gaining weight in gpp

[boldwarrior]

"Bold" - but do you agree with the following comment:

... "rep ranges of 4-8 are more suitable for growth then 10+. "

(because I almost always worked on reps of 1-6 and sets from 1 to 6, as the basis of 99% of the weights work I advocated, with no real scientific basis for it, just observation of what worked pretty well in achieving the strength and bodyweight outcomes I was looking for).

Is there a scientific basis, hormonal spikes or otherwise kk

This type of Q. and following sub Q's can get very tricky, and even more so on this site with its rules. Leaving answers being best left unsaid at times as the answers can breach rules!!
however,
with your guys working on 1-6 reps etc, them being the track guys yar? And i take it, they are also mainly trying to gain Strength v's size, (400m after all - how big do you want to be)
From my experience, i have shown no size in lean tissue that would indicate 3-5reps making one "bigger". ie, noticable size aka bodybuilding.
higher reps, from 6-12 have shown size increases, as long as short recoverys, done every 3 days etc is also followed.

Its getting to the old arguement of Mike Mentzer v's Arnold talk again!! (does it ever stop?) Mike converted a lot of guys in the 80's, and his beliefs still linger. Talk to any REal bodybuilder who actually used to be Skinny, and they will tell you, to get big, "Pump weights", to get strong, "lift" heavy. THe amount of Bodybuilders who were already big then switched to the Heavy Duty style, who have been trashed, injured etc etc is stagering.

So, im not really going to get too much into it, brings out arguments, so im leaving it here.

[Sharmer]

This opens up some interesting questions. What is the relative importance of GH levels vs the protein sparing effect of closer spacing of meals etc? (nighttime GH levels are higher in a fasting state- ie nothing after dinner).
Would moving the workouts towards the AM allow enough time to enhance a nutritional response and also allow for a GH spike at night?
Is this why there's been a trend towards earlier training sessions in recent years?
We sat somewhere in the middle, I'd guess, using Glutamine/ZMA at night but without a carb source and training early afternoon.
Second, how would you decide the relative importance of therapy when it's not possible to "do it all"?
I created a set of tables for massage priority for Vanc 04 based on concentrating the most aggressive therapy to enhance the upswing of muscle recovery between speed days and fill in the sessions as the budget allows.
Perhaps the hot/cold showers create a hormonal response and can bridge the gap where massage isn't available and complement it where it is.

Charlie you bring up some very tough questions. Timing of resistance training doesn’t seem to influence GH spikes, yet it does influence cortisol. This is a significant finding in itself.

Cortisol and Growth Hormone Responses to Exercise at Different Times of Day1

Jill A. Kanaley2, Judy Y. Weltman, Karen S. Pieper3, Arthur Weltman and Mark L. Hartman
Division of Endocrinology and Metabolism, Department of Medicine (J.A.K., A.W., M.L.H.); Division of Biostatistics and Epidemiology, Department of Health Evaluation Sciences (K.S.P.); Department of Human Services (A.W.); General Clinical Research Center (J.Y.W., A.W.); and the National Science Foundation Center for Biological Timing (M.L.H.), University of Virginia, Charlottesville, Virginia 22908

Abstract
Exercise of appropriate intensity is a potent stimulus for GH and cortisol secretion. Circadian and diurnal rhythms may modulate the GH and cortisol responses to exercise, but nutrition, sleep, prior exercise patterns, and body composition are potentially confounding factors. To determine the influence of the time of day on the GH and cortisol response to acute exercise, we studied 10 moderately trained young men (24.1 ± 1.1 yr old; maximal oxygen consumption, 47.9 ± 1.4 mL/kg•min; percent body fat, 13.2 ± 0.6%). After a supervised night of sleep and a standard meal 12 h before exercise, subjects exercised at a constant velocity (to elicit an initial blood lactate concentration of 2.5 mmol/L) on a treadmill for 30 min on 3 separate occasions, starting at 0700, 1900, and 2400 h. Blood samples were obtained at 5-min intervals for 1 h before and 5 h after the start of exercise; subjects were not allowed to sleep during this period. Subjects were also studied on 3 control days under identical conditions without exercise. There were no significant differences with time of day in the mean blood lactate and submaximal oxygen consumption values during exercise. The differences over time in serum GH and cortisol concentrations between the exercise day and the control day were determined with 95% confidence limits for each time of day. Exercise stimulated a significant increase in serum GH concentrations over control day values for approximately 105–145 min (P < 0.05) with no significant difference in the magnitude of this response by time of day.

The increase in serum GH concentrations with exercise was followed by a transient suppression of GH release (for 55–90 min; P < 0.05) after exercise at 0700 and 1900 h, but not at 2400 h. Although the duration of the increase in serum cortisol concentrations after exercise was similar ( 150–155 min; P < 0.05) at 0700, 1900, and 2400 h, the magnitude of this increase over control day levels was greatest at 2400 h. This difference was significant for approximately 130 min and approximately 40 min compared to exercise at 1900 and 0700 h, respectively (P < 0.05). The cortisol response to exercise at 0700 h was significantly greater than that at 1900 h for about 55 min (P < 0.05). A rebound suppression of cortisol release for about 50 min (P < 0.05) was observed after exercise at 2400 h, but not 0700 or 1900 h. Both baseline (before exercise) and peak cortisol concentrations were significantly higher at 0700 h than at 1900 or 2400 h (P < 0.01). We conclude that time of day does not alter the GH response to exercise; however, the exercise-induced cortisol response is modulated by time of day.

