Human growth hormone responses to repeated bouts of sprint exercise with different recovery periods between bouts.

This study examined the growth hormone (GH) response to repeated bouts of sprint cycling. Eight healthy men completed three trials consisting of two 30-s sprints on a cycle ergometer separated by either 60 min (Trial A) or 240 min (Trial B) of recovery and a single 30-s sprint carried out the day after Trial B (Trial C). Trials A and B were separated by at least 7 days. Blood samples were obtained at rest and during recovery from each sprint. In Trial A, GH was elevated immediately before sprint 2, and there was no further increase in GH following the second sprint [area under the curve: 460 (SD 348) vs. 226 min.mug(-1).l(-1) (SD 182), P = 0.05]. Free insulin-like growth factor I tended to be lower immediately before sprint 2 than sprint 1 (P = 0.06). Serum free fatty acids were not different immediately before each of the sprints. In Trial B, there was a trend for a smaller GH response to the second sprint [GH area under the curve: 512 (SD 396) vs. 242 min.mug(-1).l(-1) (SD 190), P = 0.09]. Free insulin-like growth factor I tended to be lower (P = 0.06), and serum free fatty acids were higher (P = 0.01) immediately before sprint 2 than sprint 1. There was no difference in the GH response to sprinting on consecutive days (Trials B and C). In conclusion, repeated bouts of sprint cycling on the same day result in an attenuation or even ablation of the exercise-induced increase in GH, depending on the recovery interval between sprints.     

The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men.

A single 30-s sprint is a potent physiological stimulus for growth hormone (GH) release. However, repeated bouts of sprinting attenuate the GH response, possibly due to negative feedback via elevated systemic free fatty acids (FFA). The aim of the study was to use nicotinic acid (NA) to suppress lipolysis to investigate whether serum FFA can modulate the GH response to exercise. Seven nonobese, healthy men performed two trials, consisting of two maximal 30-s cycle ergometer sprints separated by 4 h of recovery. In one trial (NA), participants ingested NA (1 g 60 min before, and 0.5 g 60 and 180 min after sprint 1); the other was a control (Con) trial. Serum FFA was not significantly different between trials before sprint 1 but was significantly lower in the NA trial immediately before sprint 2 [NA vs. Con: mean (SD); 0.08 (0.05) vs. 0.75 (0.34) mmol/l, P < 0.05]. Peak and integrated GH were significantly greater following sprint 2 compared with sprint 1 in the NA trial [peak GH: 23.3 (7.0) vs. 7.7 (11.9) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 316 (527) microg.l(-1).60 min(-1), P < 0.05] and compared with sprint 2 in the Con trial [peak GH: 23.3 (7.0) vs. 5.2 (2.3) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 206 (118) microg.l(-1).60 min(-1), P < 0.05]. In conclusion, suppressing lipolysis resulted in a significantly greater GH response to the second of two sprints, suggesting a potential role for serum FFA in negative feedback control of the GH response to repeated exercise.     

Thermoregulatory and metabolic responses to repeated bouts of prolonged cycle-ergometer exercise in man

Changes in body temperature, oxygen uptake (VO2), heart rate (HR), sweating rate and plasma osmolarity were examined in 10 human subjects, performing four successive 30 min exercise-bouts of the same intensity (50% VO2 max) separated by 30 min rest periods. In spite of the rest intervals and replacement of body fluid loss there was a progressive increase in VO2. HR, rectal (Tre) and mean body (Tb) temperatures in consecutive exercise bouts. The thermoregulatory efficiency showed an increasing tendency, and a delay in the sweating response at the beginning of each exercise was shortened. It is concluded that a drift in metabolic and temperature responses to exercise, reported throughout a long-term continuous work, occurs also in the euhydrated subjects performing a prolonged intermittent exercise. It is not caused by an impaired thermoregulation during exercise but rather by insufficient restitution of metabolic processes during rest intervals.     

Glucoregulatory and hormonal responses to repeated bouts of intense exercise in normal male subjects.

