Effect of 6-Week Sprint Training on Long-Distance Running Performance in Highly Trained Runners.

PURPOSE: Long-distance running performance has been reported to be associated with sprint performance in highly trained distance runners. Therefore, we hypothesized that sprint training could enhance distance running and sprint performance in long-distance runners. This study examined the effect of 6-week sprint training on long-distance running and sprint performance in highly trained distance runners. METHODS: Nineteen college runners were divided into control (n = 8) and training (n = 11) groups. Participants in the training group performed 12 sprint training sessions in 6 weeks, while those in the control group performed 12 distance training sessions. Before and after the interventions, maximal oxygen uptake (V˙O2max), O2 cost during submaximal running (290 m·min-1 and 310 m·min-1 of running velocity), and time to exhaustion (starting at 290 m·min-1 and increased 10 m·min-1 every minute) were assessed on a treadmill. Additionally, the 100-m and 400-m sprinting times and 3000-m running time were determined on an all-weather track. RESULTS: In the control group, no measurements significantly changed after the intervention. In the training group, the time to exhaustion, 100-m and 400-m sprinting times, and 3000-m running time improved significantly, while V˙O2max and O2 cost did not change. CONCLUSIONS: These results showed that 6-week sprint training improved both sprint and long-distance running performance in highly trained distance runners without a change in aerobic capacity. Improvement in the time to exhaustion without a change in V˙O2max suggests that the enhancement of long-distance running performance could be attributable to improved anaerobic capacity.

Gastrointestinal function following endurance exercise under different environmental temperatures.

PURPOSE: We determined the effects of different environmental temperatures on exercise-induced gastrointestinal (GI) damage and delayed gastric emptying (GE) rate. METHODS: Eleven trained males completed three trials on different days, consisting of (1) exercise in a thermoneutral environment (CON, 23 °C), (2) exercise in a hot environment (HOT, 35 °C), and (3) exercise in a cold environment (COLD, 10 °C). The subjects performed high-intensity interval-type endurance exercises in all trials. Blood intestinal fatty acid binding protein (I-FABP) levels was determine before and after exercise. We evaluated Tmax (time when the 13C-excretion/h reached a maximum level) as an indication of the GE rate during post-exercise. RESULTS: Rectal temperature during exercise was significantly higher (P < 0.001) in the HOT (38.7 ± 0.3 °C) trial compared with the CON (38.2 ± 0.3 °C) and COLD (38.2 ± 0.3 °C) trials, with no significant difference between the CON and COLD trials. Plasma I-FABP level after exercise (relative to the pre-exercise level) were significantly greater (P = 0.005) in the HOT trial (92.9 ± 69.6%) than in the CON (37.2 ± 31.6%) and COLD (37.6 ± 41.8%) trials. However, there was no significant difference between the CON and COLD trials. Moreover, the Tmax was delayed significantly (P = 0.006) in the HOT trial compared with the CON and COLD trials, with no significant difference between the CON and COLD trials. CONCLUSION: GI function following endurance exercise was similar between thermoneutral and cold environments, while endurance exercise in a hot environment exacerbated GI function compared with thermoneutral and cold environments.

Sodium L-Aspartate Supplementation Improves Repeated-Sprint Performance.

Aspartate supplementation has been reported to improve endurance performance by facilitating the tricarboxylic acid cycle flux. The present study was performed to investigate the effects of aspartate supplementation on repeated-sprint performance and blood pH. Following an overnight fast, fourteen healthy males completed three sets of 10 × 6 s maximal sprints after consuming sodium L-aspartate (ASP) or placebo (PLA), in a double-blind manner. Both supplements were taken twice on each test day (2 × 4.5 g). Exercise performance (e.g., cadence and power output) and blood variables (e.g., pH and plasma amino acid levels) were measured. The ASP trial evidenced significantly higher plasma aspartate concentration during the first (ASP, 45.3 ± 9.2 µM; PLA, 6.1 ± 0.8 µM) and the second exercise sets (ASP, 24.2 ± 4.5 µM; PLA, 6.6 ± 0.9 µM) and peak cadence during the second set (ASP, 153 ± 3 rpm; PLA, 152 ± 3 rpm) compared with the PLA trial (all p < 0.05). The peak power output during the second exercise set (ASP, 743 ± 32 W; PLA, 734 ± 31 W; p = 0.060) and the blood pH immediately before (ASP, 7.280 ± 0.020; PLA, 7.248 ± 0.016; p = 0.087) and after the third exercise set (ASP, 7.274 ± 0.019; PLA, 7.242 ± 0.018; p = 0.093) tended to be higher in the ASP than in the PLA trial. In conclusion, ASP supplementation partially improved repeated-sprint performance (peak cadence during the second exercise set). However, it did not affect the mean power output.

