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1007/s00421-012-2487-5
ORIGINAL ARTICLE
Received: 24 April 2012 / Accepted: 29 August 2012 / Published online: 13 September 2012 Springer-Verlag 2012
Abstract Exercise is a potent stimulus for release of growth hormone (GH), cortisol, testosterone and prolactin, and prolonged exercise inhibits insulin secretion. These responses seem to be specic to the type of exercise but this has been poorly characterised primarily because they have not been compared during exercise performed by the same individuals. We investigated hormone responses to resistance, sprint and endurance exercise in young men using a repeated measures design in which each subject served as their own control. Eight healthy non-obese young adults (1825 years) were studied on four occasions in random order: 30-s cycle ergometer sprint (Sprint), 30-min resistance exercise bout (Resistance), 30-min cycle at 70 % VO2max (Endurance), and seated rest in the laboratory (Rest). Cortisol, GH, testosterone, prolactin, insulin and glucose concentrations were measured for 60 min after the four different interventions. Endurance and sprint exercise signicantly increased GH, cortisol, prolactin and testosterone. Sprint exercise also increased insulin concentrations, whereas this decreased in response to endurance exercise. Resistance exercise signicantly increased only
testosterone and glucose. Sprint exercise elicited the largest response per unit of work, but the smallest response relative to mean work rate in all hormones. In conclusion, the nature and magnitude of the hormone response were inuenced by exercise type, perhaps reecting the roles of these hormones in regulating metabolism during and after resistance, sprint and endurance exercise. Keywords Exercise Cortisol Growth hormone Prolactin Insulin
Introduction There has been a great deal of interest in the impact of different types of exercise on health, and benecial roles of sprint exercise (Richards et al. 2010; Whyte et al. 2010) and resistance exercise (Breen et al. 2011) for metabolic health have been identied alongside the traditionally accepted benets of sustained exercise (Garber et al. 2011). This is important in the context of promoting physical activity and exercise options that individuals enjoy and to which they will adhere, since different types of exercise appeal to different people. For example, high intensity interval exercise has been reported to be preferred over continuous exercise in recreationally active men (Bartlett et al. 2011) and individuals with coronary heart disease (Guiraud et al. 2011). Understanding the physiological responses to different types of exercise is also important for identifying ways to maximise their benecial effects. In addition, this knowledge will be helpful in determining what changes should be made in hormones such as insulin and cortisol in patients with conditions such as Type 1 diabetes and/or Addisons disease to best mimic normal responses to different forms of exercise.
Communicated by Fabio Fischetti. K. A. Stokes (&) K. L. Gilbert D. Thompson Department for Health, University of Bath, Claverton Down, Bath BA2-7AY, UK e-mail: k.stokes@bath.ac.uk G. M. Hall Anaesthesia and Intensive Care Medicine, St Georges, University of London, SW17-0RE, London, UK R. C. Andrews Diabetes and Metabolism, School of Clinical Sciences, Learning and Research, Southmead Hospital, University of Bristol, Bristol BS10-5NB, UK
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Physical exertion can elicit marked elevations in growth hormone (GH), prolactin, testosterone and cortisol, and prolonged exercise results in a decrease in circulating insulin concentrations (Galbo 1985). The magnitude of the hormone response is inuenced by factors such as duration, intensity (Brandenberger and Follenius 1975; Felsing et al. 1992) and type (e.g. resistance, sprint, endurance) of exercise (Kraemer et al. 1990; Pritzlaff et al. 1999; Few 1974). Hence, it is likely that the different and specic metabolic demands of resistance, sprint and endurance exercise inuence the hormone responses to these exercise bouts. Characterising these responses is an important step in improving understanding of the roles of exerciseinduced hormone release. There is a large degree of inter-individual variability in hormone responses to exercise, even when individuals are homogenous for age, gender, mass and physical tness (Stokes 2003; Galbo 1985). In this context, it is difcult to know whether previous descriptions of hormone responses to one specic type of exercise can be compared with another, that is, whether any differences are genuine differences in the hormone response, or an artefact of comparing different individuals between studies. To our knowledge, no research has investigated the hormone responses to sprint, resistance, and endurance exercise within the same group of individuals to establish whether the specic metabolic demands of these exercise types impact upon hormone responses. The GH response to resistance and endurance exercise within the same individual has been studied, but the response to sprint exercise was not addressed (Consitt et al. 2007; Kindermann et al. 1982) and the effect of these exercise bouts on other hormones that might inuence metabolism was not studied (Consitt et al. 2007; Gilbert et al. 2008). The aim of this study was to characterise the response of selected hormones to three bouts of exercise with very different metabolic demands (resistance, sprint and endurance exercise) performed by the same individuals.