Glucose turnover and its regulation were studied during and after two identical bouts of intense exhaustive exercise separated by 1 h to define differences in response. Six lean young postabsorptive male subjects exercised at approximately 100% maximal O2 uptake (3.7 +/- 0.3 l/min) for 13.0 +/- 0.7 min for the first (EX1) and 13.2 +/- 0.8 min for the second (EX2) bout. Plasma glucose increased during EX1 and peaked at 7.0 +/- 0.6 mmol/l in early recovery but to 5.8 +/- 0.5 mmol/l (P less than 0.05) after EX2, and both the hyperglycemic and the hyperinsulinemic responses were less after EX2 (P less than 0.015, analysis of variance). The hyperglycemia was due to lesser increments in glucose utilization (Rd) (3-fold resting) than glucose production (Ra) (7-fold) toward exhaustion and for 7 min of recovery. The rise in Rd was more rapid (P less than 0.05) and metabolic clearance rate was greater during (P = 0.015) and from 9 to 60 min after EX2, and Ra also remained higher during recovery (P less than 0.05). Marked and similar increments in plasma norepinephrine (18-fold) and epinephrine (14-fold) occurred with both bouts. Plasma glucagon increments were small and not different. Therefore, 1) more circulating glucose was used with EX2, 2) greater metabolic clearance rate during and after EX2 suggests local muscle adaptations due to EX1, and 3) significant correlations (P less than 0.002) between plasma norepinephrine and Ra (r = 0.82) and Ra - Rd (r = 0.52) and between epinephrine and Ra (r = 0.71) and Ra - Rd (r = 0.48) suggest a major regulatory role for the catecholamine responses.     

Enhancement of fat metabolism by repeated bouts of moderate endurance exercise.

This study compared the fat metabolism between "a single bout of prolonged exercise" and "repeated bouts of exercise" of equivalent exercise intensity and total exercise duration. Seven men performed three trials: 1) a single bout of 60-min exercise (Single); 2) two bouts of 30-min exercise, separated by a 20-min rest between exercise bouts (Repeated); and 3) rest. Each exercise was performed with a cycle ergometer at 60% of maximal oxygen uptake. In the Single and Repeated trials, serum glycerol, growth hormone, plasma epinephrine, and norepinephrine concentrations increased significantly (P<0.05) during the first 30-min exercise bout. In the Repeated trial, serum free fatty acids (FFA), acetoacetate, and 3-hydroxybutyrate concentrations showed rapid increases (P<0.05) during a subsequent 20-min rest period. During the second 30-min exercise bout, FFA and epinephrine responses were significantly greater in the Repeated trial than in the Single trial (P<0.05). Moreover, the Repeated trial showed significantly lower values of insulin and glucose than the Single trial. During the 60-min recovery period after the exercise, FFA, glycerol, and 3-hydroxybutyrate concentrations were significantly higher in the Repeated trial than in the Single trial (P<0.05). The relative contribution of fat oxidation to the energy expenditure showed significantly higher values (P<0.05) in the Repeated trial than in the Single trial during the recovery period. These results indicate that repeated bouts of exercise cause enhanced fat metabolism compared with a single bout of prolonged exercise of equivalent total exercise duration.     

Oral arginine attenuates the growth hormone response to resistance exercise.

This study investigated the combined effect of resistance exercise and arginine ingestion on spontaneous growth hormone (GH) release. Eight healthy male subjects were studied randomly on four separate occasions [placebo, arginine (Arg), placebo + exercise (Ex), arginine + exercise (Arg+Ex)]. Subjects had blood sampled every 10 min for 3.5 h. After baseline sampling (30 min), subjects ingested a 7-g dose of arginine or placebo (blinded, randomly assigned). On the exercise days, the subject performed 3 sets of 9 exercises, 10 repetitions at 80% one repetition maximum. Resting GH concentrations were similar on each study day. Integrated GH area under the curve was significantly higher on the Ex day (508.7 +/- 169.6 min.ng/ml; P < 0.05) than on any of the other study days. Arg+Ex (260.5 +/- 76.8 min.ng/ml) resulted in a greater response than the placebo day but not significantly greater than the Arg day. The GH half-life and half duration were not influenced by the stimulus administered. The GH secretory burst mass was larger, but not significantly, on the Arg, Ex, and Arg+Ex day than the placebo day. Endogenous GH production rate (Ex > Arg+Ex > Arg > placebo) was greater on the Ex and Arg+Ex day than on the placebo day (P < 0.05) but there were no differences between the Ex and Arg+Ex day. Oral arginine alone (7 g) stimulated GH release, but a greater GH response was seen with exercise alone. The combined effect of arginine before exercise attenuates the GH response. Autonegative feedback possibly causes a refractory period such that when the two stimuli are presented there will be suppression of the somatotrope.     