The Impact of Heat Acclimation on Gastrointestinal Function following Endurance Exercise in a Hot Environment.

To determine the effects of heat acclimation on gastrointestinal (GI) damage and the gastric emptying (GE) rate following endurance exercise in a hot environment. Fifteen healthy men were divided into two groups: endurance training in hot (HOT, 35 °C, n = 8) or cool (COOL, 18 °C, n = 7) environment. All subjects completed 10 days of endurance training (eight sessions of 60 min continuous exercise at 50% of the maximal oxygen uptake (V·O2max). Subjects completed a heat stress exercise tests (HST, 60 min exercise at 60% V·O2max) to evaluate the plasma intestinal fatty acid-binding protein (I-FABP) level and the GE rate following endurance exercise in a hot environment (35 °C) before (pre-HST) and after (post-HST) the training period. We assessed the GE rate using the 13C-sodium acetate breath test. The core temperature during post-HST exercise decreased significantly in the HOT group compared to the pre-HST (p = 0.004) but not in the COOL group. Both the HOT and COOL groups showed exercise-induced plasma I-FABP elevations in the pre-HST (p = 0.002). Both groups had significantly attenuated exercise-induced I-FABP elevation in the post-HST. However, the reduction of exercise-induced I-FABP elevation was not different significantly between both groups. GE rate following HST did not change between pre- and post-HST in both groups, with no significant difference between two groups in the post-HST. Ten days of endurance training in a hot environment improved thermoregulation, whereas exercise-induced GI damage and delay of GE rate were not further attenuated compared with training in a cool environment.

Heat acclimation does not attenuate hepcidin elevation after a single session of endurance exercise under hot condition.

PURPOSE: We sought to determine the effects of heat acclimation on endurance exercise-induced hepcidin elevation under hot conditions. METHODS: Fifteen healthy men were divided into two groups: endurance training under hot conditions (HOT, 35 °C, n = 8) and endurance training under cool conditions (CON, 18 °C, n = 7). All subjects completed 10 days of endurance training (8 sessions in total), consisting of 60 min of continuous exercise at 50% of maximal oxygen uptake ([Formula: see text]) under their assigned environment condition. Subjects completed a heat stress exercise test (HST, 60 min exercise at 60% [Formula: see text]) to evaluate the exercise-induced thermoregulatory and hepcidin responses under hot conditions (35 °C) before (pre-HST) and after (post-HST) the training period. RESULTS: Core temperature during exercise in the post-HST decreased significantly in the HOT group compared to pre-HST (P = 0.004), but not in the CON group. The HOT and CON groups showed augmented exercise-induced plasma interleukin-6 (IL-6) elevation in the pre-HST (P = 0.002). Both groups had significantly attenuated increases in exercise-induced IL-6 in the post-HST; however, the reduction of exercise-induced IL-6 elevation was not different significantly between both groups. Serum hepcidin concentrations increased significantly in the pre-HST and post-HST in both groups (P = 0.001), no significant difference was observed between both groups during each test or over the study period. CONCLUSION: 10 days of endurance training period under hot conditions improved thermoregulation, whereas exercise-induced hepcidin elevation under hot conditions was not attenuated following the training.

Comparison of energy expenditure and substrate oxidation between walking and running in men and women.

PURPOSE: The present study compared energy metabolism between walking and running at equivalent speeds during two incremental exercise tests. METHODS: Thirty four university students (18 males, 16 females) were recruited. Each participant completed two trials, consisting of walking (Walk) and running (Run) trials on different days, with 2-3 days apart. Exercise on a treadmill was started from initial stage of 3 min (3.0 k/m in Walk trial, 5.0 km/h in Run trial), and the speed for walking and running was progressively every minute by 0.5 km/h. The changes in metabolic variables, heart rate (HR), and rating of perceived exertion (RPE) during exercise were compared between the trials. RESULTS: Energy expenditure (EE) increased with speed in each trial. However, the Walk trial had a significantly higher EE than the Run trial at speeds exceeding 92 ± 2 % of the maximal walking speed (MWS, p < 0.01). Similarly, carbohydrate (CHO) oxidation was significantly higher in the Walk trial than in the Run trial at above 92 ± 2 %MWS in males (p < 0.001) and above 93 ± 1 %MWS in females (p < 0.05). CONCLUSION: These findings suggest that EE and CHO oxidation during walking increase non-linearly with speed, and walking at a fast speed causes greater metabolic responses than running at the equivalent speed in young participants.

