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Research in Sports Medicine: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/gspm20
Effects of Acute Exposure to Mild Simulated Hypoxia on Hormonal Responses to Low-intensity Resistance Exercise in Untrained Men a
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a
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Jen-Yu Ho , Tai-Yu Huang , Yi-Chieh Chien , Ying-Chen Chen & Shuia
Yu Liu a
Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan b
Department of Physical Education, National Taiwan Normal University, Taipei, Taiwan Published online: 20 Jun 2014.
To cite this article: Jen-Yu Ho, Tai-Yu Huang, Yi-Chieh Chien, Ying-Chen Chen & Shui-Yu Liu (2014) Effects of Acute Exposure to Mild Simulated Hypoxia on Hormonal Responses to Low-intensity Resistance Exercise in Untrained Men, Research in Sports Medicine: An International Journal, 22:3, 240-252, DOI: 10.1080/15438627.2014.915834 To link to this article: http://dx.doi.org/10.1080/15438627.2014.915834
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Research in Sports Medicine, 22:240–252, 2014 © 2014 Taylor & Francis ISSN: 1543-8627 print/1543-8635 online DOI: 10.1080/15438627.2014.915834
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Effects of Acute Exposure to Mild Simulated Hypoxia on Hormonal Responses to Low-intensity Resistance Exercise in Untrained Men JEN-YU HO Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan
TAI-YU HUANG Department of Physical Education, National Taiwan Normal University, Taipei, Taiwan
YI-CHIEH CHIEN, YING-CHEN CHEN, and SHUI-YU LIU Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan
This study examined hormonal responses to low-intensity resistance exercise under mild simulated hypoxia. Ten resistance untrained men performed five sets of 15 repetitions of squat exercise at 30% of 1RM under normobaric hypoxia (FiO2 = 15%) and normoxia in a cross-over and counter-balanced design. Blood lactate (LAC), growth hormone (GH), total testosterone (T) and cortisol (C) were measured at pre-exercise, immediately post-exercise and 15 minutes post-exercise. LAC, GH and T significantly increased immediately after squat exercise in both trials (p < 0.05). While T returned to baseline, GH remained significantly greater at 15 minutes postexercise. Cortisol significantly decreased immediately after and 15 minutes post-exercise in both trials (p < 0.05). No significant differences were observed between two trials in LAC, GH, T and C. It was concluded that low-intensity resistance exercise performed under mild simulated hypoxia does not induce greater anabolic hormonal responses in resistance untrained men.
Received 12 October 2013; accepted 14 March 2014. This study was funded by the National Science Council in Taiwan (Grant No. NSC1002410-H-003-002) and partially supported by a grant for ‘Aim for the Top University Plan’ from National Taiwan Normal University and the Ministry of Education of Taiwan. Address correspondence to Jen-Yu Ho, Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan. E-mail: [email protected] 240
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KEYWORDS anabolic hormones, intermittent hypoxic training, weight training
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INTRODUCTION The use of living and training at real altitude (i.e., classic altitude training) to augment endurance performance at sea level has gained popularity in endurance athletes over the past decades (Dufour et al., 2006). However, previous studies have observed muscle mass loss and decrease in muscle fiber size following long-term exposure to severe altitude (Hoppeler et al., 1990; MacDougall et al., 1991). To cope with the detrimental effects of long-term altitude training, one of the modified training regimens referring to ‘living-low and training-high, (LLTH)’ (Roels et al., 2005) or known as ‘intermittent hypoxic training’ has been developed. The LLTH applies simulated hypoxia (i.e., simulated through the use of an altitude simulation tent or room) only during all or a limited number of training sessions while subjects recover in normoxia for optimal muscle recovery. In the past two decades, LLTH has been extensively studied. While LLTH has been demonstrated to improve endurance capacity at sea level in some studies (Geiser et al., 2001; Meeuwsen, Hendriksen, & Holewijn, 2001), other studies have not observed the benefits of LLTH (Truijens, Toussaint, Dow, & Levine, 2003; Ventura et al., 2003). The physiological benefits of LLTH still remain controversial (Hoppeler, Klossner, & Vogt, 2008). Most studies that examined the effectiveness of intermittent hypoxic training have emphasized muscular adaptations observed with endurance training. Less attention has been given to examining the roles of hypoxia in other types of training modalities. Resistance training is another modality of exercise that has grown in popularity. Resistance training has been extensively studied in the past few decades, particularly for its role in improving athletic performance by increasing muscular strength, power, and hypertrophy (Kraemer & Ratamess, 2000). Resistance exercise and training have been shown to elicit significant acute hormonal responses that are critical for muscular adaptations, especially muscle hypertrophy (Kraemer & Ratamess, 2003). Some anabolic hormones, such as growth hormone, testosterone and insulin-like growth factor-I, have been significantly secreted in response to a bout of resistance exercise (Spiering et al., 2008) and play a substantial role in promoting muscle hypertrophy. It is generally accepted that intensity of 70– 80% 1RM (e.g., 6–12RM) is required to promote anabolic hormonal responses and muscle hypertrophy (Kraemer, Fleck, & Evans, 1996). In recent years, Kon et al. (2010, 2012) hypothesized that the use of systemic simulated hypoxia can further maximize the anabolic hormonal responses following resistance exercise. Their hypotheses were based on the positive results observed from occlusion training studies. Several previous
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studies have reported that low-intensity exercise combined with moderate vascular occlusion markedly induced greater growth hormone responses (Takarada et al., 2000a) and subsequently increased muscle size and strength (Takarada et al., 2000b; Teramoto & Golding, 2006). It has been suggested that local hypoxia of skeletal muscles by using blood flow restriction to the exercising muscles may result in a greater accumulation of metabolites and lead to an increase in growth hormone secretions (Goto, Ishii, Kizuka, & Takamatsu, 2005; Takarada et al., 2000a). However, it is important to note that the physiological effects of whole body exposure to systemic simulated hypoxia may be different from effects of local hypoxia of working muscles by using blood flow restriction. In agreement with their hypotheses, Kon et al. (2010, 2012) reported that performing bench press and leg press at 70% and 50% of 1RM in normobaric hypoxic conditions (FiO2 = 13%) caused greater accumulation of metabolites (i.e., blood lactate) and a greater anabolic hormone response than that in the normoxic condition. Their findings suggest that hypoxia plays an important role in enhancing the GH responses to moderate- to high-intensity resistance exercise. While performing moderate to high intensity resistance exercise is usually suggested to promote anabolic hormonal responses and muscle hypertrophy, it is unclear whether performing lowintensity resistance exercise under systemic simulated hypoxia could also produce greater anabolic hormonal responses. Further studies are required for clarification. If low-intensity resistance exercise combined with systemic simulated hypoxia can induce greater anabolic hormonal responses, this training regimen may be used in rehabilitation training programs for those who cannot perform high-intensity resistance exercise to gain muscle strength and hypertrophy. Thus, the purpose of the present study was to determine the effects of acute exposure to mild simulated hypoxia on hormonal responses to low-intensity resistance exercise.
METHODS Participants Ten healthy male subjects (age 23.6 ± 1.3 years; weight 68.2 ± 5.9 kg; 1RM 91.5 ± 11.8 kg) volunteered to participate in this study. The subjects were either completely untrained or recreationally active college students. All subjects had not been involved with any resistance training for at least 6 months prior to the study. Subjects were excluded from the study if they had any preexisting medical condition or orthopedic limitations that put them at risk while performing the squat exercises. After a detailed description of the experimental procedures and possible risks of this study was provided, subjects gave written informed consent. All procedures were approved by the University Institutional Review Board for use with human subjects.