written and oral information about the protocol. The study was approved by the NHS Local Research Ethics Committee and was carried out according to the Declaration of Helsinki. Design The study was a repeated measures design with one study group completing four trials (resistance, sprint, endurance, rest). Trial order was randomised using a latin square, with participants nding out on the day which trial they would be performing. Each trial was separated by at least 7 days. Preliminary testing Subjects attended the laboratory on two separate occasions for preliminary tests. Each subjects one repetition maximum (1RM) was determined using a Concept-2 DYNO (Nottingham, UK) for: seated bench press, leg press and seated bench pull. On a second visit, subjects practised working against a resistance equivalent to 75 % of their 1RM, during a set of 10 repetitions of each of the exercises. In the second visit (prior to the resistance exercise), subjects also completed an incremental submaximal exercise test to determine the relationship between work rate and oxygen uptake, followed by an incremental test to exhaustion to determine each subjects maximal oxygen _ O2max). Both tests were carried out on a cycle uptake (V ergometer (Monark, 824 E, Sweden). In the submaximal test, subjects cycled continuously at 60 pedal revolutions per minute at four progressively higher exercise intensities (applied resistance of 1.5, 2.0, 2.5 and 3.0 kg) with each stage lasting 4 min. Expired gas samples were collected in the nal minute of each stage. In the maximal test, subjects cycled continuously at 60 pedal revolutions per minute at progressively higher exercise intensities with each stage lasting 3 min. The starting load was based on heart rate data from the submaximal test and the applied resistance was increased by 0.5 kg every 3 min such that the test lasted between 9 and 12 min. Expired gas samples were taken in the last minute of each stage and for a nal minute when the subject signalled that they could only manage one _ O2 more minute. From these data (the work rate vs. V _ relationship from the submaximal test and V O2max from the maximal test), the work rate required to obtain an exercise _ O2maxwas calculated. During intensity equivalent to 70 % V this visit, subjects were also familiarised with a 30-s sprint protocol on a cycle ergometer (Monark, 824 E, Sweden). Experimental protocol On the morning of each trial, subjects arrived following an overnight fast. Subjects recorded their dietary intake in
Methods Subjects Eight healthy men aged 1825 [mean (SD); 22 (1) year, mass _ O2max 53 (6) ml kg-1 min-1], who were 84 (15) kg, V recreationally active but not trained in any specic sport, volunteered to participate in this study. Subjects were excluded from the investigation if they smoked, took regular prescribed medication, had ever received endocrine therapy, had experienced recent weight gain/loss, or were shift workers. All subjects gave informed consent after receiving
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Analytical methods Whole blood glucose was immediately determined (YSI 2300 STAT plus, Yellow Springs, Ohio, USA), and the remaining blood dispensed into serum tubes and refrigerated for 60 min before centrifugation (Heraeus Biofuge Primo R, Kendro Laboratory Products Plc., Bishops Stortford, England) at 5,000g for 10 min at 4 C. Serum was frozen at -80 C for subsequent analysis for concentrations of GH, cortisol, prolactin, insulin and testosterone by routine ELISA (Diagnostic System Laboratories Inc., Webster, TX, USA): GH (DSL-10-1900; standards and controls were calibrated to the World Health Organisation International Reference Reagent for GH 88/624) intra-assay precision coefcient of variation (CV) \ 4.3 %, inter-assay precision CV \ 6.6 %; prolactin (DSL-104500) intra-assay CV \ 8.2 % inter-assay CV \ 10.4 %; testosterone (DSL-10-4000) intra-assay CV \ 6.8 %, interassay CV \ 4.9 %; cortisol (DSL-10-2000) intra-assay CV \ 6.2 %. Insulin concentrations were determined using RIA (Diagnostic System Laboratories Inc., Webster, TX, USA; DSL-1600), intra-assay CV \ 8.3 %. Statistical analysis All data are presented as mean (SD). Area under curve (AUC) was calculated using the trapezoid method for 70-min from the pre-exercise sample. This time period incorporated the exercise bout plus 40 min of recovery for the resistance and endurance trials and the exercise bout plus 60 min of recovery in the sprint trial. Due to the disparity in exercise time and work done in the three exercise trials, AUC was also adjusted for the total work completed (kJ) in each trial and the work rate (W) in each trial. Data were analysed using SPSS version 10 (SPSS Inc., Chicago, USA). One-way analysis of variance (ANOVA) with repeated measures was used to investigate the differences in AUC and adjusted AUC between trials. Two-way ANOVA was used to investigate differences in pre-exercise to peak/nadir concentrations of hormones between trials. Signicant effects were followed up using Bonferroni adjusted t tests. Signicance was accepted at P B 0.05.