Ground reaction force and electromyograms of lower limb muscles during fast walking.

Background: Physically active status is an important contributor to individual health. Walking is regarded as commonly accepted exercise for exercise promotion. Particularly, interval fast walking (FW), consisting of alternating between fast and slow walking speeds, has gained popularity from practical viewpoints. Although previous studies have determined the short- and long-term effects of FW programs on endurance capacity and cardiovascular variables, factors affecting these outcomes have not been clarified. In addition to physiological variables, understanding of mechanical variables and muscle activity during FW would be a help to understand characteristics of FW. In the present study, we compared the ground reaction force (GRF) and lower limb muscle activity between fast walking (FW) and running at equivalent speeds. Method: Eight healthy men performed slow walking (45% of the maximum walking speed; SW, 3.9 ± 0.2 km/h), FW (85% of the maximum walking speed, 7.4 ± 0.4 km/h), and running at equivalent speeds (Run) for 4 min each. GRF and average muscle activity (aEMG) were evaluated during the contact, braking, and propulsive phases. Muscle activities were determined for seven lower limb muscles: gluteus maximus (GM), biceps femoris (BF), rectus femoris (RF), vastus lateralis (VL), gastrocnemius medialis (MG), soleus (SOL), and tibialis anterior (TA). Results: The anteroposterior GRF was greater in FW than in Run during the propulsive phase (p < 0.001), whereas the impact load (peak and average vertical GRF) was lower in FW than in Run (p < 0.001). In the braking phase, lower leg muscle aEMGs were higher during Run than during SW and FW (p < 0.001). However, in the propulsive phase, soleus muscle activity was greater during FW than during Run (p < 0.001). aEMG of tibialis anterior was higher during FW than during SW and Run in the contact phase (p < 0.001). No significant difference between FW and Run was observed for HR and RPE. Conclusion: These results suggest that the average muscle activities of lower limbs (e.g., gluteus maximus, rectus femoris, and soleus) during the contact phase were comparable between FW and running, however, the activity patterns of lower limb muscles differed between FW and running, even at equivalent speeds. During running, muscles were mainly activated in the braking phase related to impact. In contrast, during FW, soleus muscle activity during the propulsive phase was increased. Although cardiopulmonary response was not different between FW and running, exercise using FW might be useful for health promotion among individuals who cannot exercise at high-intensity.

Relationship between respiratory muscle endurance and dyspnea during high-intensity exercise in trained distance runners.

We hypothesized that the trained distance runners, who have a relatively high respiratory muscle endurance, but not high respiratory muscle strength, have lower dyspneic sensations during submaximal running. Twenty-one male collegiate distance runners participated. Incremental respiratory endurance tests (IRET) and maximal inspiratory mouth pressure (PImax) measurements were performed under resting conditions. A submaximal exercise test was also performed on a treadmill at two different speeds (16 and 18 km/h) for 4 min each, and the subjects reported the rate of dyspnea (range: 0-10). The time to endpoint during the IRET, an index of respiratory muscle endurance, ranged from 9.4 to 18.8 min, and PImax, as an index of inspiratory muscle strength, ranged from 74.1 to 137.0 cmH2O. The dyspnea rating during running at 16 and 18 km/h ranged from 1 to 6 and from 4 to 8, respectively. The relative exercise intensity was approximately 80 % of peak oxygen uptake (VO2peak) at 16 km/h and 90 %VO2peak at 18 km/h. The time to endpoint during the IRET was significantly negatively correlated with dyspnea during running at 18 km/h (r = -0.459, P = 0.040), but not at 16 km/h (r = -0.161, P = 0.470). There was no significant correlation between PImax and dyspnea during running at 16 km/h (r = -0.003, P = 0.989) or 18 km/h (r = 0.070, P = 0.755). These results suggest that dyspneic sensations during high-intensity running are related to respiratory muscle endurance, but not inspiratory muscle strength, in trained distance runners.