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Experimental Design
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After the familiarization session, all subjects performed the back squat one repetition maximum (1RM) test under normoxia. Subjects then participated in two experimental trials in a cross-over and counterbalanced manner separated by one week: (1) performing acute squat exercise in mild normobaric hypoxia (FiO2 = 15%, hypoxia trial); and (2) performing acute squat exercise in normoxia (FiO2 = 21.0%, normoxia trial). In both trials, all subjects performed a low-intensity back squat (five sets of 15 repetitions at 30% of 1RM squat with 90 seconds rest between sets) followed by 15 minutes of recovery in normoxia. Blood samples were collected at pre-exercise (Pre), immediately postexercise (Post) and 15 minutes into recovery from exercise (15 min).
Squat One Repetition Maximum (1RM) Test After completing the familiarization session, all subject’s squat 1RM strength was measured in normoxia using Cybex Free Weight Squat Rack (Cybex International, Medway, MA, USA). Subjects were instructed to avoid consumption of alcohol and caffeine and intense exercise at least 48 hours before the strength test. The 1RM test used the method described by Kraemer and Fry (1995). Briefly, subjects performed back squats for 8–10 repetitions at 50% of their estimated 1RM followed by another set of 3–5 repetitions at 85% of estimated 1RM. Subsequently, three to five one repetition trials were used to determine their squat 1RM strength.
Simulated Hypoxic Exposure A hypoxia trial was performed in the hypoxic tent (FiO2 = 15%, equivalent to 2300 m altitude) (CAT-315 Walk-In Tent, Colorado Altitude Training, Louisville, CO, USA). The barometric pressure in the tent was equivalent to sea level (760 mmHg). To verify and maintain the hypoxic condition in the tent (FiO2 = 14.5%15%), the oxygen concentration was continuously monitored by using an oxygen analyzer (Handi Plus, Maxtec, Salt Lake City, UT, USA) throughout the hypoxia trial. Once the hypoxic condition in the tent was verified, subjects entered into the tent and rested for 10 minutes before performing the squat exercise in hypoxia. Arterial oxygen saturation (SpO2) was monitored by pulse oximeter (Novametrix Medical Systems, Wallingford, CT, USA). SpO2 was recorded before entering the tent, after 10 minutes of rest in the tent and immediately after the squat exercise. A normoxia trial was also performed in the tent but subjects performed the squat exercise under normoxic condition (FiO2 = 21.0%, barometric pressure was equivalent to 760 mmHg).
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Acute Squat Exercise Test All subjects were instructed to refrain from intense exercise and alcohol consumption for at least 48 hours before the squat exercise test. In the morning following 8–10 hours of overnight fasting, subjects reported to the laboratory. After 10-minute rest, the first blood draw was collected under normoxia. Subjects then warmed up for 5 minutes before the exercise test. The exercise test consisted of five sets of 15 repetitions at 30% of 1RM squat with 90 seconds rest intervals between sets. Subjects were instructed to perform the squat exercise in a smooth and controlled manner during both experimental trials. Arterial oxygen saturation (SpO2) was recorded before and after squat exercise. Subjects performed the squat exercise test under a hypoxic condition or a normoxic condition first. After one week of rest, subjects performed an exercise test again under another condition in a cross-over design. Subjects were asked to closely replicate their daily diet (from the first trial) during their second experimental trial to reduce the possible influences of diet on hormonal responses to resistance exercise.
Blood Collection and Analyses On the day of the acute squat exercise test, a pre-exercise blood sample was collected after subjects had rested quietly for 10 minutes under normoxia. Blood samples were also collected immediately post-exercise (under hypoxia during the hypoxia trial and under normoxia during the normoxia and control trials) and at 15 minutes post-exercise under normoxia. All blood samples were collected in a sitting position. Whole blood was centrifuged at 3000 RPM for 10 minutes and the resulting serum was aliquoted and stored at –80°C until subsequent analyses. Blood lactate (LAC), growth hormone (GH), total testosterone (T) and cortisol concentrations (C) were measured at a local clinical laboratory. During all trials, blood collection was standardized, being drawn in the morning (within an hour) to avoid some confounding effects from diurnal hormonal variations.
Statistical Analysis The dependent variables in this study (SpO2, LAC, GH, T and C) were analyzed using two-way repeated measures ANOVA (trial × time). All data sets satisfied statistical requirements for the linear approaches used. When a significant F score resulted, a Fisher’s least significant difference (LSD) post hoc test was used to determine the pair-wise differences between means. The test–retest reliability of the blood and 1RM tests used in this study showed intra-class Rs ≥ 0.92. The level of significance for all the tests was set at P ≤ 0.05. All data are presented as means ± standard deviation (s).
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RESULTS Arterial Oxygen Saturation (SpO2) during Squat Exercise
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SpO2 was significantly decreased during the hypoxia trial by 6.4 ± 3.6% (p < 0.001) when compared with the normoxia trial after 10 minutes rest in the tent. SpO2 remained significantly lower (p < 0.001) than the normoxia trial after squat exercise in the hypoxia trial. However, following 15 minutes of recovery in normoxia, SpO2 returned to 97.2 ± 0.4% in the hypoxia trial and were not significantly different when compared with the normoxia trial. In contrast, during the normoxia trial, SpO2 remained within 97.4–98.0% throughout the trial (Figure 1).
Blood Lactate Concentrations Figure 2 shows the blood lactate concentrations measured before and immediately after the squat exercise. Acute squat exercise significantly increased blood lactate concentrations above pre-exercise values at post-exercise (95% CI = 5.04 to 6.48) in both the hypoxia and normoxia trials (p < 0.001). However, blood lactate concentrations were not significantly different between the hypoxia and normoxia trials at any time point (p = 0.344).
Serum Hormone Concentrations Growth hormone and total testosterone significantly increased above the preexercise value at post-exercise in both the hypoxia and normoxia trials (95%
FIGURE 1 Changes in arterial oxygen saturation (SpO2) during squat exercise (mean ± s). HR = hypoxic resistance exercise; NR = normoxic resistance exercise; Rest 1 = before entering the tent; Rest 2 = after 10 minutes of rest in the tent; Post = Post-exercise; 15 min = 15 minutes of recovery in normoxia. * = p < 0.05 vs Rest 1; & = p < 0.05 vs NR
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FIGURE 2 Changes in blood lactate concentrations before and after squat exercise (mean ± s). HR = hypoxic resistance exercise; NR = normoxic resistance exercise; Pre = Pre-exercise; Post = Postexercise * = p < 0.05 vs Pre.
CI = 0.19 to 1.04 for growth hormone, 95% CI = 5.81 to 7.83 for total testosterone; p < 0.05; see Figures 3(a) and 3(b)). While total testosterone returned to pre-exercise value after 15 minutes, growth hormone remained significantly higher than pre-exercise value after 15 minutes (95% CI = 0.32 to 1.51; p = 0.020). There were no significant differences at any time point between hypoxia and normoxia trials for growth hormone and total testosterone concentrations (p > 0.05). In contrast, serum cortisol concentrations (Figure 3(c)) significantly reduced below pre-exercise value at post-exercise (95% CI = 10.15 to 12.43) and remained significantly lower than pre-exercise after 15 minutes (95% CI = 9.19 to 12.25) in both trials (p < 0.05). However, cortisol concentrations were not significantly different between the hypoxia and normoxia trials at any time point (p = 0.505).