the 48 h before the rst trial and reproduced this diet prior to subsequent trials. Participants refrained from consuming alcohol for 24 h and performing strenuous exercise in the 48 h before each trial. On arrival at the laboratory, a cannula (BD Venon Pro, Beckton Dickinson & Co., Sweden) was inserted into an antecubital forearm vein for blood sampling. The cannula was kept patent by periodic ushing with isotonic saline. A resting blood sample was taken with the subject in a seated position at least 30 min after cannula insertion, just before the warm-up. Further blood samples were taken in a seated position immediately post-exercise, and 20, 40 and 60 min post-exercise (Fig. 1). In the resistance trial, subjects completed a warm-up (4-min treadmill walk at 5 km h-1 and self-selected stretches) before commencing the resistance exercise. Resistance exercise lasted 30 min. Subjects completed ve sets, with each set comprising 10 repetitions at 75 % 1RM for seated bench press, followed by leg press, followed by seated bench pull, with a 60 s rest between exercises and 180 s of rest between sets. An estimate of total work performed (kJ) during the trial was calculated by the sum of the force exerted (N) multiplied by the distance (m) for each repetition. Work rate (W) was calculated by dividing total work performed by the time spent carrying out the exercise (8 min). In the sprint trial, subjects performed a warm-up (cycling for 4 min at 60 W, 30 s at 80 W, and then 30 s at 100 W) on a friction-loaded cycle ergometer. Following a 5-min rest period, an all-out 30-s sprint from a rolling start was performed against an applied resistance equivalent to 7.5 % (75 N/kN) of the subjects body mass as previously described (Stokes et al. 2008). In the endurance trial, subjects cycled for 30 min at a pedal cadence of 60 rpm against a resistance required to elicit a _ O2max. Work performed work rate equivalent to 70 % V was calculated using the applied resistance and the distance covered (ywheel circumference multiplied by ywheel revolutions). In the rest trial, subjects rested in the laboratory in a seated position for the duration of the trial.
Results Serum hormones Growth hormone concentrations were signicantly different between trials (P = 0.034) and over time (P = 0.002). There was also a different pattern of GH concentrations between trials (interaction; P = 0.050). Post hoc t tests
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Fig. 2 Serum GH (a), prolactin (b), testosterone (c), cortisol (d) and insulin (e) and blood glucose (f) concentrations during the rest (open diamonds), resistance (lled diamonds), sprint (lled squares) and endurance (lled triangles) trials. Letters identify signicant
differences between pre-exercise and maximum change from preexercise in the resistance (a), sprint (b), endurance (c) trials and from peak to nadir values in the sprint trial (d)
revealed a signicant increase from pre-exercise to peak GH concentrations in response to both sprint (P = 0.014) and endurance (P = 0.009) exercise (Fig. 2a). There was a signicant trial effect for GH AUC, and post hoc t tests
revealed signicantly greater GH AUC in the endurance trial compared to both resistance (P = 0.014) and rest (P = 0.024) trials (Table 1), but no signicant difference between sprint and endurance trials.
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Table 1 Hormone responses to different exercise bouts. Data displayed as AUC (units per 70 min), AUC/kJ (hormone response per unit of work performed in trial) and AUC/W (hormone response relative to mean work rate in each trial) Rest GH (ug/L/70 min) AUC AUC/kJ AUC/W Prolactin (mIU/L/70 min) AUC AUC/kJ AUC/W Insulin (mU/L/70 min) AUC AUC/kJ AUC/W AUC AUC/kJ AUC/W Cortisol (nmol/L/70 min) AUC AUC/kJ AUC/W
a b c d
Resistance
Sprint
Endurance
232 (332) 4.3 (6.9) 2.1 (3.3) 15,782 (6049) 262 (137) 126 (66)c
a
401 (264) 19.7 (14.1) 0.6 (0.4) 24,204 (9,948)b,d 1191 (527) 36 (15)
a,b a
758 (498)b,d 2.3 (1.7) 4.1 (3.0)c 17,720 (5,627) 52 (17) 94 (31)c 261 (157) 0.8 (0.5) 1.4 (0.9)c 1807 (304) 5.3 (1.4) 9.5 (2.5)c 35,979 (7,081)b,d 104 (29) 188 (52)c
537 (323)a 26.7 (18)a,b 0.8 (0.5) 1,626 (287) 78.5 (19.2)a,b 2.4 (0.6) 34,459 (10,223)d 1,681 (642) 50 (19)
a,b
Testosterone (nmol/L/70 min) 1,709 (346) 27.9 (9.7)a 13.4 (4.6)a,c 28,485 (8,381) 467 (209)
a
224 (100)c
Signicantly greater than endurance trial (P \ 0.05) Signicantly greater than resistance trial (P \ 0.05) Signicantly greater than sprint trial (P \ 0.05) Signicantly greater than rest trial (P \ 0.05)