Effects of combined hot and hypoxic conditions on muscle blood flow and muscle oxygenation during repeated cycling sprints.

PURPOSE: The purpose of the present study was to determine muscle blood flow and muscle oxygenation during repeated-sprint exercise under combined hot and hypoxic conditions. METHODS: In a single-blind, cross-over research design, 11 active males performed three sets of 5 × 6-s maximal sprints with 30-s active recovery on a cycling ergometer under control (CON; 23 °C, 50% rH, 20.9% FiO2), normobaric hypoxic (HYP; 23 °C, 50% rH, 14.5% FiO2), or hot + normobaric hypoxic (HH; 35 °C, 50% rH, 14.5% FiO2) conditions. The vastus lateralis muscle blood flow after each set and muscle oxygenation during each sprint were evaluated using near-infrared spectroscopy methods. RESULTS: Despite similar repeated-sprint performance among the three conditions (peak and mean power outputs, percent decrement score), HH was associated with significantly higher muscle blood flow compared with CON after the first set (CON: 0.61 ± 0.10 mL/min/100 g; HYP: 0.81 ± 0.13 mL/min/100 g; HH: 0.99 ± 0.16 mL/min/100 g; P < 0.05). The tissue saturation index was significantly lower in HYP than in CON during the latter phase of the exercise (P < 0.05), but it did not differ between HH and CON. CONCLUSION: These findings suggest that a combination of normobaric hypoxia and heat stress partially facilitated the exercise-induced increase in local blood flow, but it did not enhance tissue desaturation.

Impact of Three Consecutive Days of Endurance Training Under Hypoxia on Muscle Damage and Inflammatory Responses.

Purpose: The purpose of this study was to determine the effect of 3 consecutive days of endurance training under hypoxia on muscle damage, inflammation, and performance responses. Methods: Nine active healthy males completed two trials in different periods, consisting of either 3 consecutive days of endurance training under hypoxia [fraction of inspired oxygen (Fio2): 14.5%, HYP] or normoxia (Fio2: 20.9%, NOR). They performed daily 90-min sessions of endurance training consisting of high-intensity endurance interval pedaling [10 × 4-min pedaling at 80% of maximal oxygen uptake ( V ˙ o 2max ) with 2 min of active rest at 30% of V ˙ o 2max ] followed by 30-min continuous pedaling at 60% of V ˙ o 2max during 3 consecutive days (days 1-3). Venous blood sample, muscular performance of lower limb, and score of subjective feelings were determined every morning (days 1-4) to evaluate muscle damage and inflammation. On day 4, subjects performed an incremental exercise test (IET) to evaluate the performance response. Results: Pedaling workload during daily endurance training was significantly lower in the HYP trial (interval exercise: 166 ± 4 W) than in the NOR trial (194 ± 8 W; P < 0.0001). Serum creatine kinase (CK) and high-sensitivity C-reactive protein (hsCRP) concentrations did not significantly change during days 1-4 in either trial. Maximal voluntary contraction (MVC) of knee extension (P < 0.0001) and drop jump (DJ) index (P = 0.004) were significantly decreased with training in both trials, with no significant difference between trials. The muscle soreness and fatigue scores significantly increased in both trials (P < 0.0001). However, the HYP trial showed a significantly lower score of fatigue on day 4 compared with the NOR trial (P = 0.004). Maximal aerobic power output during IET on day 4 did not significantly differ between trials. Conclusion: Three consecutive days of endurance training under hypoxia induced comparable levels of muscle damage, inflammation, and performance responses compared with the same training under normoxia.

Hepcidin response to three consecutive days of endurance training in hypoxia.

PURPOSE: The purpose of this study was to determine the effects of 3 consecutive days of endurance training in hypoxia on hepcidin responses. METHOD: Nine active healthy males completed two trials, consisting of 3 consecutive days of endurance training in either hypoxia [fraction of inspired oxygen (FiO2): 14.5%) or normoxia (FiO2: 20.9%). On days 1-3, participants performed one 90 min session of endurance training per day, consisting of high-intensity endurance interval exercise [10 × 4 min of pedaling at 80% of maximal oxygen uptake ([Formula: see text]O2max) with 2 min of active rest at 30% of [Formula: see text]O2max] followed by 30 min of continuous exercise at 60% of [Formula: see text]O2max. Venous blood samples were collected prior to exercise each day during the experimental period (days 1-4) to determine serum hepcidin, iron, ferritin, haptoglobin, and ketone body concentrations. RESULT: Serum iron (p < 0.0001), ferritin (p = 0.005) and ketone body (p < 0.0001) concentrations increased significantly in both trials on days 2-4 compared with day 1, with no significant differences between trials. No significant changes in serum haptoglobin concentrations were observed throughout the experimental period in either trial. Serum hepcidin concentrations also increased significantly on days 2-4 compared with day 1 in both trials (p = 0.004), with no significant differences observed between trials. CONCLUSION: 3 consecutive days of endurance training in hypoxia did not affect hepcidin concentrations compared with endurance training in normoxia.