DISCUSSION The major finding of the present study was that the low-intensity squat exercise (30% of 1RM) performed under mild simulated hypoxia (FiO2 = 15%) did not significantly induce greater hormonal responses in growth hormone, total testosterone and cortisol than that of normoxia. While Kon et al. (2010, 2012) have demonstrated significant hypoxia-induced effects on hormonal responses to moderate- to high-intensity resistance exercise under more severe hypoxia, our data suggest that resistance exercise intensity and hypoxia severity may play a role in inducing the physiological benefits when performing resistance exercises under hypoxia.
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FIGURE 3 Changes in (a) growth hormone concentrations (b) total testosterone concentrations (c) cortisol concentrations before and after squat exercise (mean ± s). HR = hypoxic resistance exercise; NR = normoxic resistance exercise; Pre = Pre-exercise; Post = Postexercise; 15 min = 15 minutes of recovery in normoxia. * = p < 0.05 vs Pre.
During the hypoxia trial, SpO2 significantly decreased to 91.4% and remained lower than baseline values throughout the hypoxia trial. In contrast, during the normoxia trial, SpO2 remained the same within 97.4–98.0% throughout the trial (Figure 1). Previous research reported that SpO2 decreased from 98% to 92% after hypoxia inhalation testing with inspired oxygen of 15% (Kelly et al., 2006). The SpO2 data of this study ensured that subject’s exposure to hypoxia was correctly controlled during the hypoxia trial. Previous studies have shown that exercise-induced metabolic stress is positively associated with accumulation of blood lactate following exercise (Goto et al., 2005). Resistance exercise of moderate- to high-intensity may be necessary to induce greater metabolic stress and blood lactate accumulation. However, when resistance exercise is performed in hypoxic conditions, highintensity exercise and associated recruitment of fast-twitch fibers would not be necessarily required for regional accumulation of lactate (Moritani, Sherman, Shibata, Matsumoto, & Shinohara, 1992). Several recent studies that combined low-intensity resistance exercise (20%1RM) with moderate vascular occlusion
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have demonstrated greater accumulation of blood lactate (Takarada et al., 2000a). In addition, Kon et al. (2010, 2012) have also reported higher blood lactate concentrations following resistance exercise in systemic hypoxic conditions than in normoxic conditions. In the present study, despite the fact that blood lactate concentrations significantly increased after the squat exercise in both trials, blood lactate concentrations were not significantly different between hypoxia and normoxia trials (Figure 2). The conflicting results between our study and previous studies could be due to differences in experimental design, including resistance exercise intensity and hypoxia severity. In the studies conducted by Kon et al. (2010, 2012), resistance exercise was performed at higher intensity (50% and 70% of 1RM) under more severe hypoxic conditions (FiO2 = 13%) when compared with the research design we used (30% of 1RM; FiO2 = 15%). In our study, lowintensity at 30% of 1RM was used to examine whether systemic hypoxia can mimic vascular occlusion in inducing greater blood lactate responses following low-intensity resistance exercise. In addition, Kon et al. have observed beneficial effects on blood lactate responses when performing moderate- to high-intensity resistance exercise under systemic hypoxia. Further investigation is warranted as to whether performing low-intensity resistance exercise under systemic hypoxia could also produce positive effects. Based on our findings, it is possible that when applying systemic hypoxia, low-intensity resistance exercise may have not been sufficient to cause hypoxia-induced effects on muscle recruitment and associated accumulation of blood lactate. Moreover, hypoxia severity may also play a role. A mild hypoxic condition of FiO2 = 15% (equivalent to 2300 m altitude) was used in this study because exercise training, preferably at 2000–2500 m above sea level, has been commonly suggested when performing hypoxic training (Wilber, 2007). Based on our findings, it is plausible that a severe hypoxic condition is required to recruit more fast-twitch fibers and lead to greater regional accumulation of blood lactate. More studies are warranted to examine further the potential influence of resistance exercise intensity and hypoxia severity on hypoxiainduced physiological benefits. Growth hormone (GH) is an important anabolic hormone mediating muscle hypertrophy following resistance training (Kraemer & Ratamess, 2003). In the present study, we showed GH increased immediately after exercise and remained greater at 15 minutes post-exercise in both trials (Figure 3(a)). However, GH responses were not significantly greater in hypoxic condition than in normoxic condition. Our results are in contrast to Kon et al.’s (2010, 2012) studies that have demonstrated hypoxia induced greater GH responses after resistance exercise. This could be due to a lack of significant blood lactate differences observed after squat exercise between hypoxia and normoxia trials in our study. Hakkinen and Pakarinen (1993) reported high correlations between GH and blood lactate. It has been
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suggested that H+ accumulation resulted from lactate may be the primary factor stimulating GH secretions from the hypothalamus pituitary (Goto et al., 2005; Takarada et al., 2000a). Therefore, similar GH responses between hypoxia and normoxia trials could have resulted from similar blood lactate concentrations between hypoxia and normoxia trials in our study. In addition to GH responses, resistance exercise has been shown to elicit a significant increase in serum total testosterone in most studies in men (Tremblay, Copeland, & Van Helder, 2003). In our study, total testosterone significantly increased at post-exercise but returned to the pre-exercise value at 15 minutes in both trials (Figure 3(b)). No significant differences were observed between hypoxia and normoxia trials at any time point. Our results agree with Kon et al.’s (2010, 2012) studies that no significant differences in total testosterone between hypoxia and normoxia trials were observed. It is plausible that hypoxia-induced metabolic stress has no effect on total testosterone responses to resistance exercise. Cortisol is a catabolic hormone produced from the adrenal cortex in response to the stress of exercise. As a stress hormone, the degree of cortisol response to resistance exercise may depend on metabolic challenges from exercise stress (Goto et al., 2005). Metabolically demanding protocols high in total volume, moderate- to high-intensity with short rest intervals have elicited the greatest acute cortisol response (Häkkinen, & Pakarinen, 1993; Kraemer et al., 1993). Many studies have reported significant elevations in cortisol following an acute bout of resistance exercise (Häkkinen, Pakarinen, Alén, Kauhanen, & Komi, 1988; Kraemer et al., 1999). In this study, low-intensity resistance exercise, however, did not elicit an increase in cortisol concentration. Instead, cortisol concentrations were significantly lower than the pre-exercise value at post-exercise and 15 minutes of recovery in both hypoxia and normoxia trials (Figure 3(c)). The results of present study are in agreement with results from Kon et al.’s (2012) study, in which cortisol did not significantly change following moderate-intensity resistance exercise (50% of 1RM) in both hypoxic and normoxic conditions. In contrast, Kon et al. (2010) observed that cortisol significantly increased after high-intensity resistance exercise (70% of 1RM) in hypoxic conditions (FiO2 = 13%) but not in normoxic conditions. Therefore, in our study, the lower cortisol concentrations could have resulted from the metabolic stress of low-intensity squat exercise (30% of 1RM) being overwhelmed by the diurnal variation of cortisol (i.e., cortisol is at its highest level between 6–8AM and gradually falls during the day). Moreover, the metabolic stress of performing resistance exercise under mild hypoxia (FiO2 = 15%) may not be sufficient to cause greater serum cortisol in hypoxia than in normoxia. Therefore, no significant differences in cortisol between hypoxia and normoxia trials were observed in this study.