Prolactin concentrations were signicantly different between trials (P = 0.004), but there was no main effect of time (P = 0.076). There was a different pattern of prolactin concentrations between trials (interaction; P = 0.007) and post hoc t tests revealed a signicant elevation from pre-exercise to peak prolactin concentrations in response to both sprint (P = 0.050) and endurance (P = 0.003) exercise (Fig. 2b). There was a signicant trial effect for prolactin AUC, and post hoc t tests revealed signicantly greater prolactin AUC in the sprint trial compared to the rest (P = 0.035) and resistance (P = 0.032) trials (Table 1). Prolactin AUC was not signicantly different in sprint and endurance trials. Testosterone concentrations were not different between trials (P = 0.373), but there was a change over time (P \ 0.001) and this change was different between trials (interaction; P = 0.002). Post hoc t tests revealed a signicant elevation from pre-exercise to peak testosterone concentrations in response to resistance (P = 0.020), sprint (P = 0.001) and endurance (P = 0.002) exercise (Fig. 2c). There were no signicant differences in testosterone AUC between trials (Table 1).
Cortisol concentrations were signicantly different between trials (P = 0.006) and there was a change over time (P = 0.003). There was also a different pattern of response between trials (interaction; P \ 0.001), and post hoc tests revealed a signicant elevation from pre-exercise to peak cortisol concentration in response to sprint (P = 0.004) and endurance (P = 0.001) exercise (Fig. 2d). There was a signicant trial effect cortisol AUC, and post hoc t tests revealed a signicantly greater cortisol AUC in the endurance trial compared to both rest (P \ 0.001) and resistance (P = 0.022) trials. The sprint trial also resulted in signicantly greater cortisol AUC than rest (P \ 0.001; Table 1), but the response to sprint exercise was not signicantly different from responses to resistance or endurance exercise. Insulin concentrations were signicantly different between trials (P = 0.001) and there was a change over time (P = 0.001). There was also a different pattern of response between trials (interaction; P = 0.001), and post hoc tests revealed a signicant elevation from pre-exercise to peak insulin concentrations in response to sprint (P = 0.051) exercise, and a signicant decrease from
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pre-exercise insulin to nadir (P = 0.031) in the endurance trial (Fig. 2e). There was a signicant trial effect for insulin AUC, and post hoc t tests revealed that both sprint and resistance exercise elicited a signicantly greater insulin response than endurance exercise (P = 0.016 and P = 0.03, respectively; Table 1). Due to limited sample volume, no insulin data are available for the rest trial. When data were presented per unit of work completed in each trial, the sprint trial elicited the greatest response for all hormones measured, and the endurance trial elicited the smallest response for all hormones measured (Table 1). When data were corrected for work rate within the three exercise bouts, sprint exercise elicited the smallest response in all hormones measured. Resistance exercise elicited the greatest response per Watt for prolactin, testosterone, insulin and cortisol with endurance eliciting the largest GH response (Table 1). Blood glucose Glucose concentrations were not different between trials (P = 0.135), but there was a change over time (P \ 0.001) and the pattern of change was different between trials (interaction; P = 0.001). Post hoc tests revealed a signicant elevation from pre-exercise to peak glucose concentrations in response to sprint (P \ 0.001) and resistance exercise (both P = 0.026) and a signicant decrease from peak to nadir glucose concentrations in response to sprint (P = 0.016) exercise (Fig. 2f). There were no signicant differences in glucose AUC between trials. Work performed, work rate and intensity Total work performed during the endurance trial [351 (39) kJ] was signicantly greater than that performed during both the resistance [64 (11) kJ; P \ 0.001] and sprint [21 (3) kJ; P \ 0.001] trials, and the resistance trial involved signicantly more work than the sprint trial (P \ 0.001). Mean work rate during the sprint trial [706 (96) W] was signicantly greater than during both the resistance [133 (24) W; P \ 0.001] and endurance [195 (21); P \ 0.001] trials, and the endurance trial was also performed at a signicantly higher intensity than the resistance trial (P = 0.001). Plasma volume changes Data were not corrected for changes in plasma volume. The greatest changes were observed between pre-exercise and 30 min after the start of exercise (-16, -16, -18 and -4 % in resistance, sprint, endurance, and rest trials, respectively). By 60 min after the start of exercise, plasma volume had returned to approximate values seen pre-exercise (0, 0, -1 and -2 % in resistance, sprint, endurance, and rest trials, respectively).
