Resistance exercise (RE) protocols are often developed for specific training goals. Although some protocols are designed to maximize muscle strength, others may focus on maximizing muscle hypertrophy. Strength protocols typically involve high intensities (≥85% 1 repetition maximum [1RM]), low volumes (2–6 sets; ≤6 repetitions), and longer rest intervals (3–5 minutes), whereas hypertrophy protocols typically involve moderate intensities (67–85% 1RM), high volumes (3–6 sets; 8–12 repetitions), and shorter rest intervals (30–90 seconds) (27). Modification of program variables surrounding RE prescription (i.e., exercise intensity, volume, and rest interval length) have been suggested to promote distinct responses among several circulating anabolic hormones following an acute bout of RE (29,30). However, examination of the acute response of hormones involved in fluid regulation (e.g., aldosterone) following RE is limited.
Aldosterone (ALD) is a principal component of fluid regulation, which responds to changes in circulating electrolytes and plasma volume (PV) causing increased thirst and renal water and sodium (Na+) retention in an attempt to maintain body fluid homeostasis (2). Significant elevations in ALD have been reported following aerobic exercise (21,23); however, to our knowledge, only 1 study has examined the ALD response to RE. During their investigation, Kraemer et al. (17) reported no change in ALD concentrations following a single set of leg press performed to volitional fatigue. It should be noted, however, that 1 set to failure is not a typical training scheme used in a multiexercise RE protocol and may not accurately exemplify the ALD response to a full-length training session.
Changes in PV, osmolality (Posm), and circulating electrolytes are generally thought to be dependent on the intensity (5,8,18,20,22) and duration (5,18,25) of endurance exercise. However, the impact of acute program variables on mechanisms of fluid regulation during RE remains relatively unknown. In limited studies, moderate-to high-intensity RE (e.g., 70–87% 1RM) has been shown to elicit increases in Posm (17,26) and plasma Na+ (24,26) and reductions in PV (6,26) and plasma potassium (K+) (16,26) during recovery. However, no studies to our knowledge have compared the effects of different RE paradigms on changes in these fluid regulatory variables. Thus, the purpose of this investigation was to examine the influence of high-volume and high-intensity RE protocols on the fluid regulatory response in experienced, resistance-trained men.
Experimental Approach to the Problem
To assess and compare the acute fluid regulatory response to 2 common RE protocols, subjects reported to the Human Performance Laboratory (HPL) on 3 separate occasions. During their first visit, subjects were screened and informed of all study procedures, expectations, and potential risks. In addition, subjects' maximal strength (1RM) was determined on all lifts involved in the exercise protocols. On each of the subsequent visits, subjects performed 1 of the 2 randomly assigned acute RE protocols: (a) high-volume, low-intensity (HV), or (b) low-volume, high-intensity (HI). Experimental trials were performed in a counterbalanced, randomized order, and were separated by a minimum of 1 week to ensure adequate recovery. Each subject performed experimental trials at the same time of day to avoid any potential diurnal effect. On the morning of each trial, subjects reported to the laboratory after a 10-hour overnight fast and having refrained from all forms of moderate to vigorous exercise for the previous 72 hours. Additionally, subjects were asked to provide a 24-hour dietary log preceding the first experimental trial and were instructed to replicate the content, quantity, and timing of their daily diet during the 24 hours before the second experimental trial. Subjects were also instructed to consume 0.5 L of water the night before and the morning of each experimental trial. As hydration status has shown to impact RE performance (14) and endocrine responses (15), subjects provided a urine sample upon arrival to the laboratory for analysis of urine-specific gravity (USG) by refractometry to ensure euhydration (defined as USG ≤1.020). Subjects were permitted to drink water ad libitum during experimental trials and volume of water consumption was recorded. Following each RE protocol, subjects remained in the HPL for all postexercise assessments. Blood samples during experimental trials were obtained at baseline (BL), immediately postexercise (IP), 30-minute postexercise (30P), and 1-hour postexercise (1H) to quantify circulating electrolytes, plasma ALD, PV, and Posm.