Muscle oxygenation, endocrine and metabolic regulation during low-intensity endurance exercise with blood flow restriction.

PURPOSE: The present study investigated the effect of endurance exercise with blood flow restriction (BFR) performed at either 25% maximal oxygen uptake (V˙O2 max) or 40% V˙O2 max) on muscle oxygenation, energy metabolism, and endocrine responses. METHODS: Ten males were recruited in the present study. The subjects performed three trials: (1) endurance exercise at 40% V˙O2 max without BFR (NBFR40), (2) endurance exercise at 25% V˙O2 max with BFR (BFR25), and (3) endurance exercise at 40% V˙O2 max with BFR (BFR40). The exercises were performed for 15 min during which the pedaling frequency was set at 70 rpm. In BFR25 and BFR40, 2 min of pressure phase (equivalent to 160 mmHg) followed by 1 min of release phase were repeated five times (5 × 3 min) throughout 15 minutes of exercise. During exercise, muscle oxygenation and concentration of respiratory gases were measured. The blood samples were collected before exercise, immediately after 15 min of exercise, and at 15, 30, and 60 minutes after completion of exercise. RESULTS: Deoxygenated hemoglobin (deoxy-Hb) level during exercise was significantly higher with BFR25 and BFR40 than that with NBFR40. BFR40 showed significantly higher total-hemoglobin (total-Hb) than NBFR40 during 2 min of pressure phase. Moreover, exercise-induced lactate elevation and pH reduction were significantly augmented in BFR40, with concomitant increase in serum cortisol concentration after exercise. Carbohydrate (CHO) oxidation was significantly higher with BFR40 than that with NBFR40 and BFR25, whereas fat oxidation was lower with BFR40. CONCLUSION: Deoxy-Hb and total Hb levels were significantly increased during 15 min of pedaling exercise in BFR25 and BFR40, indicating augmented local hypoxia and blood volume (blood perfusion) in the muscle. Moreover, low-and moderate-intensity exercise with BFR facilitated CHO oxidation.

Exogenous glucose oxidation during endurance exercise in hypoxia.

PURPOSE: Endurance exercise in hypoxia promotes carbohydrate (CHO) metabolism. However, detailed CHO metabolism remains unclear. The purpose of this study was to evaluate the effects of endurance exercise in moderate hypoxia on exogenous glucose oxidation at the same energy expenditure or relative exercise intensity. METHODS: Nine active healthy males completed three trials on different days, consisting of 30 min of running at each exercise intensity: (a) exercise at 65% of normoxic maximal oxygen uptake in normoxia [NOR, fraction of inspired oxygen (Fi O2 ) = 20.9%, 10.6 ± 0.3 km/h], (b) exercise at the same relative exercise intensity with NOR in hypoxia (HYPR, Fi O2  = 14.5%, 9.4 ± 0.3 km/h), and (c) exercise at the same absolute exercise intensity with NOR in hypoxia (HYPA, Fi O2  = 14.5%, 10.6 ± 0.3 km/h). The subjects consumed 113 C-labeled glucose immediately before exercise, and expired gas samples were collected during exercise to determine 13 C-excretion (calculated by 13 CO2 /12 CO2 ). RESULTS: The exercise-induced increase in blood lactate was significantly augmented in the HYPA than in the NOR and HYPR (p = .001). HYPA involved a significantly higher respiratory exchange ratio (RER) during exercise compared with the other two trials (p < .0001). In contrast, exogenous glucose oxidation (13 C-excretion) during exercise was significantly lower in the HYPA than in the NOR (p = .03). No significant differences were observed in blood lactate elevation, RER, or exogenous glucose oxidation between NOR and HYPR. CONCLUSION: Endurance exercise in moderate hypoxia caused a greater exercise-induced blood lactate elevation and RER compared with the running exercise at same absolute exercise intensity in normoxia. However, exogenous glucose oxidation (13 C-excretion) during exercise was attenuated compared with the same exercise in normoxia.