Discussion The aim of this study was to investigate the hormone responses induced by resistance, sprint and endurance exercise in the same individuals. The main nding was that sprint and endurance exercise elicited a signicant response in all of the hormones studied, whereas resistance exercise only elicited changes in testosterone concentrations. The different types of exercise employed in this study were designed to have very different characteristics in terms of the amount of work done and work rate and they elicited different hormone responses, pointing towards the hormone response to exercise being specic to the metabolic demands of the exercise stimulus. The ndings also suggest that approaches to hormone administration in patients with Type 1 Diabetes and/or Addisons disease should be considered with reference to the specic exercise being undertaken. The starkest difference in any response to the different types of exercise is for insulin. A single 30-s sprint elicited an increase in insulin concentrations, whereas 30 min of sub-maximal cycling resulted in a decrease in insulin concentrations. This supports previous reports that exercise stimulates either an increase or decrease in insulin concentrations depending on the metabolic demands of the exercise bout (Kindermann et al. 1982). During submaximal exercise with stable or decreasing blood glucose concentrations, as seen in the endurance trial in the present study, insulin concentrations decrease probably as a result of elevated catecholamine concentrations (Wasserman and Cherrington 1991) to ensure that the body preserves enough glycogen to maintain function beyond the demands of exercise. Increased insulin concentrations as seen following the sprint trial, and in a previous study (Stokes et al. 2002), might facilitate muscle glycogen synthesis during recovery through insulins actions on both glucose transport and on glycogen synthase activity. The signicant increase in insulin concentrations following sprint exercise in the present study is followed by a suppression of blood glucose concentrations to levels below pre-exercise. This nding might have implications for individuals who have difculty regulating blood glucose concentrations, such as individuals with impaired glucose tolerance. In this context, it is of note that as little as 2 weeks of sprint training has been shown to improve insulin sensitivity in healthy (Richards et al. 2010) as well as sedentary overweight/ obese (Whyte et al. 2010) individuals. Similarly, a role for sprint exercise in protecting against a fall in blood glucose concentrations during subsequent endurance exercise in those with Type I diabetes has been proposed (Bussau et al. 2007). Cortisol and growth hormone responses to exercise have been reported to be related to exercise intensity
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(Kindermann et al. 1982; Wahl et al. 2010). The present study was designed to harness the large differences in factors such as total work done, work rate and the metabolic demand between resistance, sprint and endurance exercise. Our ndings suggest that the hormone response is associated with the specic demands of a given exercise bout, and in order to try to account for the differences in total work performed and work rate in the exercise bouts, AUC was adjusted for these factors. Differences between trials remained when these adjustments were made, suggesting that although work done and work rate are important in regulating exercise-induced hormone release, there are other factors that play a role. In this context, it is notable that peak concentrations of both cortisol and growth hormone were observed at the end of endurance exercise, when insulin was lower than pre-exercise and blood glucose concentrations were stable. These combined responses likely promote the availability of free fatty acids toward the end of exercise and into recovery via increased lipolysis. In contrast, peak cortisol and growth hormone concentrations occurred 3040 min after sprint exercise, when insulin had returned to pre-exercise concentrations but glucose concentrations were falling. These ndings support the notion of co-ordinated primary counter-regulatory roles against insulin for both cortisol and growth hormone in the exercise context, and it is possible that these hormones have important roles to play in the regulation of post-exercise substrate utilisation (Pritzlaff et al. 2000). The present ndings also suggest that the pituitary hormones respond to a specic demand induced by the exercise bout rather than exercise acting as a stimulus for a global hypothalamic-pituitary stress response. The evidence for this is that endurance exercise stimulated the greatest release of GH while sprint exercise stimulated the greatest release of prolactin. Prolactin has previously been reported to have a pronounced response to short duration high intensity exercise, but not to endurance exercise unless it is of long duration (Rojas Vega et al. 2012). It would be interesting to carry out an investigation similar to the present study in untrained and highly trained individuals, since it is possible that a generalised stress response would be observed in untrained individuals, and a response that is more specic to the demands of the exercise in athletes (Crewther et al. 2011). Resistance exercise resulted in a small but signicant testosterone response, but not a signicant GH, prolactin or cortisol response. In contrast, previous studies have reported signicant GH and cortisol responses to resistance exercise (Kraemer et al. 1999; Kraemer and Ratamess 2005). In the present study, the cortisol response showed a gradual decline more similar to the pattern observed in the rest trial. A possible reason for these ndings might be that