Ten resistance-trained men (24.7 ± 3.4 years; 90.1 ± 11.3 kg; 176.0 ± 4.9 cm) were recruited to participate in this research study. Subjects had 6.7 ± 4.6 years of resistance training experience with an average maximum barbell back squat of 172.7 ± 25.2 kg. All subjects were free of any physical limitations that may affect performance. Additionally, all subjects were free of any medications and performance enhancing drugs, as determined by a health and activity questionnaire. Following an explanation of all procedures, risks, and benefits, each subject provided his informed consent before participation in this investigation. The research protocol was approved by the New England Institutional Review Board before subject enrollment.
Maximal Strength Testing
Before 1RM testing, subjects performed a standardized warm-up consisting of 5 minutes on a cycle ergometer against a light resistance, 10 body weight squats, 10 walking lunges, 10 walking hamstring stretches, and 10 walking quadriceps stretches. The 1RM test for the barbell back squat and leg press were performed using previously described methods (13). Subjects performed 2 warm-up sets at 40–60% and 60–80% of his perceived 1RM, respectively, before performing 3–4 subsequent trials to determine the 1RM. A 3- to 5-minute rest period was provided between each trial. For all other exercises, the 1RM was assessed using a prediction formula based on the number of repetitions performed to volitional fatigue using a given weight (1). Trials not meeting the range of motion criteria for each exercise or using improper technique were discarded.
During each experimental trial, subjects performed the standardized warm-up routine described above, followed by a lower-body RE protocol. Table 1 depicts the high-volume (HV) and high-intensity (HI) RE protocols. All subjects were familiar and experienced in using these training protocols during their recent training history. During each protocol, subjects were verbally encouraged to complete each set. If the subject was unable to complete the desired number of repetitions, spotters provided assistance until the remaining repetitions were completed. In the event of forced repetitions, the load was adjusted so that subjects were able to perform the specific number of repetitions for each subsequent set.
To control for diet, subjects were provided a standardized low protein, low carbohydrate breakfast (7 g protein, 3 g carbohydrate, and 3 g fat; Atkins Nutritionals, Inc., Denver, CO, USA) following BL assessments. Immediately following IP blood sampling, subjects were also provided a flavored drink (355 ml; 0 g protein, 2.5 g carbohydrates, 0 g fat).
During each experimental trial, all blood samples were obtained using a Teflon cannula placed in a superficial forearm vein using a 3-way stopcock with a male luer-lock adapter and plastic syringe. The cannula was maintained patent using an isotonic saline solution (Becton Dickinson, Franklin Lakes, NJ, USA). BL blood samples were obtained following a 15-minute equilibration period. IP blood samples were taken within 1 minute of exercise cessation. Subjects were instructed to lie in a supine position for 15 minutes before 30P and 1H blood draws.
At each time point, blood samples were collected into two 6 ml Vacutainer tubes—1 containing sodium heparin and the other K2EDTA (Becton Dickinson, Broken Bow, NE, USA). Whole-blood samples were used for immediate quantification of circulating electrolyte concentrations, hematocrit, and hemoglobin concentrations. The remaining blood was subsequently centrifuged at 3,000g for 15 minutes at 4° C. The resulting plasma samples were used to determine Posm or aliquoted into separate microcentrifuge tubes and frozen at −80° C for later analysis.
Whole-blood electrolyte concentrations (i.e., Na+, and K+) were determined via ion-selective electrodes (EasyLyte; Medica Corporation, Bedford, MA, USA). Hematocrit concentrations were analyzed from whole blood via microcentrifugation (CritSpin, Iris International, Inc., Westwood, MA, USA) and microcapillary technique. Hemoglobin concentrations were analyzed from whole blood using an automated analyzer (HemoCue, Cypress, CA, USA). PV shifts were then calculated using previously established methods (7). Because of the importance of molar exposure at the tissue-receptor level, blood variables were not corrected for PV shifts. Posm was measured by freezing point depressions (Model 3320, Micro-Sample Osmometer; Advanced Instruments, Inc., Norwood, MA, USA). To eliminate interassay variance, all samples were analyzed in duplicate by a single technician. Coefficient of variation for each assay was 0.6% for Na+, 0.4% for K+, 0.5% for Posm, 0.4% for hematocrit, and 0.6% for hemoglobin.
