. Both warm-ups increased 5-s peak (observed within 10 s at the beginning of maximal cycling) and 30-s mean power output during the final 30-s maximal cycling compared to no warm-up. Moreover, the high-intensity warm-up provided a greater peak(577±169 vs. 541±175 W, P=0.01) but not mean (482±109 vs. 470±135W, P=1.00) power output than the moderate-intensity warm-up. Both VO2 during the 90-s constant workload cycling and the post-warm-up blood lactate concentration were higher following the high-intensity than moderate-intensity warm-up (all P≤0.05). We show that work-matched moderate- (~40% VO2peak) and high- (~80% VO2peak) intensity warmups both improve final sprint (~30 s) performance during the late stage of a 120-s supramaximal exercise bout, and that a high-intensity warm-up provides greater improvement of short-duration (<10 s) maximal sprinting performance

Effect of hypobaria on maximal ventilation, oxygen uptake, and exercise performance during running under hypobaric normoxic conditions

During exposure to high altitude, hypoxia develops because of reductions in barometric pressure and partial pressure of O2. Although several studies have examined the effects of hypoxia on exercise performance and physiological responses, such as maximal minute ventilation (urn:x-wiley:2051817X:media:phy214002:phy214002-math-0002Emax) and maximal oxygen uptake (urn:x-wiley:2051817X:media:phy214002:phy214002-math-0003O2max), how barometric pressure reduction (hypobaria) modulates them remains largely unknown. In this study, 11 young men performed incremental treadmill running tests to exhaustion under three conditions chosen at random: normobaric normoxia (NN; 763 ± 5 mmHg of barometric pressure, equivalent to sea level), hypobaric hypoxia (HH; 492 ± 1 mmHg of barometric pressure, equivalent to 3500 m above sea level (m a.s.l.)), and hypobaric normoxia (HN; 492 ± 1 mmHg of barometric pressure while breathing 32.2 ± 0.1% O2 to match the inspiratory O2 content under NN). urn:x-wiley:2051817X:media:phy214002:phy214002-math-0004Emax was higher in HN than in NN (160.9 ± 10.7 vs. 150.7 ± 10.0 L min−1, P 0.05). Time to exhaustion was longer in HN than in NN (932 ± 83 vs. 910 ± 79 s, P < 0.05). These results suggest that reduced air density during exposure to an altitude of 3500 m a.s.l. increases maximal ventilation and extends time to exhaustion without affecting oxygen consumption or arterial oxygen saturation

Visit to the China Qinghai Duoba National Highland Sports Training Base

The Human High Performance doctoral degree program at the University of Tsukuba was established in 2015, and I (Cao Yinhang) am one of the first students in this program. For my doctoral thesis, I have been working on a project aimed at elucidating the factors that determine individual variation in the hypoxia-induced reduction in peak oxygen uptake among endurance athletes during high-altitude exposure. To gain important insight into actual high-altitude training in China, as part of my doctoral research, I visited the Qinghai Duoba National Highland Sports Training Base (Duoba Base) on July 4-7, 2016. Duoba Base is the largest and highest high-altitude training center in China. The director of the Qinghai Institute of Sports Science, Ma Fuhai, extended to me an invitation to come to Duoba Base. During my visit, I met Chinese national race walkers engaged in high-altitude training in preparation for the 2016 Summer Olympic Games. With great support from Liu Haiming, a coach of the Qinghai province race walking team, I learned how Chinese national race walkers train at high altitude, and I assessed the pulmonary function of the race walkers from Qinghai province

Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans

Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO2 partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (Tes) to reach 39°C. During heating in two separate trials, end-tidal CO2 partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) (P = 0.005) in the Control trial. This decrease was prevented by breathing CO2-enriched air throughout the heating such that end-tidal CO2 partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating (P = 1.00). The sensitivity to rising Tes (i.e., slope of the Tes − V̇E relation) did not differ between the Control and CO2-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min−1·°C−1, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO2 breathing increased MCAV relative to Control at the end of heating (P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia

Body temperature and cold sensation during and following exercise under temperate room conditions in cold‐sensitive young trained females

We evaluated cold sensation at rest and in response to exercise‐induced changes in core and skin temperatures in cold‐sensitive exercise trained females. Fifty‐eight trained young females were screened by a questionnaire, selecting cold‐sensitive (Cold‐sensitive, n = 7) and non‐cold‐sensitive (Control, n = 7) individuals. Participants rested in a room at 29.5°C for ~100 min after which ambient temperature was reduced to 23.5°C where they remained resting for 60 min. Participants then performed 30‐min of moderate intensity cycling (50% peak oxygen uptake) followed by a 60‐min recovery. Core and mean skin temperatures and cold sensation over the whole‐body and extremities (fingers and toes) were assessed throughout. Resting core temperature was lower in the Cold‐sensitive relative to Control group (36.4 ± 0.3 vs. 36.7 ± 0.2°C). Core temperature increased to similar levels at end‐exercise (~37.2°C) and gradually returned to near preexercise rest levels at the end of recovery (>36.6°C). Whole‐body cold sensation was greater in the Cold‐sensitive relative to Control group during resting at a room temperature of 23.5°C only without a difference in mean skin temperature between groups. In contrast, cold sensation of the extremities was greater in the Cold‐sensitive group prior to, during and following exercise albeit this was not paralleled by differences in mean extremity skin temperature. We show that young trained females who are sensitive to cold exhibit augmented whole‐body cold sensation during rest under temperate ambient conditions. However, this response is diminished during and following exercise. In contrast, cold sensation of extremities is augmented during resting that persists during and following exercise

Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in humans

Effects of CO2 on ventilatory and cerebrovascular responses during passive heating in human