the protocol employed did not include eccentric muscle actions. However, concentric contractions appear to be primarily responsible for the GH response to resistance exercise as the addition of eccentric contractions did not alter the GH response (Yarrow et al. 2007). This suggests another explanation for the lack of a GH, prolactin and cortisol response in the present study; possibly that the protocol employed was not sufciently demanding. As alluded to above, the hormone response to exercise depends on factors such as the exercise intensity, volume and duration of exercise and rest periods (Kraemer et al. 1990; Davis et al. 1981; Few 1974), and testosterone concentrations have been reported to either increase (Hakkinen and Pakarinen 1995; Kraemer et al. 1991) or decrease (McCall et al. 1999) in response to resistance exercise in young men depending on the protocol employed. In the present study, although testosterone concentrations were signicantly elevated in response to all exercise trials, the percent increases were very similar to the decreases seen in plasma volume, suggesting that exercise might not have caused signicant secretion of testosterone, but rather altered concentrations might be due to a reduction in plasma volume (Kindermann et al. 1982). Notwithstanding the possibility that the resistance training protocol employed in the present study was not sufciently demanding, the fact that there was no difference in the testosterone response in the three exercise trials and that there was a large GH response to endurance exercise brings into question the purported anabolic role of the GH and testosterone response to resistance exercise. This adds to the growing debate regarding the contribution of exercise-induced hormone secretion to training adaptation (West et al. 2010) and indicates that concepts of anabolic (e.g. testosterone and growth hormone) and catabolic (e.g. cortisol) hormones might be over-simplistic. In this context, it is likely that hormones are permissive within a physiological range, with excess or decit of hormones impacting on performance and health; however, we have reported an association between overnight testosterone (but not growth hormone or cortisol) concentrations and overnight protein synthesis (Betts et al. 2011), suggesting an effect of elevated testosterone, particularly at the upper end of the physiological range. Overall, it is difcult to identify specic physiological roles in adaptation for either the individual hormone or overall hormone response to exercise. However, the growth hormone response might impact upon tendon collagen synthesis (Doessing et al. 2010), while the prolactin response to exercise has been proposed to have a role in neurogenesis (Rojas Vega et al. 2012). Studies that selectively and specically block the secretion and/or action of these hormones will be helpful in uncovering the roles of the hormone response to exercise.
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If area under the curve is taken as a reection of the overall response of each of these hormones to the exercise bout, it is interesting to note the effect that calculating this in relation to the amount of work performed (AUC/kJ) and the mean work rate (AUC/W) in each exercise (Table 1). When reported without any adjustment for these variables, the endurance exercise trial resulted in the greatest growth hormone, testosterone and cortisol concentrations, but when expressed as area under the curve per unit of work, sprint exercise resulted in the greatest values for all hormones and endurance exercise resulted in the smallest. Furthermore, when expressing values relative to mean work rate, resistance exercise resulted in the greatest values for prolactin, insulin, testosterone and cortisol, although this must be considered in the context that resistance exercise did not elicit a signicant response in any hormone other than testosterone, and this interpretation is therefore a function of low work rate. If the hormone response to exercise is considered to be important, understanding how different ways of expressing the hormone response to exercise can change the interpretation of the data is important. That said, the total response of a hormone (in addition to factors such as pattern of secretion, presence of binding proteins/globulins and tissue receptor levels) is key to the biological action and so inferences must always be made with reference to the absolute (not adjusted) hormone concentrations. Nevertheless, understanding how the amount of work performed and the work rate inuence hormone responses to exercise might be useful in terms of exercise prescription. This is particularly important in the context of evolving physical activity recommendations that include a variety of exercise options (Chief Medical Ofcers of England W, Scotland, Northern Ireland 2011). For example, the responses to sprint exercise observed in the present study were achieved by completing a relatively small total amount of work in a short period of time. These robust responses might contribute to the apparent health benets reported following brief periods of sprint training (Richards et al. 2010; Whyte et al. 2010). The ndings of this study also have implications for specic patient groups. For example, it appears that in patients with Addisons disease an increase in cortisol might not be needed to mimic a normal response to resistance exercise, although this is likely to depend on the intensity and duration of the resistance exercise bout. In addition, it appears that in patients with Type 1 diabetes, insulin doses only need to be reduced with endurance exercise and perhaps not with sprint and resistance exercise where they might even need to be increased. However, since we investigated hormone responses in healthy individuals in the present study, further studies in these specic patient groups are required to conrm the translation of our results.