Resistance exercise causes greater serum hepcidin elevation than endurance (cycling) exercise.

BACKGROUND: Hepcidin is an iron regulating hormone, and exercise-induced hepcidin elevation is suggested to increase the risk of iron deficiency among athletes. OBJECTIVE: We compared serum hepcidin responses to resistance exercise and endurance (cycling) exercise. METHODS: Ten males [mean ± standard error: 172 ± 2 cm, body weight: 70 ± 2 kg] performed three trials: a resistance exercise trial (RE), an endurance exercise trial (END), and a rest trial (REST). The RE consisted of 60 min of resistance exercise (3-5 sets × 12 repetitions, 8 exercises) at 65% of one repetition maximum, while 60 min of cycling exercise at 65% of [Formula: see text] was performed in the END. Blood samples were collected before exercise and during a 6-h post-exercise (0h, 1h, 2h, 3h, 6h after exercise). RESULTS: Both RE and END significantly increased blood lactate levels, with significantly higher in the RE (P < 0.001). Serum iron levels were significantly elevated immediately after exercise (P < 0.001), with no significant difference between RE and END. Both the RE and END significantly increased serum growth hormone (GH), cortisol, and myoglobin levels (P < 0.01). However, exercise-induced elevations of GH and cortisol were significantly greater in the RE (trial × time: P < 0.001). Plasma interleukin-6 (IL-6) levels were significantly elevated after exercise (P = 0.003), with no significant difference between the trials. Plasma hepcidin levels were elevated after exercise (P < 0.001), with significantly greater in the RE (463 ± 125%) than in the END (137 ± 27%, P = 0.03). During the REST, serum hepcidin and plasma IL-6 levels did not change significantly. CONCLUSION: Resistance exercise caused a greater exercise-induced elevation in hepcidin than did endurance (cycling) exercise. The present findings indicate that caution will be required to avoid iron deficiency even among athletes in strength (power) types of events who are regularly involved in resistance exercise.

Inflammatory, Oxidative Stress, and Angiogenic Growth Factor Responses to Repeated-Sprint Exercise in Hypoxia.

The present study was designed to determine the effects of repeated-sprint exercise in moderate hypoxia on inflammatory, muscle damage, oxidative stress, and angiogenic growth factor responses among athletes. Ten male college track and field sprinters [mean ± standard error (SE): age, 20.9 ± 0.1 years; height, 175.7 ± 1.9 cm; body weight, 67.3 ± 2.0 kg] performed two exercise trials in either hypoxia [HYPO; fraction of inspired oxygen (FiO2), 14.5%] or normoxia (NOR; FiO2, 20.9%). The exercise consisted of three sets of 5 s × 6 s maximal sprints with 30 s rest periods between sprints and 10 min rest periods between sets. After completing the exercise, subjects remained in the chamber for 3 h under the prescribed oxygen concentration (hypoxia or normoxia). The average power output during exercise did not differ significantly between trials (p = 0.17). Blood lactate concentrations after exercise were significantly higher in the HYPO trial than in the NOR trial (p < 0.05). Plasma interleukin-6 concentrations increased significantly after exercise (p < 0.01), but there was no significant difference between the two trials (p = 0.07). Post-exercise plasma interleukin-1 receptor antagonist, serum myoglobin, serum lipid peroxidation, plasma vascular endothelial growth factor (VEGF), and urine 8-hydroxydeoxyguanosine concentrations did not differ significantly between the two trials (p > 0.05). In conclusion, exercise-induced inflammatory, muscle damage, oxidative stress, and VEGF responses following repeated-sprint exercise were not different between hypoxia and normoxia.

Muscle Oxygenation During Repeated Double-Poling Sprint Exercise in Normobaric Hypoxia and Normoxia.