Cyclooxygenase-1 and -2 modulate sweating but not cutaneous vasodilation during exercise in the heat in young men

We recently reported that the nonselective cyclooxygenase (COX) inhibitor ketorolac attenuated sweating but not cutaneous vasodilation during moderate‐intensity exercise in the heat. However, the specific contributions of COX‐1 and COX‐2 to the sweating response remained to be determined. We tested the hypothesis that COX‐1 but not COX‐2 contributes to sweating with no role for either COX isoform in cutaneous vasodilation during moderate‐intensity exercise in the heat. In thirteen young males (22 ± 2 years), sweat rate and cutaneous vascular conductance were measured at three forearm skin sites that were continuously treated with (1) lactated Ringer\u27s solution (Control), (2) 150 μmmol·L−1 celecoxib, a selective COX‐2 inhibitor, or (3) 10 mmol L−1 ketorolac, a nonselective COX inhibitor. Participants first rested in a non heat stress condition (≥85 min, 25°C) followed by a further 70‐min rest period in the heat (35°C). They then performed 50 min of moderate‐intensity cycling (~55% peak oxygen uptake) followed by a 30‐min recovery period. At the end of exercise, sweat rate was lower at the 150 μmol·L−1 celecoxib (1.51 ± 0.25 mg·min−1·cm−2) and 10 mmol·L−1 ketorolac (1.30 ± 0.30 mg·min−1·cm−2) treated skin sites relative to the Control site (1.89 ± 0.27 mg·min−1·cm−2) (both P ≤ 0.05). Additionally, sweat rate at the ketorolac site was attenuated relative to the celecoxib site (P ≤ 0.05). Neither celecoxib nor ketorolac influenced cutaneous vascular conductance throughout the experiment (both P > 0.05). We showed that both COX‐1 and COX‐2 contribute to sweating but not cutaneous vasodilation during moderate‐intensity exercise in the heat in young men

The nitric oxide dependence of cutaneous microvascular function to independent and combined hypoxic cold exposure

Hypoxic modulation of nitric oxide (NO) production pathways in the cutaneous microvasculature and its interaction with cold-induced reflex vasoconstriction, independent of local cooling, have yet to be identified. This study assessed the contribution of NO to nonglabrous microvasculature perfusion during hypoxia and whole body cooling with concomitant inhibition of NO synthase [NOS; via NG-nitro-l-arginine methyl ester (l-NAME)] and the nitrite reductase, xanthine oxidase (via allopurinol), two primary sources of NO production. Thirteen volunteers were exposed to independent and combined cooling via water-perfused suit (5°C) and normobaric hypoxia (FIO2, 0.109 ± 0.002). Cutaneous vascular conductance (CVC) was assessed across four sites with intradermal microdialysis perfusion of 1) lactated Ringers solution (control), 2) 20 mmol l-NAME, 3) 10 µmol allopurinol, or 4) combined l-NAME/allopurinol. Effects and interactions were assessed via four-way repeated measures ANOVA. Independently, l-NAME reduced CVC (43%, P < 0.001), whereas allopurinol did not alter CVC (P = 0.5). Cooling decreased CVC (P = 0.001), and the reduction in CVC was consistent across perfusates (~30%, P = 0.9). Hypoxia increased CVC (16%, P = 0.01), with this effect abolished by l-NAME infusion (P = 0.04). Cold-induced vasoconstriction was blunted by hypoxia, but importantly, hypoxia increased CVC to a similar extent (39% at the Ringer site) irrespective of environmental temperature; thus, no interaction was observed between cold and hypoxia (P = 0.1). l-NAME restored vasoconstriction during combined cold-hypoxia (P = 0.01). This investigation suggests that reflex cold-induced cutaneous vasoconstriction acts independently of NO suppression, whereas hypoxia-induced cutaneous vasodilatation is dependent on NOS-derived NO production

Wearing graduated compression stockings augments cutaneous vasodilation but not sweating during exercise in the heat

The activation of cutaneous vasodilation and sweating are essential to the regulation of core temperature during exercise in the heat. We assessed the effect of graduated compression induced by wearing stockings on cutaneous vasodilation and sweating during exercise in the heat (30°C). On two separate occasions, nine young males exercised for 45 min or until core temperature reached ~1.5°C above baseline resting while wearing either (1) stockings causing graduated compression (graduate compression stockings, GCS), or (2) loose‐fitting stockings without compression (Control). Forearm vascular conductance was evaluated by forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure to estimate cutaneous vasodilation. Sweat rate was estimated using the ventilated capsule technique. Core and skin temperatures were measured continuously. Exercise duration was similar between conditions (Control: 42.2 ± 3.6 min vs. GCS: 42.2 ± 3.6 min, P = 1.00). Relative to Control, GCS increased forearm vascular conductance during the late stages (≥30 min) of exercise (e.g., at 40 min, 15.6 ± 5.6 vs. 18.0 ± 6.0 units, P = 0.01). This was paralleled by a greater sensitivity (23.1 ± 9.1 vs. 32.1 ± 15.0 units°C−1, P = 0.043) and peak level (14.1 ± 5.1 vs. 16.3 ± 5.7 units, P = 0.048) of cutaneous vasodilation as evaluated from the relationship between forearm vascular conductance with core temperature. However, the core temperature threshold at which an increase in forearm vascular conductance occurred did not differ between conditions (Control: 36.9 ± 0.2 vs. GCS: 37.0 ± 0.3°C, P = 0.13). In contrast, no effect of GCS on sweating was measured (all P > 0.05). We show that the use of GCS during exercise in the heat enhances cutaneous vasodilation and not sweating