EXERCISE OF appropriate intensity is a potent stimulus for GH and cortisol secretion. The GH and cortisol responses to exercise are both dependent on the relative exercise workload, but other factors modulate these hormonal responses, including the mode and duration of exercise, anaerobic vs. aerobic exercise, prior meal ingestion, and fitness level of the subject (1, 2, 3, 4, 5, 6, 7, 8, 9, 10). Underlying pulsatile and circadian/diurnal rhythms of these hormones potentially may modulate the exercise response observed (11, 12, 13, 14, 15, 16).

At rest, GH secretion is pulsatile and is influenced by age, gender, nutrition, sleep, body composition, fitness, and sex steroid hormones (17). During a 24-h period, spontaneous GH secretion is maximal at night in close association with slow wave sleep (11, 12, 17, 18). The GH response to an iv bolus injection of GHRH is maximal at night, particularly during slow wave sleep (13, 14). Circadian and/or diurnal rhythms may influence GH secretion independently of sleep, as GH secretion is still maximal at night when subjects are kept awake (12). Food ingestion may account in part for the lower levels of GH secretion during the day; ingestion of high fat meals is known to blunt the GH response to exercise (4, 17).
Cortisol secretion is also pulsatile. The amplitude and frequency of cortisol secretory pulses are modulated by a circadian rhythm (15, 16). Circulating cortisol concentrations are maximal in the early morning hours just before awakening as a result of increased cortisol secretory pulse amplitude and frequency. The amplitude of cortisol secretory pulses progressively decreases throughout the day until cortisol concentrations are quite low in the evening (16). This circadian rhythm is largely independent of sleep, although an inhibitory effect of nocturnal, but not diurnal, sleep on cortisol concentrations has been documented in humans (18). Meals stimulate cortisol release in humans. Exercise performed immediately after food ingestion results in a blunted cortisol response to the exercise stimulus (1, 2).

Few studies have assessed the impact of time of day on the GH and cortisol responses to exercise. Two studies reported no effect of time of day on the GH response to exercise. One study was limited by the omission of an appropriate control (nonexercise) day (19). The second study employed a low exercise intensity and infused iv glucose during the test (20). Four studies have reported that the cortisol response to exercise is similar in the morning and evening (2, 19, 21, 22). The statistical methods used in these studies did not allow inspection of possible differences over time in the cortisol response to exercise compared with resting conditions at different times of day. A fifth study employed a low exercise intensity that elicited a cortisol response in the afternoon, but no response in the morning or evening (20).

The present study examined the influence of time of day on the GH and cortisol responses to exercise. Hormonal responses to exercise in the early morning and early evening and at midnight were compared with those on identical control (nonexercise) days. This study controlled for the confounding effects of meals and sleep and employed a statistical approach that enabled the difference in hormone concentrations to be compared across time with 95% confidence limits.

Subjects and Methods
Subjects
Ten healthy, moderately trained, male subjects completed this study. All subjects underwent a detailed medical history and physical examination and provided informed, written consent in accordance with the guidelines established by the University of Virginia human investigation committee. The subjects were nonsmokers, were not taking any medication known to affect GH or cortisol secretion, had not undergone transmeridian travel in the past 8 weeks, were not night shift workers and regularly went to bed between 2200–2400 h. Screening laboratory data revealed normal hepatic, renal, metabolic, hematological, thyroid, and gonadal function.

Experimental design
Body composition and aerobic exercise capacity [maximal oxygen consumption (VO2 max)] were determined approximately 1 week before the first admission. Subjects were admitted to the General Clinical Research Center (GCRC) on six separate occasions for hormonal measurements. Three of the admissions were exercise days, and three admissions were control days. The study times for the admissions were 0600–1200, 1800–2400, and 2300–0500 h. The exercise times in each of these study periods were 0700, 1900, and 2400 h, respectively. These times were chosen because they are three popular times for recreational exercise (before and after day shift work and after evening shift work). These times also encompass the diurnal rhythms of both cortisol and GH secretion. Although the daily peak of cortisol secretion usually occurs earlier than 0700 h, it was not feasible to conduct the exercise studies at 0400 or 0500 h. Controls were studied at the same time of day as the exercise group, but no exercise occurred. The order of all six admissions was randomized.

VO2 max
Maximal oxygen consumption was determined using a continuous treadmill protocol. The treadmill velocity was initially set at 100 m/min at 0% grade, and every 3 min the velocity was increased by 10 m/min. Subjects were verbally encouraged throughout the test, and the test was terminated when the subject reached volitional fatigue. Metabolic measures were collected using standard open circuit spirometric techniques (2900Z metabolic cart, SensorMedics, Yorba Linda, CA). VO2 max was chosen as the highest VO2 attained during the test. From an indwelling venous catheter located in a forearm vein, blood samples were taken at rest and at the end of each 3-min stage while the subjects continued running. A saline solution (0.9% NaCl) was infused after each blood sample to prevent clotting. Samples were analyzed immediately for lactate concentrations with an automated lactate analyzer (model 2700, YSI, Inc., Yellow Springs, OH).