Atrial natriuretic peptide stimulates lipid mobilization during repeated bouts of endurance exercise

Atrial natriuretic peptide (ANP) controls lipolysis in human adipocytes. Lipid mobilization is increased during repeated bouts of exercise, but the underlying mechanisms involved in this process have not yet been delineated. The relative involvement of catecholamine- and ANP-dependent pathways in the control of lipid mobilization during repeated bouts of exercise was thus investigated in subcutaneous adipose tissue (SCAT) by microdialysis. The study was performed in healthy males. Subjects performed two 45-min exercise bouts (E1 and E2) at 50% of their maximal oxygen uptake separated by a 60-min rest period. Extracellular glycerol concentration (EGC), reflecting SCAT lipolysis, was measured in a control probe perfused with Ringer solution and in two other probes perfused with either Ringer plus phentolamine (alpha(1/2)-AR antagonist) or Ringer plus both phentolamine and propranolol (beta-AR antagonist). Plasma epinephrine, plasma glycerol, and EGC were 1.7-, 1.6-, and 1.2-fold higher in E2 than in E1, respectively. Phentolamine potentiated exercise-induced EGC increase during E2 only. Propranolol reduced the lipolytic rate during both E1 and E2 compared with the probe with phentolamine. Plasma ANP concentration increased more during E2 than during E1 and was correlated with the increase in EGC in the probe containing phentolamine plus propranolol. The results suggest that ANP is involved in the control of lipolysis during exercise and that it contributes to stimulation of lipolysis during repeated bouts of exercise.     

Effects of vitamin E supplementation on recovery from repeated bouts of resistance exercise

The purpose of this study was to examine the effects of vitamin E (VE) supplementation (1200 IU/day) on recovery responses to repeated bouts of resistance exercise. Non-resistance trained men were assigned to supplement with VE (n = 9) or placebo (PL; n = 9) for 3 weeks and then perform 3 resistance exercise sessions separated by 3 days of recovery (EX-1, EX-2, and EX-3). Performance was assessed at EX-1, EX-2, and EX-3. Fasting morning blood samples and perceived muscle soreness were obtained before EX-1 and for 10 consecutive days. Muscle soreness peaked after EX-1 and gradually returned to baseline values by day 6. Lower and upper body maximal strength and explosive power were significantly (p < or = 0.05) decreased at EX-2 and EX-3 (approximately 10%). Plasma malondialdehyde (MDA) was significantly elevated on days 7 and 8. There were no significant differences between VE and PL in muscle soreness, performance measures, or plasma MDA. Creatine kinase (CK) area under the curve from day 1 to day 10 was significantly greater for VE because of a nearly 2-fold greater increase in CK after EX-1 in VE, compared with PL (404 +/- 146 and 214 +/- 179 U/L, respectively). VE supplementation was not effective at attenuating putative markers of membrane damage, oxidative stress, and performance decrements after repeated bouts of whole-body concentric/eccentric resistance exercise.     

Ergogenic and metabolic effects of oral glucocorticoid intake during repeated bouts of high-intensity exercise

All systemically administered glucocorticoids (GC) are prohibited in-competition, because of the potential ergogenic effects. Although short-term GC intake has been shown to improve performance during submaximal exercise, literature on its impact during brief intense exercise appears to be very scant. The purpose of this study was to examine the ergogenic and metabolic effects of prednisone during repeated bouts of high-intensity exercise. In a double-blind randomized protocol, ten recreational male athletes followed two 1-week treatments (Cor: prednisone, 60 mg/day or Pla: placebo). At the end of each treatment, they hopped on their dominant leg for 30 s three times consecutively and then hopped until exhaustion, with intervals of 5 min of passive recovery. Blood and saliva samples were collected at rest and 3 min after each exercise bout to determine the lactate, interleukin-6, interleukin-10, TNF-alpha, DHEA and testosterone values. The absolute peak force of the dominant leg was significantly increased by Cor but only during the first 30-s hopping bout (p < 0.05), whereas time to exhaustion was not significantly changed after Cor treatment vs Pla (Pla: 119.9 ± 24.7; Cor: 123.1 ± 29.5 s). Cor intake lowered basal and end-exercise plasma interleukin-6 and saliva DHEA (p < 0.01) and increased interleukin-10 (p < 0.01), whereas no significant change was found in blood lactate and TNF-alpha or saliva testosterone between Pla and Cor. According to these data, short-term glucocorticoid intake did not improve endurance performance during repeated bouts of high-intensity exercise, despite the significant initial increase in absolute peak force and anti-inflammatory effect.     

