Explore the vast range of titles available.

PurposeThis study determined the effect of a single session of sprint interval training in hypoxia on muscle glycogen content among athletes.MethodsTen male college track and field sprinters (mean ± standard error of the mean: age, 21.1 ± 0.2 years; height, 177 ± 2 cm; body weight, 67 ± 2 kg) performed two exercise trials under either hypoxia [HYPO; fraction of inspired oxygen (FiO2), 14.5%] or normoxia (NOR: FiO2, 20.9%). The exercise consisted of 3 × 30 s maximal cycle sprints with 8-min rest periods between sets. Before and immediately after the exercise, the muscle glycogen content was measured using carbon magnetic resonance spectroscopy in vastus lateralis and vastus intermedius muscles. Moreover, power output, blood lactate concentrations, metabolic responses (respiratory oxygen uptake and carbon dioxide output), and muscle oxygenation were evaluated.ResultsExercise significantly decreased muscle glycogen content in both trials (interaction, P = 0.03; main effect for time, P < 0.01). Relative changes in muscle glycogen content following exercise were significantly higher in the HYPO trial (− 43.5 ± 0.4%) than in the NOR trial (− 34.0 ± 0.3%; P < 0.01). The mean power output did not significantly differ between the two trials (P = 0.80). The blood lactate concentration after exercise was not significantly different between trials (P = 0.31).ConclusionA single session of sprint interval training (3 × 30 s sprints) in hypoxia caused a greater decrease in muscle glycogen content compared with the same exercise under normoxia without interfering with the power output.

Hepcidin is an iron regulating hormone, and exercise-induced hepcidin elevation is suggested to increase the risk of iron deficiency among athletes. We compared serum hepcidin responses to resistance exercise and endurance (cycling) exercise. 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). 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. 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.

PurposeAcute resistance exercise decreases endothelial function in sedentary individuals but not in strength-trained (ST) individuals. However, the underlying mechanism(s) of vascular protection in ST individuals remains unclear. Herein, we compared catecholamines, endothelin-1 (ET-1), and nitric oxide (NOx) releases after acute resistance exercise between sedentary and ST individuals.MethodsThe untrained (UT) group comprised 12 male individuals with no regular training, while the ST group comprised 12 male individuals. Participants performed a session of resistance exercise, which consisted of 3 sets of 10 repetitions at 75% of one repetition maximum. Heart rate (HR) and blood pressure were measured during resistance exercise. Brachial artery flow-mediated dilation (FMD), blood pressure, HR, and blood collection were undertaken before and 10, 30, and 60 min after the resistance exercise.ResultsNo significant difference was found in baseline brachial artery FMD between the groups (P > 0.05). Brachial artery FMD was significantly reduced in the UT group (P < 0.05) but it was prevented in the ST group after the resistance exercise. Significant differences were found at 10, 30, and 60 min after the resistance exercise in brachial artery ΔFMD from baseline between groups (P < 0.05). Blood pressure, HR, plasma epinephrine, norepinephrine, dopamine, serum endothelin-1, and plasma NOx responses did not differ between groups throughout the experimental period.ConclusionIn conclusion, preserved endothelial function in response to acute resistance exercise in ST male individuals is independent of catecholamines, ET-1, and NOx responses.

Background This study determined the effect of repeated sprint training in hypoxia (RSH) in female athletes. Methods Thirty-two college female athletes performed repeated cycling sprints of two sets of 10 × 7-s sprints with a 30-s rest between sprints twice per week for 4 weeks under either normoxic conditions (RSN group; F i O 2 , 20.9%; n = 16) or hypoxic conditions (RSH group; F i O 2 , 14.5%; n = 16). The repeated sprint ability (10 × 7-s sprints) and maximal oxygen uptake ( V ˙ O 2 max ) were determined before and after the training period. Results After training, when compared to pre-values, the mean power output was higher in all sprints during the repeated sprint test in the RSH group but only for the second half of the sprints in the RSN group ( P  ≤ 0.05). The percentage increases in peak and mean power output between before and after the training period were significantly greater in the RSH group than in the RSN group (peak power output, 5.0 ± 0.7% vs. 1.5 ± 0.9%, respectively; mean power output, 9.7 ± 0.9% vs. 6.0 ± 0.8%, respectively; P  < 0.05). V ˙ O 2 max did not change significantly after the training period in either group. Conclusion Four weeks of RSH further enhanced the peak and mean power output during repeated sprint test compared with RSN.