We compared upper limb muscle oxygenation responses during repeated double-poling sprint exercise in normobaric hypoxia and normoxia. Eight male kayakers completed a repeated double-poling sprint exercise (3 × 3 × 20-s maximal sprints, 40-s passive recovery, 5-min rest) in either hypoxia (HYP, FiO2 = 14.5%) or normoxia (NOR, FiO2 = 20.9%). Power output, muscle oxygenation of triceps brachii muscle (using near infrared spectroscopy), arterial oxygen saturation, and cardiorespiratory variables were monitored. Mean power output tended to be lower (-5.2%; P = 0.06) in HYP compared with NOR, while arterial oxygen saturation (82.9 ± 0.9% vs. 90.5 ± 0.8%) and systemic oxygen uptake (1936 ± 140 vs. 2408 ± 83 mL⋅min-1) values were lower (P < 0.05). Exercise-induced increases in deoxygenated hemoglobin (241.7 ± 46.9% vs. 175.8 ± 27.2%) and total hemoglobin (138.0 ± 18.1% vs. 112.1 ± 6.7%) were greater in HYP in reference to NOR (P < 0.05). Despite moderate hypoxia exacerbating exercise-induced elevation in blood perfusion of active upper limb musculature, power output during repeated double-poling exercise only tended to be lower.

The Effects of Endurance Exercise in Hypoxia on Acid-Base Balance, Potassium Kinetics, and Exogenous Glucose Oxidation.

PURPOSE: To investigate the carbohydrate metabolism, acid-base balance, and potassium kinetics in response to exercise in moderate hypoxia among endurance athletes. METHODS: Nine trained endurance athletes [maximal oxygen uptake (VO2max): 62.5 ± 1.2 mL/kg/min] completed two different trials on different days: either exercise in moderate hypoxia [fraction of inspired oxygen (FiO2) = 14.5%, HYPO] or exercise in normoxia (FiO2 = 20.9%, NOR). They performed a high-intensity interval-type endurance exercise consisting of 10 × 3 min runs at 90% of VO2max with 60 s of running (active rest) at 50% of VO2max between sets in hypoxia (HYPO) or normoxia (NOR). Venous blood samples were obtained before exercise and during the post-exercise. The subjects consumed 13C-labeled glucose immediately before exercise, and we collected expired gas samples during exercise to determine the 13C-excretion (calculated as 13CO2/12CO2). RESULTS: The running velocities were significantly lower in HYPO (15.0 ± 0.2 km/h) than in NOR (16.4 ± 0.3 km/h, P < 0.0001). Despite the lower running velocity, we found a significantly greater exercise-induced blood lactate elevation in HYPO compared with in NOR (P = 0.002). The bicarbonate ion concentration (P = 0.002) and blood pH (P = 0.002) were significantly lower in HYPO than in NOR. There were no significant differences between the two trials regarding the exercise-induced blood potassium elevation (P = 0.87) or 13C-excretion (HYPO, 0.21 ± 0.02 mmol⋅39 min; NOR, 0.14 ± 0.03 mmol⋅39 min; P = 0.10). CONCLUSION: Endurance exercise in moderate hypoxia elicited a decline in blood pH. However, it did not augment the exercise-induced blood K+ elevation or exogenous glucose oxidation (13C-excretion) compared with the equivalent exercise in normoxia among endurance athletes. The findings suggest that endurance exercise in moderate hypoxia causes greater metabolic stress and similar exercise-induced elevation of blood K+ and exogenous glucose oxidation compared with the same exercise in normoxia, despite lower mechanical stress (i.e., lower running velocity).

Effects of Respiratory Muscle Endurance Training in Hypoxia on Running Performance.

PURPOSE: We hypothesized that respiratory muscle endurance training (RMET) in hypoxia induces greater improvements in respiratory muscle endurance with attenuated respiratory muscle metaboreflex and consequent whole-body performance. We evaluated respiratory muscle endurance and cardiovascular response during hyperpnoea and whole-body running performance before and after RMET in normoxia and hypoxia. METHODS: Twenty-one collegiate endurance runners were assigned to control (n = 7), normoxic (n = 7), and hypoxic (n = 7) groups. Before and after the 6 wk of RMET, incremental respiratory endurance test and constant exercise tests were performed. The constant exercise test was performed on a treadmill at 95% of the individual's peak oxygen uptake (V˙O2peak). The RMET was isocapnic hyperpnoea under normoxic and hypoxic conditions (30 min·d). The initial target of minute ventilation during RMET was set to 50% of the individual maximal voluntary ventilation, and the target increased progressively during the 6 wk. Target arterial oxygen saturation in the hypoxic group was set to 90% in the first 2 wk, and thereafter it was set to 80%. RESULTS: Respiratory muscle endurance was increased after RMET in the normoxic and hypoxic groups. The time to exhaustion at 95% V˙O2peak exercise also increased after RMET in the normoxic (10.2 ± 2.4 to 11.2 ± 2.6 min) and hypoxic (11.5 ± 2.6 to 12.6 ± 3.0 min) groups, but not in the control group (9.6 ± 3.2 to 9.4 ± 4.0 min). The magnitude of these changes did not differ between the normoxic and the hypoxic groups (P = 0.84). CONCLUSION: These results suggest that the improvement of respiratory muscle endurance and blunted respiratory muscle metaboreflex could, in part, contribute to improved endurance performance in endurance-trained athletes. However, it is also suggested that there are no additional effects when the RMET is performed in hypoxia.