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CONCLUSION In conclusion, performing low-intensity squat exercise (30% 1RM) under mild normobaric hypoxia (FiO2 = 15%, equivalent to 2300 m altitude) did not significantly induce greater blood lactate, growth hormone, total testosterone and cortisol responses when compared with a similar exercise regimen in normoxic conditions. The results of our study suggest that the use of mild simulated hypoxia during resistance exercise may not be effective for enhancing greater anabolic hormonal responses to low-intensity resistance exercise in previously resistance untrained men. Further studies are needed for clarification regarding the effects of intensity and hypoxia severity on hypoxiainduced physiological benefits.
REFERENCES Dufour, S.P., Ponsot, E., Zoll, J., Doutreleau, S., Lonsdorfer-Wolf, E., Geny, B., Lampert, E., Fluck, M., Hoppeler, H., Billat, V., Mettauer, B., Richard, R., & Lonsdorfer, J. (2006). Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity. Journal of Applied Physiology, 100, 1238–1248. Geiser, J., Vogt, M., Billeter, R., Zuleger, C., Belforti, F., & Hoppeler, H. (2001). Training high–living low: Changes of aerobic performance and muscle structure with training at simulated altitude. International Journal of Sports Medicine, 22, 579–585. Goto, K., Ishii, N., Kizuka, T., & Takamatsu, K. (2005). The impact of metabolic stress on hormonal responses and muscular adaptations. Medicine and Science in Sports and Exercise, 37, 955–963. Häkkinen, K., Pakarinen, A., Alén, M., Kauhanen, H., & Komi, P.V. (1988). Neuromuscular and hormonal responses in elite athletes to two successive strength training sessions in one day. European Journal of Applied Physiology, 57, 133–139. Häkkinen, K., & Pakarinen, A. (1993). Acute hormonal responses to two different fatiguing heavy-resistance protocols in male athletes. Journal of Applied Physiology, 74, 882–887. Hoppeler, H., Kleinert, E., Schlegel, C., Claassen, H., Howald, H., & Cerretelli, P. (1990). Muscular exercise at high altitude: II morphological adaptation of skeletal muscle to chronic hypoxia. International Journal of Sports Medicine, 11, S3–S9. Hoppeler, H., Klossner, S., & Vogt, M. (2008). Training in hypoxia and its effects on skeletal muscle tissue. Scandinavian Journal of Medicine & Science in Sports, 18, S38–S49. Kelly, P.T., Swanney, M.P., Frampton, C., Seccombe, L.M., Peters, M.J., & Beckert, L.E. (2006). Normobaric hypoxia inhalation test vs. response to airline flight in healthy passengers. Aviation, Space, and Environmental Medicine, 77, 1143–1147.
Downloaded by [University of North Carolina] at 10:25 04 October 2014
Effects of Acute Exposure to Mild Simulated Hypoxia
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Kon, M., Ikeda, T., Homma, T., Akimoto, T., Suzuki, Y., & Kawahara, T. (2010). Effects of acute hypoxia on metabolic and hormonal responses to resistance exercise. Medicine and Science in Sports and Exercise, 42, 1279–1285. Kon, M., Ikeda, T., Homma, T., Akimoto, T., & Suzuki, Y. (2012). Effects of low intensity resistance exercise under acute systemic hypoxia on hormonal responses. Journal of Strength and Conditioning Research, 26, 611–617. Kraemer, W. J., Fleck, S. J., Dziados, J. E., et al. (1993). Changes in hormonal concentrations after different heavy-resistance exercise protocols in women. Journal of Applied Physiology, 75, 594–604. Kraemer, W.J., & Fry, A. C. (1995). Strength testing: Development and evaluation of methodology. In P.J. Maud & C. Foster (Eds.), Physiological assessment of human fitness (pp. 115–138). Champaign, IL: Human Kinetics. Kraemer, W.J., Fleck, S.J., & Evans, W.J. (1996). Strength and power training: Physiological mechanisms of adaptation. In J.O. Holloszy (Ed.), Exercise and sport science reviews (pp. 363–397). Philadelphia, PA: Williams & Wilkins. Kraemer, W.J., Fleck, S.J., Maresh, C.M., Ratamess, N.A., Gordon, S.E., Goetz K.L., et al. (1999). Acute hormonal responses to a single bout of heavy resistance exercise in trained power lifters and untrained men. Journal of Applied Physiology, 24, 524–537. Kraemer, W.J., & Ratamess, N.A. (2000). Physiology of resistance training: Current issues. In W.B. Saunders (Ed.), Orthopedics & physical therapy clinics in North America: Exercise & technology (pp. 467–513). Philadelphia, PA: W.B. Saunders. Kraemer, W.J., & Ratamess, N.A. (2003). Endocrine responses and adaptations to strength and power training. In P.V. Komi (Ed.), Strength and power in sport (pp. 361–386). Malden, MA: Blackwell Scientific Publications. MacDougall, J.D., Green, H.J., Sutton, J.R., Coates, G., Cymerman, A.Y.P., & Houston, C.S. (1991). Operation Everest II: Structural adaptations in skeletal muscle in response to extreme simulated altitude. Acta Physiologica Scandinavica, 142, 421–427. Meeuwsen, T., Hendriksen, I.J., & Holewijn, M. (2001). Training-induced increases in sea-level performance are enhanced by acute intermittent hypobaric hypoxia. European Journal of Applied Physiology, 84, 283–290. Moritani, T., Sherman, W.M., Shibata, M., Matsumoto, T., & Shinohara, M. (1992). Oxygen availability and motor unit activity in humans. European Journal of Applied Physiology and Occupational Physiology, 64, 552–556. Roels, B., Millet, G.P., Marcoux, C.J., Coste, O., Bentley, D.J., & Candau, R.B. (2005). Effects of hypoxic interval training on cycling performance. Medicine and Science in Sports and Exercise, 37, 138–146. Spiering, B.A, Kraemer, W.J., Anderson, J.M., Armstrong, L.E., Nindl, B.C., Volek, J.S., et al. (2008). Effects of elevated circulating hormones on resistance exercise-induced Akt signaling. Medicine and Science in Sports Exercise, 40, 1039–1048. Takarada, Y., Nakamura, Y., Aruga, S., Onda, T., Miyazaki, S., & Ishii, N. (2000a). Rapid increase in plasma growth hormone after low intensity resistance exercise with vascular occlusion. Journal of Applied Physiology, 88, 61–65.
Downloaded by [University of North Carolina] at 10:25 04 October 2014
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Takarada, Y., Takazawa, H., Sato, Y., Takebayashi, S., Tanaka, Y., & Ishii, N. (2000b). Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. Journal of Applied Physiology, 88, 2097–2106. Teramoto, M., & Golding, L.A. (2006). Low-intensity exercise, vascular occlusion, and muscular adaptations. Research in Sports Medicine, 14, 259–271. Tremblay, M.S., Copeland, J.L., & Van Helder, W. (2003). Effect of training status and exercise mode on endogenous steroid hormones in men. Journal of Applied Physiology, 96, 531–539. Truijens, M.J., Toussaint, H.M., Dow, J., & Levine, B.D. (2003). Effect of high-intensity hypoxic training on sea-level swimming performance. Journal of Applied Physiology, 94, 733–743. Ventura, N., Hoppeler, H., Seiler, R., Binggeli, A., Mullis, P., & Vogt, M. (2003). The response of trained athletes to six weeks of endurance training in hypoxia or normoxia. International Journal of Sports Medicine, 24, 166–172. Wilber, R.L. (2007). Introduction to altitude/hypoxic training symposium. Medicine and Science in Sports Exercise, 39, 1587–1589.