Body composition
Percent body fat was assessed by hydrostatic weighing as previously described (10). Briefly, each subject was weighed in air on an Accu-Weigh beam scale (Metro Equipment Company, Sunnyvale, CA) accurate to 0.1 kg and subsequently weighed underwater with a 9-kg Chatillon autopsy scale (Chatillon, New York, NY) accurate to 10 g. Residual volume was measured on land using an O2 dilution technique (23). Relative body fat was converted from body density using the equation of Brozek et al. (24).
Study day protocol

Subjects were admitted to the GCRC the evening before the study and slept in the GCRC to standardize sleeping conditions (lights out at 2200 h) before the study day. All subjects were given a standard meal that contained 16 Cal/kg BW (50% carbohydrate, 30% fat, and 20% protein) 12 h before the start of blood sampling. After the standard meal, subjects fasted until the study was completed 18 h later. With the exception of the exercise tests, subjects refrained from vigorous activity, but were allowed to walk around the GCRC unit. An indwelling cannula was inserted in a forearm vein 1 h before the start of blood sampling. Serial blood sampling (2.5 mL/sample) was initiated 1 h after iv placement, and samples were taken at 5-min intervals over 6 h. On three of the visits, subjects exercised at a constant velocity on the treadmill for 30 min (starting at 0700, 1900, and 2400 h). The initial velocity chosen was the velocity associated with a blood lactate concentration of 2.5 mmol/L on the incremental VO2 max treadmill test. This velocity was chosen so that the lactate response to 30 min of exercise would not exceed 4.0 mmol/L (25). During the submaximal exercise test, metabolic measures were collected using standard open circuit spirometry as described above. Subjects were not allowed to sleep during the blood-sampling period. As the subjects were significantly sleep deprived during the 2300–0500 h study periods, electroencephalographic monitoring was performed to record any possible episodes of sleep. No episodes of sleep exceeding 9 min occurred.

Assays
Serum GH was measured in duplicate with an immunoradiometric assay (IRMA) using standards diluted in human serum (Nichols Institute Diagnostics, San Juan Capistrano, CA). The assay sensitivity was 0.2 µg/L, and the mean inter- and intraassay coefficients of variation (CVs) were 8.6% and 4.9%, respectively. This assay was chosen (instead of a chemiluminescence assay) because the primary end point of interest was the peak GH response to exercise rather than the low concentrations of GH between pulses. At the time the study was conducted (1993–1994), the GH chemiluminescence assay had not been fully validated for the concentration range of interest in exercise studies. Cortisol was measured with a chemiluminescence assay (Nichols Institute Diagnostics). The assay sensitivity was 38.6 nmol/L, and the mean inter- and intraassay coefficients of variation (CVs) were 7.0% and 8.4%, respectively. The samples from all study days for each subject were run in the same assay. Serum hormone concentrations were determined by a procedure previously described (26). Briefly, standard curves were evaluated by weighted nonlinear least squares analysis using three different response functions. Uncertainties (SD) associated with each hormone concentration were estimated empirically, considering the variance associated with both the assay response and standard curve evaluations. The standard curve parameters and response function to the variably weighted response data were optimized. Confidence limits for the standard curve parameters were then calculated (26). The function yielding the lowest absolute sum of squared residuals was chosen for analyzing the samples.
Deconvolution analysis of hormone concentrations

Integrated serum GH and cortisol concentrations (area under the curve) for the 6-h time periods were calculated as previously described (27). A multiple parameter deconvolution method was employed to derive quantitative estimates of GH secretory events from the serum GH concentrations (28). This was done to allow simultaneous estimates of the subject-specific monoexponential half-life of endogenous GH. It was assumed that a Gaussian distribution of secretory rates approximates each pulse of GH secretion (29). The sensitivity of the GH IRMA did not allow for estimation of basal GH secretion, so GH secretory rates were assumed to decay to zero (11). GH secretory pulses were considered significant if the fitted amplitude could be distinguished from zero (e.g. pure noise) with 95% statistical certainty. The GH secretory pulse half-duration, GH half-life of elimination, and GH distribution volume were assumed to be constant throughout the study period for each individual (11). The mass of GH secreted per pulse was estimated as the area of the calculated secretory pulse (28). The endogenous GH production rate for each 6-h period was estimated as the product of the number of secretory pulses and the mean GH mass secreted per pulse. Deconvolution analysis was not performed on the serum cortisol concentrations due to the long half-life of cortisol and the short duration (6 h) of blood sampling.

Statistical analysis
Results are expressed as the mean ± SE, unless otherwise stated. A one-way ANOVA with repeated measures was used to examine blood lactate and VO2 responses to submaximal exercise. A 2 x 3 ANOVA (condition x time of day) with repeated measures was employed to determine mean differences in integrated hormone concentrations, peak hormone concentrations, and attributes of GH secretion and clearance. Mean comparisons were examined when mean differences were observed. An level of P < 0.05 was chosen a priori.