Circulating concentrations of plasma ALD were assessed by enzyme-linked immunosorbent assay (EIA5298; DRG International, Inc., Mountainside, NJ, USA). Analysis was conducted using a spectrophotometer (BioTek Eon, Winooski, VT, USA). To eliminate interassay variance, all samples were thawed once and analyzed in duplicate by a single technician. The coefficient of variation for ALD was 2.5%.
Before statistical procedures, all data were assessed for normal distribution, homogeneity of variance, and sphericity. If assumptions of sphericity were violated, a Greenhouse-Geisser correction was applied. Between-trial differences in biochemical changes were analyzed using a 2 -way (trial × time) analysis of variance. In the event of a significant F ratio, LSD post hoc tests were used for pairwise comparisons. Area under the curve (AUC) was also calculated for ALD using a standard trapezoidal method and was further analyzed by paired samples t-tests. For effect size, partial eta-squared statistics were calculated. According to Green et al. (11), 0.01, 0.06, and 0.14 were interpreted as small, medium, and large effect sizes, respectively. Significance was accepted at an alpha level of p ≤ 0.05, whereas trends toward significance were acknowledged at an alpha level of p ≤ 0.10. All data are reported as mean ± SD.
Preexercise Hydration Status and Workout Volume
All subjects were adequately hydrated (USG ≤1.020) before each trial, and there was no significant difference between trials for baseline USG (p = 0.980). No significant differences were observed between trials for water consumption during each protocol (p = 0.337, HV: 2,007.5 ± 679.5 ml; HI: 2,400.0 ± 765.9 ml). However, a significant difference (p = 0.010) was noted in workout volume—calculated as sets × load × repetitions—between HV (45,300 kg) and HI (33,633 kg). The HV training protocol also resulted in significantly higher plasma lactate responses than HI. These results though are reported elsewhere (9).
Plasma Volume Shifts
No significant trial × time interaction was noted for PV shifts (F = 1.901; p = 0.179; η2 = 0.096), but significant time effects were observed (F = 8.608; p = 0.004; η2 = 0.324). The PV shift from BL to 30P (6.26 ± 7.71%) was significantly greater (p < 0.001) than those observed from BL to IP (−4.81 ± 6.59%) and BL to 1H (4.19 ± 10.27%).
Changes in Posm are displayed in Table 2. A significant time × trial interaction was observed for Posm (F = 8.655; p < 0.001; η2 = 0.325). During HV, Posm was significantly greater at IP (p < 0.001), 30P (p = 0.002), and 1H (p = 0.006) compared with HI. In addition, Posm was significantly elevated from BL at IP (p < 0.001 during HV), whereas Posm was significantly reduced from BL at 30P (p = 0.037), and trended (p = 0.056) toward reduction at 1H during HI.
Changes in plasma electrolyte concentrations are also displayed in Table 2. A significant time × trial interaction was observed for Na+ (F = 13.029; p < 0.001; η2 = 0.420). Plasma Na+ concentrations were significantly greater during HV than HI at IP (p < 0.001) and 30P (p = 0.001). During HV, plasma Na+ concentrations were significantly elevated from BL at IP (p = 0.001) but became significantly reduced from BL at 1H (p = 0.008). Furthermore, a trend toward a reduced Na+ concentration was noted from BL at 30P (p = 0.059) during HV. During HI, Na+ concentrations were significantly reduced from BL at both 30P (p = 0.001) and 1H (p = 0.003).
A significant time × trial interaction was also observed for plasma K+ concentrations (F = 4.513; p = 0.007; η2 = 0.200). Plasma K+ concentrations were significantly lower during HV compared with HI at IP only (p < 0.001). During HV, plasma K+ concentrations were significantly reduced from BL at IP (p = 0.046) but recovered to become significantly elevated at 1H (p = 0.006). Potassium concentrations tended (p = 0.082) to remain elevated at 30P. During HI, K+ concentrations were significantly elevated from BL at IP (p = 0.025), 30P (p = 0.007), and 1H (p = 0.004).
Changes in ALD concentrations are displayed in Figure 1. A trend was observed for a time × trial interaction (F = 3.487; p = 0.056; η2 = 0.162). Plasma ALD concentrations tended to be higher during HV compared with HI. Significant time effects were noted for ALD (F = 55.723; p < 0.001; η2 = 0.756). Compared with BL, ALD was significantly elevated (p < 0.001) at IP, 30P, and 1H. Similarly, AUC analysis indicated a trend between trials (p = 0.070) suggesting that ALD concentrations during HV tended to be higher than those observed during HI.