Conclusion This study has shown that selected hormones respond differently to the exercise models investigated in the same individuals, indicating a specic response to the demands of the exercise, rather than a global exercise-induced hormone response. These variations in the nature and magnitude of the hormone responses might reect the specic roles of these hormones in regulating metabolism in the face of differing demands during and after resistance, sprint and endurance exercise, which might, in turn, impact upon adaptation to training.
Acknowledgments The authors would like to acknowledge Concept-2 for the loan of the DYNO resistance exercise machine used in this study. Conict of interest to declare. The authors do not have any conicts of interest
References
Bartlett JD, Close GL, MacLaren DPM, Gregson W, Drust B, Morton JP (2011) High-intensity interval running is perceived to be more enjoyable than moderate-intensity continuous exercise: implications for exercise adherence. J Sports Sci 29(6):547553. doi: 10.1080/02640414.2010.545427 Betts JA, Beelen M, Stokes KA, Saris WHM, van Loon LJC (2011) Endocrine responses during overnight recovery from exercise: impact of nutrition and relationships with muscle protein synthesis. Int J Sport Nutr Exerc Metab 21(5):398409 Brandenberger G, Follenius M (1975) Inuence of timing and intensity of muscular exercise on temporal patterns of plasma cortisol levels. J Clin Endocrinol Metab 40(5):845849 Breen L, Philp A, Shaw CS, Jeukendrup AE, Baar K, Tipton KD (2011) Benecial effects of resistance exercise on glycemic control are not further improved by protein ingestion. PLoS One 6 (6). doi:10.1371/journal.pone.0020613 Bussau VA, Ferreira LD, Jones TW, Fournier PA (2007) A 10-s sprint performed prior to moderate-intensity exercise prevents early post-exercise fall in glycaemia in individuals with type 1 diabetes. Diabetologia 50(9):18151818. doi:10.1007/s00125007-0727-8 Chief Medical Ofcers of England W, Scotland, Northern Ireland (2011) Start active, stay active: a report on physical activity from the four home countries Chief Medical Ofcers. doi: http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/ PublicationsPolicyAndGuidance/DH_128209 Consitt LA, Bloomer RJ, Wideman L (2007) The effect of exercise type on immunofunctional and traditional growth hormone. Eur J Appl Physiol 100(3):321330. doi:10.1007/s00421-007-0431-x Crewther BT, Cook C, Cardinale M, Weatherby RP, Lowe T (2011) Two emerging concepts for elite athletes the short-term effects of testosterone and cortisol on the neuromuscular system and the dose-response training role of these endogenous hormones. Sports Med 41(2):103123. doi:10.2165/11539170-00000000000000 Davis HA, Gass GC, Bassett JR (1981) Serum cortisol response to incremental work in experienced and naive subjects. Psychosom Med 43(2):127132
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Eur J Appl Physiol (2013) 113:775783 Doessing S, Heinemeier KM, Holm L, Mackey AL, Schjerling P, Rennie M, Smith K, Reitelseder S, Kappelgaard AM, Rasmussen MH, Flyvbjerg A, Kjaer M (2010) Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myobrillar protein synthesis. J Physiol (Lond) 588(2):341351. doi:10.1113/jphysiol.2009.179325 Felsing NE, Brasel JA, Cooper DM (1992) Effect of low and highintensity exercise on circulating growth-hormone in men. J Clin Endocrinol Metab 75(1):157162 Few JD (1974) Effect of exercise on secretion and metabolism of cortisol in man. J Endocrinol 62(2):341353 Galbo H (1985) The hormonal response to exercise. Proc Nutr Soc 44(2):257266 Garber CE, Blissmer B, Deschenes MR, Franklin BA, Lamonte MJ, Lee IM, Nieman DC, Swain DP, Amer Coll Sports M (2011) Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor tness in apparently healthy adults: guidance for prescribing exercise. Med Sci Sports Exerc 43(7):13341359. doi:10.1249/MSS. 0b013e318213fefb Gilbert KL, Stokes KA, Hall GM, Thompson D (2008) Growth hormone responses to 3 different exercise bouts in 18-to 25-and 40-to 50-year-old men. Appl Physiol Nutr Metab 33(4):706712. doi:10.1139/h08-034 Guiraud