The effects of endurance exercise in hypoxia on acid-base balance and potassium kinetics: a randomized crossover design in male endurance athletes.

BACKGROUND: Exercise-induced disturbance of acid-base balance and accumulation of extracellular potassium (K+) are suggested to elicit fatigue. Exercise under hypoxic conditions may augment exercise-induced alterations of these two factors compared with exercise under normoxia. In the present study, we investigated acid-base balance and potassium kinetics in response to exercise under moderate hypoxic conditions in endurance athletes. METHODS: Nine trained middle-to-long distance athletes [maximal oxygen uptake (VO2max) 57.2 ± 1.0 mL/kg/min] completed two different trials on different days, consisting of exercise in moderate hypoxia [fraction of inspired oxygen (FiO2) = 14.5%, H trial] and exercise in normoxia (FiO2 = 20.9%, N trial). They performed interval endurance exercise (8 × 4 min pedaling at 80% of VO2max alternated with 2-min intervals of active rest at 40% of VO2max) under hypoxic or normoxic conditions. Venous blood samples were obtained to determine blood lactate, pH, bicarbonate ion, and K+ concentrations before exercise, during exercise, and after exercise. RESULTS: The blood lactate concentrations increased significantly with exercise in both trials. Exercise-induced blood lactate elevations were significantly greater in the N trial than in the H trial at all time points (P = 0.012). Bicarbonate ion concentrations (P = 0.001) and blood pH (P = 0.019) during exercise and post-exercise periods were significantly lower in the N trial than in the H trial. A significantly greater exercise-induced elevation in blood K+ concentration was produced in the N trial than in the H trial during exercise and immediately after exercise (P = 0.03). CONCLUSIONS: High-intensity interval exercise on a cycle ergometer under moderate hypoxic conditions did not elicit a decrease in blood pH or elevation in K+ levels compared with an equivalent level of exercise under normoxic conditions.

Impact of Endurance Exercise in Hypoxia on Muscle Damage, Inflammatory and Performance Responses.

Sumi, D, Kojima, C, and Goto, K. Impact of endurance exercise in hypoxia on muscle damage, inflammatory and performance responses. J Strength Cond Res 32(4): 1053-1062, 2018-This study evaluated muscle damage and inflammatory and performance responses after high-intensity endurance exercise in moderate hypoxia among endurance athletes. Nine trained endurance athletes completed 2 different trials on different days: exercise under moderate hypoxia (H trial, FiO2 = 14.5%) and normoxia (N trial, FiO2 = 20.9%). They performed interval exercises (10 × 3-minute running at 95% of V[Combining Dot Above]O2max with 60-second of active rest at 60% of V[Combining Dot Above]O2max) followed by 30-minute of continuous running at 85% of V[Combining Dot Above]O2max under either hypoxic or normoxic conditions. Venous blood samples were collected 4 times: before exercise, 0, 60, and 120-minute after exercise. The time to exhaustion (TTE) during running at 90% of V[Combining Dot Above]O2max was also determined to evaluate endurance capacity 120-minute after the training session. The H trial induced a significantly greater exercise-induced elevation in the blood lactate concentration than did the N trial (p = 0.02), whereas the elevation in the exercise-induced myoglobin concentration (muscle damage marker) was significantly greater in the N trial than in the H trial (p = 0.005). There was no significant difference in plasma interleukin-6 (inflammatory marker) concentration between the H and N trials. The TTE was shorter in the N trial (613 ± 65 seconds) than in the H trial (783 ± 107 seconds, p = 0.02). In conclusion, among endurance athletes, endurance exercise under moderate hypoxic conditions did not facilitate an exercise-induced muscle damage response or cause a further reduction in the endurance capacity compared with equivalent exercise under normoxic conditions.