This study examined the fluid regulatory response to 2 different RE protocols in resistance-trained men. The HV and HI protocols used were typical of those used primarily for hypertrophy and strength development, respectively (27). The main findings of this investigation indicate that RE elicits a significant decrease in PV, whereas high-volume, moderate-intensity RE protocols with short rest intervals (e.g., 1-minute) seem to result in a significant increase in Posm. Compared with HI, HV also elicited significantly greater elevations in plasma Na+ at IP and 30P and significantly lower K+ concentrations at IP only. Collectively, these changes in circulating electrolytes and fluid dynamics during HV seem to influence a trend toward an elevation in plasma ALD.
Moderate-to high-intensity RE (e.g., 70–87% 1RM) has been previously shown to cause PV decreases of up to 22% from baseline levels (4,6,10,26). These reductions in PV typically return to resting levels within 30–60 minutes of exercise cessation (4,6,10,26). The PV responses seen in this study, 2 and 8% following HI and HV, respectively, were also observed to return to preexercise values by 30P and are consistent with the aforementioned studies. Despite the transitory reduction in PV following both RE protocols, Posm continued to remain elevated through 30P during HV only. This is consistent with a previous study by Ploutz-Snyder et al. (26) who reported an elevation in Posm and a decrease in PV for approximately 45 minutes of recovery following a moderate-intensity, moderate-rest (6 × 10-RM, 2-minute) back squat protocol. However, Kraemer et al. (17) examining a single set of moderate intensity (80% 1RM) leg press exercise performed until volitional exhaustion (∼21 repetitions) reported a significant increase in Posm at IP but observed no significant change in PV. Others comparing single-set (1 × 10-RM) and multiple-set (3 × 10-RM) RE protocols (each protocol used 8 exercises with 1-minute rest between each set) reported decreases in PV (−10.3 ± 4.2% and −12.2 ± 5.1%, respectively), but no differences were noted between the training protocols (10). Similarly, Nicholson et al. (24) reported similar decreases in PV following 2 different back squat protocols (4 sets of 6 repetitions at 85% 1RM, 5-minute rest vs. 4 sets of 10 repetitions using 70% 1RM, 1.5-minute rest). In contrast, Craig et al. (6) compared a 10-RM, short rest (1-minute) RE protocol to a 5-RM, long rest (3-minute) RE protocol and reported a greater decrease in PV following the 10-RM (−22.6 ± 2.3%) vs. the 5-RM protocol (−13.0 ± 1.2%). Subjects in that study performed 3 sets of 9 exercises (whole body), with the leg press exercise being performed 3 different times during the circuit-type exercise protocol. This was consistent with other studies that also reported a greater PV decrease following high-volume RE (31). It appears that the magnitude of the PV deficit during RE may be dependent on changes in the acute program design. However, many of these studies (6,10,31) did not report on any other fluid regulatory markers (e.g., Posm, electrolytes, fluid regulatory hormones). The results of the present study appear to be more consistent with those of Gotshalk et al. (10) and Nicholson et al. (24), as no differences were noted in the PV response between the 2 contrasting RE protocols. Based on the changes observed in both the Posm and the electrolyte response to the different RE protocols, it appears that altering multiple acute program variables (e.g., training intensity, training volume, and rest) may provoke a greater change in the fluid regulatory response to RE. However, it should be noted that changes in fluid shifts provide only 1 aspect of the variables that drive the fluid regulatory response.
Both RE protocols elicited significant changes in Na+ and K+ concentrations; however, the magnitude of these changes was greater following HV. Compared with HI, plasma Na+ was significantly greater during HV at IP and 30P. This was consistent with others that reported a greater elevation in plasma Na+ following high-volume compared with low-volume training protocols (24,26).