Research in Sports Medicine: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/gspm20
Effects of Acute Exposure to Mild Simulated Hypoxia on Hormonal Responses to Low-intensity Resistance Exercise in Untrained Men a
b
a
a
Jen-Yu Ho , Tai-Yu Huang , Yi-Chieh Chien , Ying-Chen Chen & Shuia
Yu Liu a
Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan b
Department of Physical Education, National Taiwan Normal University, Taipei, Taiwan Published online: 20 Jun 2014.
To cite this article: Jen-Yu Ho, Tai-Yu Huang, Yi-Chieh Chien, Ying-Chen Chen & Shui-Yu Liu (2014) Effects of Acute Exposure to Mild Simulated Hypoxia on Hormonal Responses to Low-intensity Resistance Exercise in Untrained Men, Research in Sports Medicine: An International Journal, 22:3, 240-252, DOI: 10.1080/15438627.2014.915834 To link to this article: http://dx.doi.org/10.1080/15438627.2014.915834
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Research in Sports Medicine, 22:240–252, 2014 © 2014 Taylor & Francis ISSN: 1543-8627 print/1543-8635 online DOI: 10.1080/15438627.2014.915834
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Effects of Acute Exposure to Mild Simulated Hypoxia on Hormonal Responses to Low-intensity Resistance Exercise in Untrained Men JEN-YU HO Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan
TAI-YU HUANG Department of Physical Education, National Taiwan Normal University, Taipei, Taiwan
YI-CHIEH CHIEN, YING-CHEN CHEN, and SHUI-YU LIU Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan
This study examined hormonal responses to low-intensity resistance exercise under mild simulated hypoxia. Ten resistance untrained men performed five sets of 15 repetitions of squat exercise at 30% of 1RM under normobaric hypoxia (FiO2 = 15%) and normoxia in a cross-over and counter-balanced design. Blood lactate (LAC), growth hormone (GH), total testosterone (T) and cortisol (C) were measured at pre-exercise, immediately post-exercise and 15 minutes post-exercise. LAC, GH and T significantly increased immediately after squat exercise in both trials (p < 0.05). While T returned to baseline, GH remained significantly greater at 15 minutes postexercise. Cortisol significantly decreased immediately after and 15 minutes post-exercise in both trials (p < 0.05). No significant differences were observed between two trials in LAC, GH, T and C. It was concluded that low-intensity resistance exercise performed under mild simulated hypoxia does not induce greater anabolic hormonal responses in resistance untrained men.
Received 12 October 2013; accepted 14 March 2014. This study was funded by the National Science Council in Taiwan (Grant No. NSC1002410-H-003-002) and partially supported by a grant for ‘Aim for the Top University Plan’ from National Taiwan Normal University and the Ministry of Education of Taiwan. Address correspondence to Jen-Yu Ho, Department of Athletic Performance, National Taiwan Normal University, Taipei, Taiwan. E-mail: [email protected] 240
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KEYWORDS anabolic hormones, intermittent hypoxic training, weight training
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INTRODUCTION The use of living and training at real altitude (i.e., classic altitude training) to augment endurance performance at sea level has gained popularity in endurance athletes over the past decades (Dufour et al., 2006). However, previous studies have observed muscle mass loss and decrease in muscle fiber size following long-term exposure to severe altitude (Hoppeler et al., 1990; MacDougall et al., 1991). To cope with the detrimental effects of long-term altitude training, one of the modified training regimens referring to ‘living-low and training-high, (LLTH)’ (Roels et al., 2005) or known as ‘intermittent hypoxic training’ has been developed. The LLTH applies simulated hypoxia (i.e., simulated through the use of an altitude simulation tent or room) only during all or a limited number of training sessions while subjects recover in normoxia for optimal muscle recovery. In the past two decades, LLTH has been extensively studied. While LLTH has been demonstrated to improve endurance capacity at sea level in some studies (Geiser et al., 2001; Meeuwsen, Hendriksen, & Holewijn, 2001), other studies have not observed the benefits of LLTH (Truijens, Toussaint, Dow, & Levine, 2003; Ventura et al., 2003). The physiological benefits of LLTH still remain controversial (Hoppeler, Klossner, & Vogt, 2008). Most studies that examined the effectiveness of intermittent hypoxic training have emphasized muscular adaptations observed with endurance training. Less attention has been given to examining the roles of hypoxia in other types of training modalities. Resistance training is another modality of exercise that has grown in popularity. Resistance training has been extensively studied in the past few decades, particularly for its role in improving athletic performance by increasing muscular strength, power, and hypertrophy (Kraemer & Ratamess, 2000). Resistance exercise and training have been shown to elicit significant acute hormonal responses that are critical for muscular adaptations, especially muscle hypertrophy (Kraemer & Ratamess, 2003). Some anabolic hormones, such as growth hormone, testosterone and insulin-like growth factor-I, have been significantly secreted in response to a bout of resistance exercise (Spiering et al., 2008) and play a substantial role in promoting muscle hypertrophy. It is generally accepted that intensity of 70– 80% 1RM (e.g., 6–12RM) is required to promote anabolic hormonal responses and muscle hypertrophy (Kraemer, Fleck, & Evans, 1996). In recent years, Kon et al. (2010, 2012) hypothesized that the use of systemic simulated hypoxia can further maximize the anabolic hormonal responses following resistance exercise. Their hypotheses were based on the positive results observed from occlusion training studies. Several previous
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studies have reported that low-intensity exercise combined with moderate vascular occlusion markedly induced greater growth hormone responses (Takarada et al., 2000a) and subsequently increased muscle size and strength (Takarada et al., 2000b; Teramoto & Golding, 2006). It has been suggested that local hypoxia of skeletal muscles by using blood flow restriction to the exercising muscles may result in a greater accumulation of metabolites and lead to an increase in growth hormone secretions (Goto, Ishii, Kizuka, & Takamatsu, 2005; Takarada et al., 2000a). However, it is important to note that the physiological effects of whole body exposure to systemic simulated hypoxia may be different from effects of local hypoxia of working muscles by using blood flow restriction. In agreement with their hypotheses, Kon et al. (2010, 2012) reported that performing bench press and leg press at 70% and 50% of 1RM in normobaric hypoxic conditions (FiO2 = 13%) caused greater accumulation of metabolites (i.e., blood lactate) and a greater anabolic hormone response than that in the normoxic condition. Their findings suggest that hypoxia plays an important role in enhancing the GH responses to moderate- to high-intensity resistance exercise. While performing moderate to high intensity resistance exercise is usually suggested to promote anabolic hormonal responses and muscle hypertrophy, it is unclear whether performing lowintensity resistance exercise under systemic simulated hypoxia could also produce greater anabolic hormonal responses. Further studies are required for clarification. If low-intensity resistance exercise combined with systemic simulated hypoxia can induce greater anabolic hormonal responses, this training regimen may be used in rehabilitation training programs for those who cannot perform high-intensity resistance exercise to gain muscle strength and hypertrophy. Thus, the purpose of the present study was to determine the effects of acute exposure to mild simulated hypoxia on hormonal responses to low-intensity resistance exercise.
METHODS Participants Ten healthy male subjects (age 23.6 ± 1.3 years; weight 68.2 ± 5.9 kg; 1RM 91.5 ± 11.8 kg) volunteered to participate in this study. The subjects were either completely untrained or recreationally active college students. All subjects had not been involved with any resistance training for at least 6 months prior to the study. Subjects were excluded from the study if they had any preexisting medical condition or orthopedic limitations that put them at risk while performing the squat exercises. After a detailed description of the experimental procedures and possible risks of this study was provided, subjects gave written informed consent. All procedures were approved by the University Institutional Review Board for use with human subjects.