As GH and cortisol were measured at 5-min intervals for 6 h, paired comparisons at each time point were not appropriate. The spontaneous changes in hormone concentrations over the course of the day make statistical comparison of the areas under the hormone concentration curves for the control and exercise days potentially misleading. To assess objectively the stimulation of GH and cortisol release by exercise against a background of spontaneous pulsatile secretion modulated by diurnal and circadian rhythms, we normalized each subject’s exercise GH and cortisol concentration time trends to the subject’s control GH and cortisol concentration time trends, respectively. Both absolute and percent changes have been used to analyze such data (30). We had previously determined that absolute differences were more independent of control conditions than ratios or percent change for GH data and therefore chose differences as the method to analyze the present data (31). For the three times of day, we subtracted each subject’s serum hormone concentration at each time point during the control day from their hormone concentration at the same time point during the exercise day (exercise day minus control day). A regression curve (flexible regression spline) was derived for the change in serum hormone concentrations ( serum hormone, exercise day minus control day) over time with simultaneous (taking into account multiple time points) 95% confidence bands. These curves are smoothed versions of the raw data, with the amount of smoothing carefully chosen to be able to estimate the mean profiles without overfitting. The 95% confidence regions were derived using a variation of the bootstrap technique (see Appendix in Ref. 31 for further details). The use of this 95% confidence region avoids the problem of multiple pointwise comparisons. A significant hormone response to exercise was defined as occurring when the lower 95% confidence limit for the regression curve was more than zero. Significant suppression of hormone release was defined as occurring when the upper 95% confidence limit for the regression curve was less than zero. To compare the magnitude of the hormone response to exercise at the different times of day, we determined the difference between the regression curves (with simultaneous 95% confidence regions) at each time point for 0700 and 1900 h (0700 minus 1900 h), 0700 and 2400 h (0700 minus 2400 h), and 1900 and 2400 h (1900 minus 2400 h), as previously described (31).

Results
Subject characteristics
The subjects studied had a mean age of 24.1 ± 1.1 yr, weight of 69.8 ± 2.3 kg, and height of 174 ± 1.6 cm. The subjects had a VO2 max of 47.9 ± 1.4 mL/kg•min and a percent body fat of 13.2 ± 0.6%.

Submaximal VO2 during exercise
Each exercise bout was initiated at the same velocity to elicit initially a similar blood lactate level and VO2. Throughout the 30 min of exercise, the mean blood lactate level was 3.5 ± 0.6, 3.9 ± 0.6 and 3.9 ± 0.9 mmol at 0700, 1900, and 2400 h on the exercise day, respectively. This corresponded to a mean submaximal VO2 of 40.1 ± 0.9, 41.4 ± 0.4, and 41.8 ± 1.5 mL/kg•min, respectively ( 85% VO2 max). There were no significant differences in blood lactate or submaximal VO2 by time of day.

Mean GH and cortisol responses to exercise
The mean GH and cortisol concentrations over the 6-h period are shown in Figs. 1 and 2 . A rise in response to exercise was seen in both GH and cortisol concentrations. The effect of underlying diurnal rhythms of GH and cortisol release can be seen by inspection of the data from the control days. Spontaneous increases in mean serum GH concentrations occurred in the evening and night hours despite the fact that subjects did not sleep (Fig. 1 ). Serum cortisol concentrations rose during the early morning hours, so that baseline levels before exercise were higher before exercise at 0700 than at 1900 or 2400 h


concentrations during blood sampling at 5-min intervals between 0600–1200 h (top), 1800–2400 h (middle), and 2300–0500 h (bottom) in 10 young men studied on an exercise day and an otherwise identical control day. On exercise days, subjects exercised at a constant treadmill velocity (chosen to elicit an initial blood lactate response of 2.5 mmol/L based on an initial treadmill test) for 30 min beginning at 0700 h, 1900, and 2400 h (0 min).

Analysis of GH response to exercise
Integrated GH concentrations and attributes of GH secretory pulses and clearance rates during the 6-h periods are shown in Table 1 . No differences in the 6-h integrated GH concentrations, 6-h GH production rates, or attributes of GH secretory pulses were found among each of the three times of day in either the control or exercise conditions. The immediate GH response to exercise was also assessed by calculating the 2-h integrated GH concentrations (30-min exercise + 90-min recovery), and there were no significant differences by time of day. Analysis of the data by condition (exercise vs. control) revealed that integrated GH concentrations were about 160% higher on the exercise day than on the control day as the result of a significant increase in GH production rates (P < 0.01) with no change in the half-life of GH disappearance. This enhanced secretion was related to a significant increase in the mass of GH secreted per pulse despite a decrease in secretory pulse half-duration (P < 0.05). The exercise stimulus did not affect the number of GH secretory pulses.

Figure 3 depicts the differences over time in serum GH concentrations between the exercise and control days for each of the three times of day. In each graph, the solid line represents the regression curve for the difference, and the dotted lines represent the 95% confidence intervals. A significant GH response or suppression occurred when both 95% confidence limits for the regression curve were greater or less than zero, respectively. Inspection of these graphs reveals that at all exercise times (0700, 1900, and 2400 h), serum GH concentrations were significantly increased by the exercise stimulus compared with the control day (P < 0.05). The exercise-induced stimulation of GH release lasted approximately 145 min at 0700 h, 105 min at 1900 h, and 125 min at 2400 h. A significant suppression of GH release occurred between 205 and 260 min after the onset of exercise at 0700 h and 150 and 240 min after the onset of exercise at 1900 h (P < 0.05). There was no significant suppression of GH release after exercise at 2400 h. To compare the magnitude of the GH response to exercise at the different times of day, we determined the difference between the regression curves at each time point for 0700 and 1900 h (0700 minus 1900 h), 0700 and 2400 h (0700 minus 2400 h), and 1900 and 2400 h (1900 minus 2400 h). Regression curves with simultaneous 95% confidence bands for these differences were calculated. These graphs, which are shown in Fig. 4 , demonstrate that there were no significant differences in the GH response to exercise by time of day.

The change in serum GH concentrations (exercise day minus control day) over time at the three different times of day. The regression curve (solid line) and simultaneous 95% confidence limits (dotted line) are shown. Significant stimulation of serum GH release by exercise over control day conditions occurred when the lower 95% confidence limit for the regression curve was more than zero. Significant suppression of GH release after exercise occurred when the upper 95% confidence limit for the regression curve was less than zero. Refer to Fig. 1 for details of study design.