In contrast to the results observed in the present study, Nicholson et al. (24) reported no significant change from baseline in plasma K+ following either 4 sets of 10 repetitions (70% 1RM) or 4 sets of 6 repetitions (85% 1RM) of the back squat exercise. Considering the similarity in training intensities used in these studies, the discrepancy in the plasma K+ response may be attributed to differences in total training volume. The onset of exercise provokes an initial release of K+ ions during muscle contraction (3,18), which is partly reflected by an increase in plasma K+ (16). This initial elevation in plasma K+ is suggested to be influenced by acute program variables (e.g., exercise intensity and duration) and the muscle mass recruited (18,22). This initial elevation is thought to be followed by a rapid clearance of plasma K+ to maintain membrane potential (3,18,32). Interestingly, the postexercise reuptake of K+ has been shown to exceed its extracellular accumulation causing a reduction in plasma K+ below baseline levels following intense aerobic exercise (12,18,22) and moderate-intensity (e.g., ∼70% RM) RE (16). Although speculative, it is possible that the additional repetitions performed during HV in the present study resulted in a greater net release of K+ compared with HI, causing a greater plasma K+ clearance during recovery. Although limited research has compared the electrolyte response with different RE paradigms, the current results appear to suggest that a multiexercise protocol incorporating moderate intensity and high volume, compared with high intensity and low volume, may elicit greater changes in plasma electrolytes.
Plasma ALD was significantly elevated following both RE protocols but displayed a tendency to increase to a greater extent following HV compared with HI. To the best of our understanding, only 1 other investigation in the literature has examined the ALD response to an acute RE protocol. In that study, no significant changes were reported following a single set of leg press performed at 80% 1RM to volitional exhaustion (17). However, it is likely that the aforementioned exercise stimulus (∼21 repetitions) was either too brief or provided an insufficient workload to stimulate any change in the ALD response. Alternatively, endurance exercise has been shown to induce a significant rise in ALD, which is typically stimulated by increases in Posm and circulating electrolytes and a reduction in PV (5,19,20). Although both RE protocols produced significant reductions in PV, the changes in Posm and electrolytes were significantly greater following HV. Therefore, the current findings appear to support previous studies indicating that changes in plasma ALD are dependent on changes in PV, Posm, and electrolytes.
This investigation aimed to examine the fluid regulatory response following 2 common RE protocols. Although differences in the fluid regulatory response were observed between RE protocols, we must acknowledge potential limitations. First, fluid intake and rehydration were not controlled during exercise or the subsequent recovery period. Although all subjects were euhydrated before each trial, rehydration was allowed ad libitum so as to replicate the subjects' typical rehydration practices during exercise. Additionally, we did not assess body fluid loss (e.g., sweat) during trials. Although increased rates of perspiration and respiration during physical activity often cause insensible fluid loss (28), the extent of fluid lost during an acute bout of RE is reportedly negligible and is believed to play a minimal role in the change in fluid dynamics (6). To the best of our knowledge, this is the first investigation to compare changes in ALD in conjunction with circulating electrolytes, PV, and Posm following different RE protocols in trained men.
The results of this study indicate that RE elicits significant elevations in ALD and Posm, and change in electrolytes, which are accompanied by a reduction in PV. Although changes in PV were similar between protocols, HV resulted in greater changes in electrolytes and Posm and displayed a tendency to produce a greater ALD response compared with HI. Thus, RE paradigms incorporating high-volume, moderate-intensity training with short rest periods, typical of a training protocol designed to enhance muscle hypertrophy, appear to augment the fluid regulatory response to a greater extent than training programs designed to enhance maximal strength.
The results of this study suggest that high-volume, moderate-intensity RE stimulates a greater change in the fluid regulatory response compared with high-intensity, low volume RE. The physiological relevance for coaches pertains to the understanding that high-volume RE performed following sport practices may potentially exacerbate fluid shifts. Although the present results cannot conclude whether this poses additional risk for the athlete as regards dehydration or heat illness, they provide potential interest for future examination.
The authors thank Alyssa N. Varanoske, David D. Church, Edward H. Robinson IV, Kyle S. Beyer, Ran Wang, Michael B. LaMonica, Mattan W. Hoffman, Gerald T. Mangine, and Joshua J. Riffe for their assistance during data collection. The authors have no conflicts of interest to declare.
1. Brzycki M. Strength testing—predicting a one-rep max from reps-to-fatigue. J Phys Educ Recreation Dance 64: 88–90, 1993.
2. Cheuvront SN, Kenefick RW. Dehydration: Physiology, assessment, and performance effects. Compr Physiol 4: 257–285, 2014.