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Experimental Design
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After the familiarization session, all subjects performed the back squat one repetition maximum (1RM) test under normoxia. Subjects then participated in two experimental trials in a cross-over and counterbalanced manner separated by one week: (1) performing acute squat exercise in mild normobaric hypoxia (FiO2 = 15%, hypoxia trial); and (2) performing acute squat exercise in normoxia (FiO2 = 21.0%, normoxia trial). In both trials, all subjects performed a low-intensity back squat (five sets of 15 repetitions at 30% of 1RM squat with 90 seconds rest between sets) followed by 15 minutes of recovery in normoxia. Blood samples were collected at pre-exercise (Pre), immediately postexercise (Post) and 15 minutes into recovery from exercise (15 min).
Squat One Repetition Maximum (1RM) Test After completing the familiarization session, all subject’s squat 1RM strength was measured in normoxia using Cybex Free Weight Squat Rack (Cybex International, Medway, MA, USA). Subjects were instructed to avoid consumption of alcohol and caffeine and intense exercise at least 48 hours before the strength test. The 1RM test used the method described by Kraemer and Fry (1995). Briefly, subjects performed back squats for 8–10 repetitions at 50% of their estimated 1RM followed by another set of 3–5 repetitions at 85% of estimated 1RM. Subsequently, three to five one repetition trials were used to determine their squat 1RM strength.
Simulated Hypoxic Exposure A hypoxia trial was performed in the hypoxic tent (FiO2 = 15%, equivalent to 2300 m altitude) (CAT-315 Walk-In Tent, Colorado Altitude Training, Louisville, CO, USA). The barometric pressure in the tent was equivalent to sea level (760 mmHg). To verify and maintain the hypoxic condition in the tent (FiO2 = 14.5%15%), the oxygen concentration was continuously monitored by using an oxygen analyzer (Handi Plus, Maxtec, Salt Lake City, UT, USA) throughout the hypoxia trial. Once the hypoxic condition in the tent was verified, subjects entered into the tent and rested for 10 minutes before performing the squat exercise in hypoxia. Arterial oxygen saturation (SpO2) was monitored by pulse oximeter (Novametrix Medical Systems, Wallingford, CT, USA). SpO2 was recorded before entering the tent, after 10 minutes of rest in the tent and immediately after the squat exercise. A normoxia trial was also performed in the tent but subjects performed the squat exercise under normoxic condition (FiO2 = 21.0%, barometric pressure was equivalent to 760 mmHg).
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Acute Squat Exercise Test All subjects were instructed to refrain from intense exercise and alcohol consumption for at least 48 hours before the squat exercise test. In the morning following 8–10 hours of overnight fasting, subjects reported to the laboratory. After 10-minute rest, the first blood draw was collected under normoxia. Subjects then warmed up for 5 minutes before the exercise test. The exercise test consisted of five sets of 15 repetitions at 30% of 1RM squat with 90 seconds rest intervals between sets. Subjects were instructed to perform the squat exercise in a smooth and controlled manner during both experimental trials. Arterial oxygen saturation (SpO2) was recorded before and after squat exercise. Subjects performed the squat exercise test under a hypoxic condition or a normoxic condition first. After one week of rest, subjects performed an exercise test again under another condition in a cross-over design. Subjects were asked to closely replicate their daily diet (from the first trial) during their second experimental trial to reduce the possible influences of diet on hormonal responses to resistance exercise.
Blood Collection and Analyses On the day of the acute squat exercise test, a pre-exercise blood sample was collected after subjects had rested quietly for 10 minutes under normoxia. Blood samples were also collected immediately post-exercise (under hypoxia during the hypoxia trial and under normoxia during the normoxia and control trials) and at 15 minutes post-exercise under normoxia. All blood samples were collected in a sitting position. Whole blood was centrifuged at 3000 RPM for 10 minutes and the resulting serum was aliquoted and stored at –80°C until subsequent analyses. Blood lactate (LAC), growth hormone (GH), total testosterone (T) and cortisol concentrations (C) were measured at a local clinical laboratory. During all trials, blood collection was standardized, being drawn in the morning (within an hour) to avoid some confounding effects from diurnal hormonal variations.
Statistical Analysis The dependent variables in this study (SpO2, LAC, GH, T and C) were analyzed using two-way repeated measures ANOVA (trial × time). All data sets satisfied statistical requirements for the linear approaches used. When a significant F score resulted, a Fisher’s least significant difference (LSD) post hoc test was used to determine the pair-wise differences between means. The test–retest reliability of the blood and 1RM tests used in this study showed intra-class Rs ≥ 0.92. The level of significance for all the tests was set at P ≤ 0.05. All data are presented as means ± standard deviation (s).
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RESULTS Arterial Oxygen Saturation (SpO2) during Squat Exercise
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SpO2 was significantly decreased during the hypoxia trial by 6.4 ± 3.6% (p < 0.001) when compared with the normoxia trial after 10 minutes rest in the tent. SpO2 remained significantly lower (p < 0.001) than the normoxia trial after squat exercise in the hypoxia trial. However, following 15 minutes of recovery in normoxia, SpO2 returned to 97.2 ± 0.4% in the hypoxia trial and were not significantly different when compared with the normoxia trial. In contrast, during the normoxia trial, SpO2 remained within 97.4–98.0% throughout the trial (Figure 1).
Blood Lactate Concentrations Figure 2 shows the blood lactate concentrations measured before and immediately after the squat exercise. Acute squat exercise significantly increased blood lactate concentrations above pre-exercise values at post-exercise (95% CI = 5.04 to 6.48) in both the hypoxia and normoxia trials (p < 0.001). However, blood lactate concentrations were not significantly different between the hypoxia and normoxia trials at any time point (p = 0.344).
Serum Hormone Concentrations Growth hormone and total testosterone significantly increased above the preexercise value at post-exercise in both the hypoxia and normoxia trials (95%
FIGURE 1 Changes in arterial oxygen saturation (SpO2) during squat exercise (mean ± s). HR = hypoxic resistance exercise; NR = normoxic resistance exercise; Rest 1 = before entering the tent; Rest 2 = after 10 minutes of rest in the tent; Post = Post-exercise; 15 min = 15 minutes of recovery in normoxia. * = p < 0.05 vs Rest 1; & = p < 0.05 vs NR
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FIGURE 2 Changes in blood lactate concentrations before and after squat exercise (mean ± s). HR = hypoxic resistance exercise; NR = normoxic resistance exercise; Pre = Pre-exercise; Post = Postexercise * = p < 0.05 vs Pre.
CI = 0.19 to 1.04 for growth hormone, 95% CI = 5.81 to 7.83 for total testosterone; p < 0.05; see Figures 3(a) and 3(b)). While total testosterone returned to pre-exercise value after 15 minutes, growth hormone remained significantly higher than pre-exercise value after 15 minutes (95% CI = 0.32 to 1.51; p = 0.020). There were no significant differences at any time point between hypoxia and normoxia trials for growth hormone and total testosterone concentrations (p > 0.05). In contrast, serum cortisol concentrations (Figure 3(c)) significantly reduced below pre-exercise value at post-exercise (95% CI = 10.15 to 12.43) and remained significantly lower than pre-exercise after 15 minutes (95% CI = 9.19 to 12.25) in both trials (p < 0.05). However, cortisol concentrations were not significantly different between the hypoxia and normoxia trials at any time point (p = 0.505).