Serum creatine kinase activity following repeated bouts of isometric exercise with different muscle groups

The purpose of this study was to examine the relationship between the muscle mass involved in exercise and post-exercise serum creatine kinase (CK) elevation. Twelve untrained college-aged men completed three isometric exercises: one arm flexion (OAF), two arm flexion (TAF) and one leg knee extension (OLE). These exercises were balanced over subjects and days and separated by two week intervals. Each exercise consisted of 40 maximal isometric concentrations lasting for 10 s with a 20 s rest between contractions. Relative increases in serum CK for OAF, TAF, and OLE were 181 +/- 70% (SD), 222 +/- 69% and 297 +/- 67%, respectively. An ANOVA using a latin square design for analysis of carry over effects showed that these CK increases were not significantly different (p greater than 0.05). However, the increase in serum CK following the first exercise (379 +/- 90%), regardless of what it was (OAF, TAF, or OLE), was significantly greater (p less than 0.05) than those following bouts 2 and 3 (155 +/- 29%; 167 +/- 54%). Regression analysis indicated that post-exercise serum CK elevation was not related to the amount of muscle mass involved in the exercise (r = 0.30, p greater than 0.05) nor to muscle tension developed (r = 0.28, p greater than 0.05). We conclude that post-exercise serum CK elevation is not necessarily related to the muscle mass involved in the exercise. Because each exercise involved the use of different muscle groups, factors outside the exercising muscle may contribute to post-exercise serum enzyme activity.     

Leukocyte counts and lymphocyte responsiveness associated with repeated bouts of strenuous endurance exercise.

This study compared leukocyte counts and lymphocyte responsiveness during and after a second bout of high-intensity endurance exercise on the same day with the response to a similar but single bout of exercise. Nine athletes participated in three 24-h trials: 1) rest in bed (Rest); 2) one bout of exercise (One); and 3) two bouts of exercise (Two). All bouts consisted of 75 min at approximately 75% of maximal O(2) uptake on a cycle ergometer. Lymphocytes in whole blood were stimulated with monoclonal antibodies against CD2 and assessed by flow cytometry for expression of the early activation molecule CD69. The second bout of exercise in the Two trial was associated with significantly increased concentrations of total leukocytes, neutrophils, lymphocytes, CD4(+), CD8(+), and CD56(+) cells and a significantly decreased percentage of CD56(+) cells expressing CD69 compared with a single bout. Additionally, there was a significantly decreased CD69 fluorescence in CD56(+) cells postexercise. These differences suggest a "carry-over" effect in the immune system from a first to a second bout of exercise on the same day.     

Concurrent aerobic exercise interferes with the satellite cell response to acute resistance exercise

The addition of aerobic exercise (AE) to a resistance exercise (RE) program (concurrent exercise, CE) can interfere with maximum muscle fiber growth achieved with RE. Further, CE appears to markedly affect the growth of myosin heavy chain (MHC) I, but not MHC IIa fibers. The mechanism responsible for this "interference" is unclear. Satellite cell (SC) responsiveness to exercise appears to influence muscle adaptation but has not yet been examined following acute concurrent exercise. Thus, we assessed the fiber-type-specific SC response to RE, AE, and CE exercise. Eight college-aged males completed the following two exercise trials: the RE trial, which consisted of unilateral leg extensions and presses (4 sets ≥ 10 repetitions: 75% 1 repetition maximum, RM); and the AE/CE trial, which included an identical RE protocol with the opposite leg, immediately followed by subjects cycling for 90 min (60% W(max)). Muscle biopsies were obtained from the vastus lateralis before and 4 days after each session. Samples were cross-sectioned, stained with antibodies against NCAM, Ki-67, and MHC I, counterstained with DAPI, and analyzed for SC density (SC per fiber), SC activation, and fiber type. SC density increased to a greater extent following RE (38 ± 10%), compared with CE (-6 ± 8%). Similarly, MHC I muscle fiber SC density displayed a greater increase following RE (46 ± 14%), compared with AE (-7 ± 17%) and CE (-8 ± 8%). Our data indicate that the SC response to RE is blunted when immediately followed by AE, at least in MHC I muscle fibers, and possibly MHC II fibers. This suggests that the physiological environment evoked by AE might attenuate the eventual addition of myonuclei important for maximum muscle fiber growth and consequent force-producing capacity.     