Comparison of the magnitudes of the GH response to exercise over control conditions at the three different times of day. The difference between the regression curves at each time point for 0700 and 1900 h (0700 minus 1900 h), 0700 and 2400 h (0700 minus 2400 h), and 1900 and 2400 h (1900 minus 2400 h) are shown in the top, middle, and bottom panels, respectively. Regression curves (solid line) with simultaneous 95% confidence bands (dotted lines) for these differences are shown. There were no significant differences in the GH responses to exercise among the three times of day. Refer to Fig. 1 for details of the study design.

Analysis of cortisol response to exercise
Integrated cortisol concentrations on the control days were 127,643 ± 6,460, 44,006 ± 6,630, and 74,770 ± 14,298 min•nmol/L for the 0700, 1900, and 2400 h study days, respectively. On the exercise days, the integrated cortisol concentrations were 135,919 ± 12,232, 65,123 ± 7,325, and 103,942 ± 13,363 min•nmol/L for the 0700, 1900, and 2400 h study days, respectively. ANOVA of these integrated concentrations revealed a significant effect of time of day across conditions (P < 0.01), demonstrating the dominant effect of the circadian rhythm in cortisol release. This effect is further illustrated by the mean baseline cortisol concentrations (1 h before exercise), which were greater (P < 0.01) at 0700 h (411.1 ± 49.7 nmol/L) than at 1900 and 2400 h (168.3 ± 16.6 and 162.8 ± 46.9 nmol/L, respectively). The effect of exercise on integrated cortisol concentrations did not reach statistical significance (P = 0.071), and the interaction between time of day and condition also did not reach statistical significance. Peak cortisol concentrations in response to exercise were significantly greater at 0700 h (729.2 ± 85.2 nmol/L) than at 1900 h (454.0 ± 66.3 nmol/L) or 2400 h (634.6 ± 76.9 nmol/L; P < 0.01); the peak concentration at 2400 h was significantly greater than at 1900 h (P < 0.05). These peak concentrations on the exercise days were significantly higher (P < 0.01) than the highest concentrations observed on the control days (644.8 ± 54.7, 189.5 ± 33.3, and 313.2 ± 28.5 nmol/L for 0700, 1900, and 2400 h study days, respectively). However, a significantly greater percent increase from mean baseline cortisol concentrations (1 h before exercise) to peak cortisol values occurred after exercise at 2400 h (600%; P < 0.01) compared with 1900 h (200%) and 0700 h (150%).

The differences over time in serum cortisol concentrations between the exercise and control days for each of the three times of day are shown in Fig. 5 with 95% simultaneous confidence limits. Exercise at each of the selected times of day significantly stimulated cortisol release for approximately 150–155 min (P < 0.05). There was a brief period of rebound suppression of cortisol release occurring between 240 and 290 min after exercise at 2400 h (P < 0.05), but this was not observed after exercise at 0700 and 1900 h.

The change in serum cortisol concentrations (exercise day minus control day) over time at the three different times of day. The regression curve (solid line) and simultaneous 95% confidence limits (dotted line) are shown. Refer to Figs. 1 and 3 for further details.

To compare the magnitudes of the cortisol response to exercise at the different times of day, we determined the difference between the regression curves (with simultaneous 95% confidence limits) at each time point for 0700 and 1900 h (0700 minus 1900 h), 0700 and 2400 h (0700 minus 2400 h), and 1900 and 2400 h (1900 minus 2400 h). Figure 6 demonstrates that for a brief period of time ( 55 min) the cortisol response to exercise was greater at 0700 h than at 1900 h; this difference was significant between 25 min before and 30 min after exercise began (P < 0.05). Similarly, cortisol concentrations were transiently higher ( 40 min) after exercise at 2400 h compared with exercise at 0700 h; this difference was significant between 130 and 170 min after exercise began (P < 0.05). The cortisol response to exercise was significantly greater at 2400 h than at 1900 h; this difference was significant for approximately 130 min, between 10 and 140 min after exercise began (P < 0.05).

Comparison of the magnitude of the cortisol response to exercise over control conditions at the three different times of day. Regression curves (solid line) with simultaneous 95% confidence bands (dotted lines) for the differences between the designated times of day are shown. A significant difference between two times of day for the cortisol response to exercise over control day conditions is demonstrated when either the lower or upper 95% confidence band crosses zero. Refer to Figs. 1 and 4 for further details.

Discussion
The primary purpose of this study was to investigate whether circadian and diurnal rhythms underlying the secretion of GH and cortisol modulate the responses of these hormones to aerobic exercise. Consistent with earlier reports (3, 6, 8, 9, 19, 20, 32), exercise stimulated a dramatic increase in serum GH concentrations for approximately 105–145 min. The magnitude of the GH response was independent of time of day. The exercise-induced increase in serum GH levels was followed by a transient suppression of GH release ( 55–90 min) after exercise at 0700 and 1900 h, but not at midnight. In contrast, the cortisol response to exercise was modulated by time of day. Although the duration of the increase in serum cortisol concentrations after exercise was similar ( 150–155 min) at 0700, 1900, and 2400 h, the increase over control day levels was greatest at 2400 h and smallest at 1900 h, and an intermediate response occurred at 0700 h. These differences in serum cortisol concentrations between exercise and control days were transient ( 40–130 min) and were most apparent when the effects over time were studied, as the 6-h integrated cortisol concentrations did not differ significantly at each time of day.
Both spontaneous and GHRH-stimulated GH secretion are maximal at night (11, 12, 13, 14, 17, 18). In contrast, the GH secretory response to exercise at 0700, 1900, and 2400 h did not differ significantly in the present study. Two other studies with different experimental designs have reported similar findings. Galliven et al. observed that the GH response to high intensity exercise (90% VO2 max) was similar in the morning and evening, but no comparison was made to control (nonexercise) conditions (19). Scheen et al. observed no difference in the GH secretory response to 3 h of moderate intensity (40–60% VO2 max) exercise initiated at 0500, 1430, or 2330 h compared with resting conditions (20).