DISCUSSION The major finding of the present study was that the low-intensity squat exercise (30% of 1RM) performed under mild simulated hypoxia (FiO2 = 15%) did not significantly induce greater hormonal responses in growth hormone, total testosterone and cortisol than that of normoxia. While Kon et al. (2010, 2012) have demonstrated significant hypoxia-induced effects on hormonal responses to moderate- to high-intensity resistance exercise under more severe hypoxia, our data suggest that resistance exercise intensity and hypoxia severity may play a role in inducing the physiological benefits when performing resistance exercises under hypoxia.
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FIGURE 3 Changes in (a) growth hormone concentrations (b) total testosterone concentrations (c) cortisol concentrations before and after squat exercise (mean ± s). HR = hypoxic resistance exercise; NR = normoxic resistance exercise; Pre = Pre-exercise; Post = Postexercise; 15 min = 15 minutes of recovery in normoxia. * = p < 0.05 vs Pre.
During the hypoxia trial, SpO2 significantly decreased to 91.4% and remained lower than baseline values throughout the hypoxia trial. In contrast, during the normoxia trial, SpO2 remained the same within 97.4–98.0% throughout the trial (Figure 1). Previous research reported that SpO2 decreased from 98% to 92% after hypoxia inhalation testing with inspired oxygen of 15% (Kelly et al., 2006). The SpO2 data of this study ensured that subject’s exposure to hypoxia was correctly controlled during the hypoxia trial. Previous studies have shown that exercise-induced metabolic stress is positively associated with accumulation of blood lactate following exercise (Goto et al., 2005). Resistance exercise of moderate- to high-intensity may be necessary to induce greater metabolic stress and blood lactate accumulation. However, when resistance exercise is performed in hypoxic conditions, highintensity exercise and associated recruitment of fast-twitch fibers would not be necessarily required for regional accumulation of lactate (Moritani, Sherman, Shibata, Matsumoto, & Shinohara, 1992). Several recent studies that combined low-intensity resistance exercise (20%1RM) with moderate vascular occlusion
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have demonstrated greater accumulation of blood lactate (Takarada et al., 2000a). In addition, Kon et al. (2010, 2012) have also reported higher blood lactate concentrations following resistance exercise in systemic hypoxic conditions than in normoxic conditions. In the present study, despite the fact that blood lactate concentrations significantly increased after the squat exercise in both trials, blood lactate concentrations were not significantly different between hypoxia and normoxia trials (Figure 2). The conflicting results between our study and previous studies could be due to differences in experimental design, including resistance exercise intensity and hypoxia severity. In the studies conducted by Kon et al. (2010, 2012), resistance exercise was performed at higher intensity (50% and 70% of 1RM) under more severe hypoxic conditions (FiO2 = 13%) when compared with the research design we used (30% of 1RM; FiO2 = 15%). In our study, lowintensity at 30% of 1RM was used to examine whether systemic hypoxia can mimic vascular occlusion in inducing greater blood lactate responses following low-intensity resistance exercise. In addition, Kon et al. have observed beneficial effects on blood lactate responses when performing moderate- to high-intensity resistance exercise under systemic hypoxia. Further investigation is warranted as to whether performing low-intensity resistance exercise under systemic hypoxia could also produce positive effects. Based on our findings, it is possible that when applying systemic hypoxia, low-intensity resistance exercise may have not been sufficient to cause hypoxia-induced effects on muscle recruitment and associated accumulation of blood lactate. Moreover, hypoxia severity may also play a role. A mild hypoxic condition of FiO2 = 15% (equivalent to 2300 m altitude) was used in this study because exercise training, preferably at 2000–2500 m above sea level, has been commonly suggested when performing hypoxic training (Wilber, 2007). Based on our findings, it is plausible that a severe hypoxic condition is required to recruit more fast-twitch fibers and lead to greater regional accumulation of blood lactate. More studies are warranted to examine further the potential influence of resistance exercise intensity and hypoxia severity on hypoxiainduced physiological benefits. Growth hormone (GH) is an important anabolic hormone mediating muscle hypertrophy following resistance training (Kraemer & Ratamess, 2003). In the present study, we showed GH increased immediately after exercise and remained greater at 15 minutes post-exercise in both trials (Figure 3(a)). However, GH responses were not significantly greater in hypoxic condition than in normoxic condition. Our results are in contrast to Kon et al.’s (2010, 2012) studies that have demonstrated hypoxia induced greater GH responses after resistance exercise. This could be due to a lack of significant blood lactate differences observed after squat exercise between hypoxia and normoxia trials in our study. Hakkinen and Pakarinen (1993) reported high correlations between GH and blood lactate. It has been
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suggested that H+ accumulation resulted from lactate may be the primary factor stimulating GH secretions from the hypothalamus pituitary (Goto et al., 2005; Takarada et al., 2000a). Therefore, similar GH responses between hypoxia and normoxia trials could have resulted from similar blood lactate concentrations between hypoxia and normoxia trials in our study. In addition to GH responses, resistance exercise has been shown to elicit a significant increase in serum total testosterone in most studies in men (Tremblay, Copeland, & Van Helder, 2003). In our study, total testosterone significantly increased at post-exercise but returned to the pre-exercise value at 15 minutes in both trials (Figure 3(b)). No significant differences were observed between hypoxia and normoxia trials at any time point. Our results agree with Kon et al.’s (2010, 2012) studies that no significant differences in total testosterone between hypoxia and normoxia trials were observed. It is plausible that hypoxia-induced metabolic stress has no effect on total testosterone responses to resistance exercise. Cortisol is a catabolic hormone produced from the adrenal cortex in response to the stress of exercise. As a stress hormone, the degree of cortisol response to resistance exercise may depend on metabolic challenges from exercise stress (Goto et al., 2005). Metabolically demanding protocols high in total volume, moderate- to high-intensity with short rest intervals have elicited the greatest acute cortisol response (Häkkinen, & Pakarinen, 1993; Kraemer et al., 1993). Many studies have reported significant elevations in cortisol following an acute bout of resistance exercise (Häkkinen, Pakarinen, Alén, Kauhanen, & Komi, 1988; Kraemer et al., 1999). In this study, low-intensity resistance exercise, however, did not elicit an increase in cortisol concentration. Instead, cortisol concentrations were significantly lower than the pre-exercise value at post-exercise and 15 minutes of recovery in both hypoxia and normoxia trials (Figure 3(c)). The results of present study are in agreement with results from Kon et al.’s (2012) study, in which cortisol did not significantly change following moderate-intensity resistance exercise (50% of 1RM) in both hypoxic and normoxic conditions. In contrast, Kon et al. (2010) observed that cortisol significantly increased after high-intensity resistance exercise (70% of 1RM) in hypoxic conditions (FiO2 = 13%) but not in normoxic conditions. Therefore, in our study, the lower cortisol concentrations could have resulted from the metabolic stress of low-intensity squat exercise (30% of 1RM) being overwhelmed by the diurnal variation of cortisol (i.e., cortisol is at its highest level between 6–8AM and gradually falls during the day). Moreover, the metabolic stress of performing resistance exercise under mild hypoxia (FiO2 = 15%) may not be sufficient to cause greater serum cortisol in hypoxia than in normoxia. Therefore, no significant differences in cortisol between hypoxia and normoxia trials were observed in this study.