We investigated performance, energy metabolism, acid–base balance, and endocrine responses to repeated‐sprint exercise in hot and/or hypoxic environment. In a single‐blind, cross‐over study, 10 male highly trained athletes completed a repeated cycle sprint exercise (3 sets of 3 × 10‐s maximal sprints with 40‐s passive recovery) under four conditions (control [CON; 20℃, 50% rH, FiO2: 20.9%; sea level], hypoxia [HYP; 20℃, 50% rH, FiO2: 14.5%; a simulated altitude of 3,000 m], hot [HOT; 35℃, 50% rH, FiO2: 20.9%; sea level], and hot + hypoxia [HH; 35℃, 50% rH, FiO2: 14.5%; a simulated altitude of 3,000 m]). Changes in power output, muscle and skin temperatures, and respiratory oxygen uptake were measured. Peak (CON: 912 ± 26 W, 95% confidence interval [CI]: 862–962 W, HYP: 915 ± 28 W [CI: 860–970 W], HOT: 937 ± 26 W [CI: 887–987 W], HH: 937 ± 26 W [CI: 886–987 W]) and mean (CON: 808 ± 22 W [CI: 765–851 W], HYP: 810 ± 23 W [CI: 765–855 W], HOT: 825 ± 22 W [CI: 781–868 W], HH: 824 ± 25 W [CI: 776–873 W]) power outputs were significantly greater when exercising in heat conditions (HOT and HH) during the first sprint (p < .05). Heat exposure (HOT and HH) elevated muscle and skin temperatures compared to other conditions (p < .05). Oxygen uptake and arterial oxygen saturation were significantly lower in hypoxic conditions (HYP and HH) versus the other conditions (p < .05). In summary, additional heat stress when sprinting repeatedly in hypoxia improved performance (early during exercise), while maintaining low arterial oxygen saturation. The present study investigated performance, energy metabolism, acid‐base balance, and endocrine responses to repeated sprint exercise in a hot and/or hypoxic environment. Our findings suggest that additional heat stress to hypoxia enhances repeated sprint performance with maintaining low arterial oxygen saturation.

PURPOSE: The purpose of the present study was to investigate the effect of whole-body cryotherapy (WBC) treatment after exercise on appetite regulation and energy intake. METHODS: Twelve male athletes participated in two trials on different days. In both trials, participants performed high-intensity intermittent exercise. After 10 min following the completion of the exercise, they were exposed to a 3-min WBC treatment (−140 °C, WBC trial) or underwent a rest period (CON trial). Blood samples were collected to assess plasma acylated ghrelin, serum leptin, and other metabolic hormone concentrations. Respiratory gas parameters, skin temperature, and ratings of subjective variables were also measured after exercise. At 30 min post-exercise, energy and macronutrient intake were evaluated during an ad libitum buffet meal test. RESULTS: Although appetite-regulating hormones (acylated ghrelin and leptin) significantly changed with exercise (p = 0.047 for acylated ghrelin and p < 0.001 for leptin), no significant differences were observed between the trials. Energy intake during the buffet meal test was significantly higher in the WBC trial (1371 ± 481 kcal) than the CON trial (1106 ± 452 kcal, p = 0.007). CONCLUSION: Cold exposure using WBC following strenuous exercise increased energy intake in male 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 (VO 2max ) 57.2 ± 1.0 mL/kg/min] completed two different trials on different days, consisting of exercise in moderate hypoxia [fraction of inspired oxygen (F i O 2 ) = 14.5%, H trial] and exercise in normoxia (F i O 2  = 20.9%, N trial). They performed interval endurance exercise (8 × 4 min pedaling at 80% of VO 2max alternated with 2-min intervals of active rest at 40% of VO 2max ) 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.

Hepcidin is an iron regulating hormone, and exercise-induced hepcidin elevation is suggested to increase the risk of iron deficiency among athletes. We compared serum hepcidin responses to resistance exercise and endurance (cycling) exercise. 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 x 12 repetitions, 8 exercises) at 65% of one repetition maximum, while 60 min of cycling exercise at 65% of VO2max 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). 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 x 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. 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.