The present data suggest that aerobic exercise of sufficient intensity is able to override any diurnal or circadian rhythms underlying GH release when the potentially confounding variables of meals and sleep are controlled. This latter point is important, because subjects ate a standard meal 12 h before each exercise bout and were not allowed to sleep during blood sampling. These conditions differ from normal daily life, where meal ingestion may blunt the GH response to exercise (4). In addition, exercising in the evening may decrease GH secretion during the first few hours of sleep (33).

The increase in serum GH concentrations with exercise was related to an approximately 2-fold increase in GH secretion rates with no significant change in the half-life of GH disappearance, as estimated by deconvolution analysis. Exercise increased ( 2-fold) the mass of GH secreted per pulse and decreased ( 20%) the secretory pulse half-duration, but did not change the number of GH secretory pulses compared with control conditions. These effects of exercise on GH secretory pulse attributes were similar to our previous observations (32). In the present study there were no significant effects of time of day on GH secretory pulse attributes in response to exercise.

After the increase in serum GH concentrations with exercise, a significant suppression of GH release occurred between 2.5 and 4 h after the onset of exercise at 0700 and 1900 h. This may reflect autonegative feedback of GH on its own secretion, as suggested by studies in rats (34). It is unlikely that pituitary stores of GH were depleted, because repeated bouts of exercise (70% VO2 max) elicit similar GH secretory responses even if spaced by only 1 h of rest (32). The absence of a similar rebound suppression of GH release after exercise at 2400 h may reflect the diurnal rhythm of enhanced GH secretion at night even when subjects are awake (12). As the sensitivity of the GH IRMA used in this study was insufficient to measure GH concentrations below 0.2 µg/L, it is possible that the magnitude and timing of the suppression of GH release after exercise may not have been precisely determined.
The circadian rhythm had a significant effect on the cortisol response to aerobic exercise. The increase in cortisol concentrations over control day levels was greatest at 2400 h and smallest at 1900 h, and an intermediate response occurred at 0700 h. Previous studies have reported that that the cortisol response to exercise is similar in both the morning and evening (2, 19, 21, 22), or that exercise elicits a cortisol response in the afternoon, but no response in the morning or evening (20). Three features of our experimental design may account for the differences between the present and past findings. First, an exercise intensity was employed ( 85% VO2 max) that was adequate to reliably stimulate cortisol release; a threshold of 60% VO2 max has been proposed by Few (7). Two studies reporting disparate results from the present findings used exercise intensities between 40–60% VO2 max (2, 20). Second, the study design controlled for the possible effects of meals, sleep, and prior exercise. The cortisol response to exercise is blunted by prior meal ingestion, and the postprandial increase in serum cortisol concentrations is attenuated by prior exercise (1, 2). Third, the pattern of cortisol release over time under exercise conditions was compared with that observed at rest at the identical time of day for each subject. Early studies did not include a control day and simply compared cortisol concentrations during exercise to the preexercise levels on the same day (2, 5, 7, 19). This approach does not take into account the changing cortisol concentrations over the course of the day due to the circadian rhythm. Recent studies have compared the area under the curve for serum cortisol concentrations on exercise and control (nonexercise) days (20, 21, 22). Using this approach, the cortisol response to exercise (70% VO2 max for 40 min) was reported to be similar in the morning (0800 h) and the evening (2000 h) (21). However, using area under the curve analysis or assessing peak hormone concentrations alone does not enable changes over time to be detected. The statistical method employed in the present study enabled differences in serum cortisol levels between exercise and control conditions to be assessed at each time point with 95% confidence limits. The effect of time of day on these differences could then be assessed over time with 95% confidence limits. This approach revealed that time of day does indeed modulate the cortisol response to exercise, albeit for short periods of time ( 40–130 min).

The effect of time of day on the cortisol response to exercise cannot be completely accounted for by the preexercise baseline cortisol concentrations. The highest peak cortisol concentrations after exercise occurred at 0700 h, with the second highest vales at 2400 h; the peak response at 1900 h was the lowest. In contrast, the largest percent increase from baseline to peak values was 600% at 2400 h compared with 200% and 150% at 1900 and 0700 h, respectively. As baseline cortisol levels were similar at 1900 and 2400 h, a greater increase over time occurred in response to exercise at 2400 h than at 1900 h. Furthermore, although baseline cortisol levels were significantly higher at 0700 than at 1900 h, the increases in cortisol levels over time on the exercise compared with the control days were similar at 0700 and 1900 h, with a transiently greater response at 0700 h. Thus, assessing the cortisol response to exercise in relation to the baseline cortisol concentration alone is inadequate (21).