Effect of repeated bouts of short-term exercise on plasma free and sulphoconjugated catecholamines in humans

We tested the hypothesis that measurement of plasma catecholamine sulphate concentration after exercise reflects the overall activation of the sympathoadrenergic system during the whole period of repeated bouts of short-term exercise. A group of 11 male athletes performed two exercise tests at similar average power outputs consisting of three sets each. The tests either started with one set of three very intense sprints (95% of maximal running speed) followed by two sets of three less intense sprints (85% of maximal running speed; HLX) or vice versa (LHX). Similar mean areas under the curve of free noradrenaline (NA) during HLX and LHX [622 (SEM 13) v.s. 611 (SEM 14) nmol x l(-1) min) as well as similar mean heart rates [143 (SEM 9) v.s. 143 (SEM 8) beats x min(-1)] indicated comparable sympathetic activation during both exercise tests. Even so, plasma concentration of free NA was still significantly higher at the end of LHX than of HLX [35.7 (SEM 3.5) v.s. 22.5 (SEM 2.1) nmol x l(-1), respectively], i.e. when exercise ended with the more intense set of sprints. Plasma noradrenaline sulphate (NA-S) increased with exercise intensity showing higher mean increments after the first set of HLX compared to LHX [1.83 (SEM 0.42) v.s. 1.18 (SEM 0.29) nmol x l(-1); P<0.05]. However, after the end of HLX and LHX, increments in plasma NA-S were similar [4.52 (SEM 0.76) v.s. 4.06 (SEM 0.79) nmol x l(-1)], suggesting that NA-S response changed in parallel with the overall activation of the sympathetic nervous system during repeated bouts of short-term exercise. The results supported the hypothesis that measurement of plasma NA-S immediately after repeated bouts of short-term exercise reflects overall activation of the sympathetic nervous system during prolonged periods of this type of exercise.     

Effect of aerobic training on the plasma ACTH response to exercise

The purpose of this study was to reexamine the effect of training on plasma adrenocorticotropin (ACTH) levels during exercise. Ten adult volunteers were split into a control and an experimental group. The experimental group participated in a 12-wk training program that resulted in a significant 11% increase in their mean maximal O2 uptake. The plasma ACTH response to a 150-W work rate was measured in both groups before and after the training program. The experimental group demonstrated a significant reduction in the ACTH response (11 vs. 4 pg/ml) to the work rate, whereas the control group demonstrated an unchanged response (16 vs. 13 pg/ml) over the course of the study. These data suggest that the ACTH response to an absolute submaximal work rate is blunted after training.     

Smaller muscle ATP reduction in women than in men by repeated bouts of sprint exercise.

It was hypothesized that the reduction of high-energy phosphates in muscle after repeated sprints is smaller in women than in men. Fifteen healthy and physically active women and men with an average age of 25 yr (range of 19-42 yr) performed three 30-s cycle sprints (Wingate test) with 20 min of rest between sprints. Repeated blood and muscle samples were obtained. Freeze-dried pooled muscle fibers of types I and II were analyzed for high-energy phosphates and their breakdown products and for glycogen. Accumulation of plasma ATP breakdown products, plasma catecholamines, and blood lactate, as well as glycogen reduction in type I fibers, was all lower in women than in men during sprint exercise. Repeated sprints induced smaller reduction of ATP and smaller accumulation of IMP and inosine in women than in men in type II muscle fibers, with no gender differences in changes of ATP and its breakdown products during the bouts of exercise themselves. This indicates that the smaller ATP reduction in women than in men during repeated sprints was created during recovery periods between the sprint exercises and that women possess a faster recovery of ATP via reamination of IMP during these recovery periods.