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CONCLUSION In conclusion, performing low-intensity squat exercise (30% 1RM) under mild normobaric hypoxia (FiO2 = 15%, equivalent to 2300 m altitude) did not significantly induce greater blood lactate, growth hormone, total testosterone and cortisol responses when compared with a similar exercise regimen in normoxic conditions. The results of our study suggest that the use of mild simulated hypoxia during resistance exercise may not be effective for enhancing greater anabolic hormonal responses to low-intensity resistance exercise in previously resistance untrained men. Further studies are needed for clarification regarding the effects of intensity and hypoxia severity on hypoxiainduced physiological benefits.
REFERENCES Dufour, S.P., Ponsot, E., Zoll, J., Doutreleau, S., Lonsdorfer-Wolf, E., Geny, B., Lampert, E., Fluck, M., Hoppeler, H., Billat, V., Mettauer, B., Richard, R., & Lonsdorfer, J. (2006). Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity. Journal of Applied Physiology, 100, 1238–1248. Geiser, J., Vogt, M., Billeter, R., Zuleger, C., Belforti, F., & Hoppeler, H. (2001). Training high–living low: Changes of aerobic performance and muscle structure with training at simulated altitude. International Journal of Sports Medicine, 22, 579–585. Goto, K., Ishii, N., Kizuka, T., & Takamatsu, K. (2005). The impact of metabolic stress on hormonal responses and muscular adaptations. Medicine and Science in Sports and Exercise, 37, 955–963. Häkkinen, K., Pakarinen, A., Alén, M., Kauhanen, H., & Komi, P.V. (1988). Neuromuscular and hormonal responses in elite athletes to two successive strength training sessions in one day. European Journal of Applied Physiology, 57, 133–139. Häkkinen, K., & Pakarinen, A. (1993). Acute hormonal responses to two different fatiguing heavy-resistance protocols in male athletes. Journal of Applied Physiology, 74, 882–887. Hoppeler, H., Kleinert, E., Schlegel, C., Claassen, H., Howald, H., & Cerretelli, P. (1990). Muscular exercise at high altitude: II morphological adaptation of skeletal muscle to chronic hypoxia. International Journal of Sports Medicine, 11, S3–S9. Hoppeler, H., Klossner, S., & Vogt, M. (2008). Training in hypoxia and its effects on skeletal muscle tissue. Scandinavian Journal of Medicine & Science in Sports, 18, S38–S49. Kelly, P.T., Swanney, M.P., Frampton, C., Seccombe, L.M., Peters, M.J., & Beckert, L.E. (2006). Normobaric hypoxia inhalation test vs. response to airline flight in healthy passengers. Aviation, Space, and Environmental Medicine, 77, 1143–1147.
Downloaded by [University of North Carolina] at 10:25 04 October 2014
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Kon, M., Ikeda, T., Homma, T., Akimoto, T., Suzuki, Y., & Kawahara, T. (2010). Effects of acute hypoxia on metabolic and hormonal responses to resistance exercise. Medicine and Science in Sports and Exercise, 42, 1279–1285. Kon, M., Ikeda, T., Homma, T., Akimoto, T., & Suzuki, Y. (2012). Effects of low intensity resistance exercise under acute systemic hypoxia on hormonal responses. Journal of Strength and Conditioning Research, 26, 611–617. Kraemer, W. J., Fleck, S. J., Dziados, J. E., et al. (1993). Changes in hormonal concentrations after different heavy-resistance exercise protocols in women. Journal of Applied Physiology, 75, 594–604. Kraemer, W.J., & Fry, A. C. (1995). Strength testing: Development and evaluation of methodology. In P.J. Maud & C. Foster (Eds.), Physiological assessment of human fitness (pp. 115–138). Champaign, IL: Human Kinetics. Kraemer, W.J., Fleck, S.J., & Evans, W.J. (1996). Strength and power training: Physiological mechanisms of adaptation. In J.O. Holloszy (Ed.), Exercise and sport science reviews (pp. 363–397). Philadelphia, PA: Williams & Wilkins. Kraemer, W.J., Fleck, S.J., Maresh, C.M., Ratamess, N.A., Gordon, S.E., Goetz K.L., et al. (1999). Acute hormonal responses to a single bout of heavy resistance exercise in trained power lifters and untrained men. Journal of Applied Physiology, 24, 524–537. Kraemer, W.J., & Ratamess, N.A. (2000). Physiology of resistance training: Current issues. In W.B. Saunders (Ed.), Orthopedics & physical therapy clinics in North America: Exercise & technology (pp. 467–513). Philadelphia, PA: W.B. Saunders. Kraemer, W.J., & Ratamess, N.A. (2003). Endocrine responses and adaptations to strength and power training. In P.V. Komi (Ed.), Strength and power in sport (pp. 361–386). Malden, MA: Blackwell Scientific Publications. MacDougall, J.D., Green, H.J., Sutton, J.R., Coates, G., Cymerman, A.Y.P., & Houston, C.S. (1991). Operation Everest II: Structural adaptations in skeletal muscle in response to extreme simulated altitude. Acta Physiologica Scandinavica, 142, 421–427. Meeuwsen, T., Hendriksen, I.J., & Holewijn, M. (2001). Training-induced increases in sea-level performance are enhanced by acute intermittent hypobaric hypoxia. European Journal of Applied Physiology, 84, 283–290. Moritani, T., Sherman, W.M., Shibata, M., Matsumoto, T., & Shinohara, M. (1992). Oxygen availability and motor unit activity in humans. European Journal of Applied Physiology and Occupational Physiology, 64, 552–556. Roels, B., Millet, G.P., Marcoux, C.J., Coste, O., Bentley, D.J., & Candau, R.B. (2005). Effects of hypoxic interval training on cycling performance. Medicine and Science in Sports and Exercise, 37, 138–146. Spiering, B.A, Kraemer, W.J., Anderson, J.M., Armstrong, L.E., Nindl, B.C., Volek, J.S., et al. (2008). Effects of elevated circulating hormones on resistance exercise-induced Akt signaling. Medicine and Science in Sports Exercise, 40, 1039–1048. Takarada, Y., Nakamura, Y., Aruga, S., Onda, T., Miyazaki, S., & Ishii, N. (2000a). Rapid increase in plasma growth hormone after low intensity resistance exercise with vascular occlusion. Journal of Applied Physiology, 88, 61–65.
Downloaded by [University of North Carolina] at 10:25 04 October 2014
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Takarada, Y., Takazawa, H., Sato, Y., Takebayashi, S., Tanaka, Y., & Ishii, N. (2000b). Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. Journal of Applied Physiology, 88, 2097–2106. Teramoto, M., & Golding, L.A. (2006). Low-intensity exercise, vascular occlusion, and muscular adaptations. Research in Sports Medicine, 14, 259–271. Tremblay, M.S., Copeland, J.L., & Van Helder, W. (2003). Effect of training status and exercise mode on endogenous steroid hormones in men. Journal of Applied Physiology, 96, 531–539. Truijens, M.J., Toussaint, H.M., Dow, J., & Levine, B.D. (2003). Effect of high-intensity hypoxic training on sea-level swimming performance. Journal of Applied Physiology, 94, 733–743. Ventura, N., Hoppeler, H., Seiler, R., Binggeli, A., Mullis, P., & Vogt, M. (2003). The response of trained athletes to six weeks of endurance training in hypoxia or normoxia. International Journal of Sports Medicine, 24, 166–172. Wilber, R.L. (2007). Introduction to altitude/hypoxic training symposium. Medicine and Science in Sports Exercise, 39, 1587–1589.