Time of day apparently influences the incremental response, but not the peak response, to pharmacological tests of cortisol secretory reserve. The peak cortisol response 30 min after an iv bolus of ACTH is similar in the morning (0800 h) and afternoon (1600 h), but cortisol concentrations rise more rapidly after ACTH administration in the afternoon than in the morning (35). The incremental cortisol response observed in response to insulin-induced hypoglycemia and ovine CRH is also greater in the afternoon than in the morning, although peak cortisol concentrations do not differ by time of day (36, 37). For clinical purposes, the peak response to ACTH is more valuable than the incremental cortisol response when assessing adrenal cortical reserve, with a peak response exceeding 550 nmol/L (20 µg/dL) considered a normal response (35, 38). In the present study mean peak cortisol responses exceeded this threshold at 0700 and 2400 h, but not at 1900 h. This suggests that the cortisol response to exercise is regulated in complex ways that differ from that observed in response to hypoglycemia, CRH, or ACTH. However, it should be pointed out that the times of day that testing was performed in the present study differed from those in previous studies of pharmacological tests, and thus a direct comparison of results is not possible.
No differences by time of day were observed for mean submaximal VO2 or blood lactate levels during exercise in the present study. Previous studies with different experimental designs have observed higher peak lactate accumulation in the afternoon during exhaustive constant power exercise (39) and greater work capacity in the afternoon and evening compared with the morning (40). In the present study the treadmill velocity was chosen to produce similar blood lactate concentrations and VO2 values. Velocity was not adjusted for changes in blood lactate levels achieved, and subjects did not exercise to exhaustion. Anecdotally, when asked which exercise bout seemed the most difficult, subjects could usually choose one time of day; however, the ratings of perceived exertion (Borg scale) obtained during each exercise bout did not reflect any time of day differences. Thus, the effect of time of day on the cortisol responses to exercise cannot be explained by differences in the physiological or psychological response to exercise.

In conclusion, when the confounding factors of meals, prior exercise, and sleep are controlled, time of day has no effect on the magnitude of the GH response to exercise. In contrast, the cortisol response to exercise is modulated by time of day. Peak cortisol concentrations in response to exercise were highest at 0700 h, followed by 2400 and 1900 h in that order. In contrast, maximal increases in cortisol concentrations over time in comparison to control day conditions occurred at 2400 h, followed by 0700 and 1900 h, in that order. These data suggest that the circadian rhythm of cortisol secretion influences the cortisol response to exercise.

[Sharmer]

This opens up some interesting questions. What is the relative importance of GH levels vs the protein sparing effect of closer spacing of meals etc? (nighttime GH levels are higher in a fasting state- ie nothing after dinner).
Would moving the workouts towards the AM allow enough time to enhance a nutritional response and also allow for a GH spike at night?
Is this why there's been a trend towards earlier training sessions in recent years?
We sat somewhere in the middle, I'd guess, using Glutamine/ZMA at night but without a carb source and training early afternoon.
Second, how would you decide the relative importance of therapy when it's not possible to "do it all"?
I created a set of tables for massage priority for Vanc 04 based on concentrating the most aggressive therapy to enhance the upswing of muscle recovery between speed days and fill in the sessions as the budget allows.
Perhaps the hot/cold showers create a hormonal response and can bridge the gap where massage isn't available and complement it where it is.

Researching findings on supplements and recovery

Effect of leucine metabolite -hydroxy- -methylbutyrate on muscle metabolism during resistance-exercise training

S. Nissen, R. Sharp, M. Ray, J. A. Rathmacher, D. Rice, J. C. Fuller Jr., A. S. Connelly, and N. Abumrad
Iowa State University, Ames 50011; Metabolic Technologies Inc., Ames, Iowa 50010; MET-Rx Inc., Irvine, California 92715; and North Shore University Hospital, Manhasset, New York 11030
Received 18 August 1995; accepted in final form 1 July 1996.
Nissen, S., R. Sharp, M. Ray, J. A. Rathmacher, D. Rice, J. C. Fuller, Jr., A. S. Connelly, and N. Abumrad. Effect of leucine metabolite -hydroxy- -methylbutyrate on muscle metabolism during resistance-exercise training. J. Appl. Physiol. 81(5): 2095-2104, 1996. The effects of dietary supplementation with the leucine metabolite -hydroxy- -methylbutyrate (HMB) were studied in two experiments. In study 1, subjects (n = 41) were randomized among three levels of HMB supplementation (0, 1.5 or 3.0 g HMB/day) and two protein levels (normal, 117 g/day, or high, 175 g/day) and weight lifted for 1.5 h 3 days/wk for 3 wk. In study 2, subjects (n = 28) were fed either 0 or 3.0 g HMB/day and weight lifted for 2-3 h 6 days/wk for 7 wk. In study 1, HMB significantly decreased the exercise-induced rise in muscle proteolysis as measured by urine 3-methylhistidine during the first 2 wk of exercise (linear decrease, P < 0.04). Plasma creatine phosphokinase was also decreased with HMB supplementation (week 3, linear decrease, P < 0.05). Weight lifted was increased by HMB supplementation when compared with the unsupplemented subjects during each week of the study (linear increase, P < 0.02). In study 2, fat-free mass was significantly increased in HMB-supplemented subjects compared with the unsupplemented group at 2 and 4-6 wk of the study (P < 0.05). In conclusion, supplementation with either 1.5 or 3 g HMB/day can partly prevent exercise-induced proteolysis and/or muscle damage and result in larger gains in muscle function associated with resistance training

This study was supported by these findings in 2000.