T, Nigam A, Juneau M, Meyer P, Gayda M, Bosquet L (2011) Acute responses to high-intensity intermittent exercise in CHD patients. Med Sci Sports Exerc 43(2):211217. doi:10.1249/ MSS.0b013e3181ebc5de Hakkinen K, Pakarinen A (1995) Acute hormonal responses to heavy resistance exercise in men and women at different ages. Int J Sports Med 16(8):507513 Kindermann W, Schnabel A, Schmitt WM, Biro G, Cassens J, Weber F (1982) Catecholamines, growth-hormone, cortisol, insulin, and sex-hormones in anaerobic and aerobic exercise. Eur J Appl Physiol Occ Med 49(3):389399 Kraemer WJ, Ratamess NA (2005) Hormonal responses and adaptations to resistance exercise and training. Sports Med 35(4):339361 Kraemer WJ, Marchitelli L, Gordon SE, Harman E, Dziados JE, Mello R, Frykman P, McCurry D, Fleck SJ (1990) Hormonal and growth-factor responses to heavy resistance exercise protocols. J Appl Physiol 69(4):14421450 Kraemer WJ, Gordon SE, Fleck SJ, Marchitelli LJ, Mello R, Dziados JE, Friedl K, Harman E, Maresh C, Fry AC (1991) Endogenous anabolic hormonal and growth-factor responses to heavy resistance exercise in males and females. Int J Sports Med 12(2):228235 Kraemer WJ, Hakkinen K, Newton RU, Nindl BC, Volek JS, McCormick M, Gotshalk LA, Gordon SE, Fleck SJ, Campbell WW, Putukian M, Evans WJ (1999) Effects of heavy-resistance training on hormonal response patterns in younger vs. older men. J Appl Physiol 87(3):982992
783 McCall GE, Byrnes WC, Fleck SJ, Dickinson A, Kraemer WJ (1999) Acute and chronic hormonal responses to resistance training designed to promote muscle hypertrophy. Can J Appl Physiol 24(1):96107 Pritzlaff CJ, Wideman L, Weltman JY, Abbott RD, Gutgesell ME, Hartman ML, Veldhuis JD, Weltman A (1999) Impact of acute exercise intensity on pulsatile growth hormone release in men. J Appl Physiol 87(2):498504 Pritzlaff CJ, Wideman L, Blumer J, Jensen M, Abbott RD, Gaesser GA, Veldhuis JD, Weltman A (2000) Catecholamine release, growth hormone secretion, and energy expenditure during exercise vs. recovery in men. J Appl Physiol 89(3):937946 Richards JC, Johnson TK, Kuzma JN, Lonac MC, Schweder MM, Voyles WF, Bell C (2010) Short-term sprint interval training increases insulin sensitivity in healthy adults but does not affect the thermogenic response to beta-adrenergic stimulation. J Physiol (Lond) 588(15):29612972. doi:10.1113/jphysiol.2010. 189886 Rojas Vega S, Hollmann W, Struder HK (2012) Inuences of exercise and training on the circulating concentration of prolactin in humans. J Neuroendocrinol 24(3):395402. doi:10.1111/j.13652826.2011.02266.x Stokes K (2003) Growth hormone responses to sub-maximal and sprint exercise. Growth Horm IGF Res 13(5):225238 Stokes KA, Nevill ME, Hall GM, Lakomy HKA (2002) Growth hormone responses to repeated maximal cycle ergometer exercise at different pedaling rates. J Appl Physiol 92(2):602608 Stokes KA, Tyler C, Gilbert KL (2008) The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men. J Appl Physiol 104(3):724728. doi: 10.1152/japplphysiol.00534.2007 Wahl P, Zinner C, Achtzehn S, Bloch W, Mester J (2010) Effect of high- and low-intensity exercise and metabolic acidosis on levels of GH, IGF-I, IGFBP-3 and cortisol. Growth Horm IGF Res 20(5):380385. doi:10.1016/j.ghir.2010.08.001 Wasserman DH, Cherrington AD (1991) Hepatic fuel metabolism during muscular work: role and regulation. Am J Physiol 260(6):E811E824 West DWD, Burd NA, Tang JE, Moore DR, Staples AW, Holwerda AM, Baker SK, Phillips SM (2010) Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow exors. J Appl Physiol 108(1):6067. doi:10.1152/japplphysiol. 01147.2009 Whyte LJ, Gill JMR, Cathcart AJ (2010) Effect of 2 weeks of sprint interval training on health-related outcomes in sedentary overweight/obese men. Metabol Clin Exp 59(10):14211428. doi: 10.1016/j.metabol.2010.01.002 Yarrow JF, Borsa PA, Borst SE, Sitren HS, Stevens BR, White LJ (2007) Neuroendocrine responses to an acute bout of eccentricenhanced resistance exercise. Med Sci Sports Exerc 39(6): 941947. doi:10.1097/mss.0b013e318043a249
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