Effects of -hydroxy- -methylbutyrate on muscle damage after a prolonged run

A. E. Knitter, L. Panton, J. A. Rathmacher, A. Petersen, and R. Sharp
Human Performance Laboratory, Iowa State University, Ames, Iowa 50011
This study examined the effects of supplemental -hydroxy- -methylbutyrate (HMB) on muscle damage as a result of intense endurance exercise. Subjects (n = 13) were paired according to their 2-mile run times and past running experience. Each pair was randomly assigned a treatment of either HMB (3 g/day) or a placebo. After 6 wk of daily training and supplementation, all subjects participated in a prolonged run (20-km course). Creatine phosphokinase and lactate dehydrogenase (LDH) activities were measured before and after a prolonged run to assess muscle damage. The placebo-supplemented group exhibited a significantly greater (treatment main effect, P = 0.05) increase in creatine phosphokinase activity after a prolonged run than did the HMB-supplemented group. In addition, LDH activity was significantly lower (treatment main effect, P = 0.003) with HMB supplementation compared with the placebo-supplemented group. In conclusion, supplementation with 3.0 g of HMB results in a decreased creatine phosphokinase and LDH response after a prolonged run. These findings support the hypothesis that HMB supplementation helps prevent exercise-induced muscle damage.

ß-Hydroxy-ß-Methylbutyrate (HMB) Supplementation in Humans Is Safe and May Decrease Cardiovascular Risk Factors

S. Nissen*1, R. L. Sharp*, L. Panton*, M. Vukovich , S. Trappe and J. C. Fuller, Jr.**
* Iowa State University, Ames, IA, Wichita State University, Wichita, KS, Ball State University, Muncie, IN and ** Metabolic Technologies Incorporated, Iowa State University Research Park, Ames, IA
1To whom correspondence and reprint requests should be addressed.

The leucine metabolite, ß-hydroxy-ß-methylbutyrate (HMB) enhances the effects of exercise on muscle size and strength. Although several reports in animals and humans indicate that HMB is safe, quantitative safety data in humans have not been reported definitively. The objective of this work was to summarize safety data collected in nine studies in which humans were fed 3 g HMB/d. The studies were from 3 to 8 wk in duration, included both males and females, young and old, exercising or nonexercising. Organ and tissue function was assessed by blood chemistry and hematology; subtle effects on emotional perception were measured with an emotional profile test (Circumplex), and tolerance of HMB was assessed with a battery of 32 health-related questions. HMB did not adversely affect any surrogate marker of tissue health and function. The Circumplex emotion profile indicated that HMB significantly decreased (improved) one indicator of negative mood (Unactivated Unpleasant Affect category, P < 0.05). No untoward effects of HMB were indicated. Compared with the placebo, HMB supplementation resulted in a net decrease in total cholesterol (5.8%, P < 0.03), a decrease in LDL cholesterol (7.3%, P < 0.01) and a decrease in systolic blood pressure (4.4 mm Hg, P < 0.05). These effects of HMB on surrogate markers of cardiovascular health could result in a decrease in the risk of heart attack and stroke. In conclusion, the objective data collected across nine experiments indicate that HMB can be taken safely as an ergogenic aid for exercise and that objective measures of health and perception of well-being are generally enhanced.
HMB meta-analysis and the clustering of data sources
Jacques Décombaz, Alexandre Bury and Corinne Hager
Nestle Research Center Nestec Ltd. CH-1000 Lausanne 26, Switzerland E-mail: jacques.decombaz@rdls.nestle.com

The following is the abstract of the article discussed in the subsequent letter:
The purpose of this study was to quantify which dietary supplements augment lean mass and strength gains during resistance training. Peer-reviewed studies between the years 1967 and 2001 were included in the analysis if they met a predetermined set of experimental criteria, among which were at least 3-wk duration and resistance-training 2 or more times a week. Lean mass and strength were normalized for meta-analysis by conversion to percent change per week and by calculating the effect size for each variable. Of the 250 supplements examined, only 6 had more than 2 studies that met the criteria for inclusion in the meta-analysis. Creatine and -hydroxy- -methylbutyrate (HMB) were found to significantly increase net lean mass gains of 0.36 and 0.28%/wk and strength gains of 1.09 and 1.40%/wk (P < 0.05), respectively. Chromium, dehydroepiandrosterone, androstenedione, and protein did not significantly affect lean gain or strength. In conclusion, two supplements, creatine and HMB, have data supporting their use to augment lean mass and strength gains with resistance training.

I know I am heading to the health store and getting me some creatine and HMB again.

[Sharmer]

Second, how would you decide the relative importance of therapy when it's not possible to "do it all"?
I created a set of tables for massage priority for Vanc 04 based on concentrating the most aggressive therapy to enhance the upswing of muscle recovery between speed days and fill in the sessions as the budget allows.
Perhaps the hot/cold showers create a hormonal response and can bridge the gap where massage isn't available and complement it where it is.

I know L carnitine causes vaso -dilation in the lower body, maybe combining this supplement with contrasts baths.

[rapsmvp]

ZMA can be used with pure glutamine (best in powder or powder in a capsule) but not calcium sources. It seems to promote deeper sleep which might have some effect on GH or T. I really don't know why but you sleep deeper, wake up more refreshed, and males do wake up "with a tent in the bed" more often. (Not very scientific!)
BTW, I got some special Glutamine powder to use recently (smells like sulfur!) which is supposed to work better. I'll tell you more about it as it goes.

I am thinking of buying some of this, but I am wondering, can't a multi vitamin with zinc/mag do just as good?

btw what I love about this forum is how things can just shoot off on a tangent