3. Clausen T. Quantification of Na+, K+ pumps and their transport rate in skeletal muscle: Functional significance. J Gen Physiol 142: 327–345, 2013.
4. Collins MA, Hill DW, Cureton KJ, DeMello JJ. Plasma volume change during heavy-resistance weight lifting. Eur J Appl Physiol Occup Physiol 55: 44–48, 1986.
5. Convertino V, Keil L, Bernauer E, Greenleaf J. Plasma volume, osmolality, vasopressin, and renin activity during graded exercise in man. J Appl Physiol Respir Environ Exerc Physiol 50: 123–128, 1981.
6. Craig S, Byrnes W, Fleck S. Plasma volume during weight lifting. Int J Sports Med 29: 89–95, 2008.
7. Dill D, Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol 37: 247–248, 1974.
8. Freund BJ, Shizuru EM, Hashiro GM, Claybaugh JR. Hormonal, electrolyte, and renal responses to exercise are intensity dependent. J Appl Physiol (1985) 70: 900–906, 1991.
9. Gonzalez AM, Hoffman JR, Townsend JR, Jajtner AR, Boone CH, Beyer KS, Baker KM, Wells AJ, Mangine GT, Robinson EH. Intramuscular anabolic signaling and endocrine response following high volume and high intensity resistance exercise protocols in trained men. Physiol Rep 3: e12466, 2015.
10. Gotshalk LA, Loebel CC, Nindl BC, Putukian M, Sebastianelli WJ, Newton RU, Häkkinen K, Kraemer WJ. Hormonal responses of multiset versus single-set heavy-resistance exercise protocols. Can J Appl Physiol 22: 244–255, 1997.
11. Green TR, Fisher J, Matthews JB, Stone MH, Ingham E. Effect of size and dose on bone resorption activity of macrophages by in vitro clinically relevant ultra high molecular weight polyethylene particles. J Biomed Mater Res 53: 490–497, 2000.
12. Hallen J, Gullestad L, Sejersted OM. K+ shifts of skeletal muscle during stepwise bicycle exercise with and without beta-adrenoceptor blockade. J Physiol 477: 149, 1994.
13. Hoffman J. Norms for Fitness, performance, and health. Champaign, IL: Human Kinetics, 2006.
14. Judelson DA, Maresh CM, Farrell MJ, Yamamoto LM, Armstrong LE, Kraemer WJ, Volek JS, Spiering BA, Casa DJ, Anderson JM. Effect of hydration state on strength, power, and resistance exercise performance. Med Sci Sports Exerc 39: 1817, 2007.
15. Judelson DA, Maresh CM, Yamamoto LM, Farrell MJ, Armstrong LE, Kraemer WJ, Volek JS, Spiering BA, Casa DJ, Anderson JM. Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism. J Appl Physiol (1985) 105: 816–824, 2008.
16. Juel C, Bangsbo J, Graham T, Saltin B. Lactate and potassium
fluxes from human skeletal muscle during and after intense, dynamic, knee extensor exercise. Acta Physiol Scand 140: 147–159, 1990.
17. Kraemer WJ, Fleck SJ, Maresh CM, Ratamess NA, Gordon SE, Goetz KL, Harman EA, Frykman PN, Volek JS, Mazzetti SA. Acute hormonal responses to a single bout of heavy resistance exercise in trained power lifters and untrained men. Can J Appl Physiol 24: 524–537, 1999.
18. Lindinger MI. Potassium
regulation during exercise and recovery in humans: Implications for skeletal and cardiac muscle. J Mol Cell Cardiol 27: 1011–1022, 1995.
19. Mandroukas K, Zakas A, Aggelopoulou N, Christoulas K, Abatzides G, Karamouzis M. Atrial natriuretic factor responses to submaximal and maximal exercise. Br J Sports Med 29: 248–251, 1995.
20. Mannix ET, Palange P, Aronoff GR, Manfredi F, Farber MO. Atrial natriuretic peptide and the renin-aldosterone axis during exercise in man. Med Sci Sports Exerc 22: 785–789, 1990.
21. McConell G, Burge C, Skinner S, Hargreaves M. Influence of ingested fluid volume on physiological responses during prolonged exercise. Acta Physiol Scand 160: 149–156, 1997.
22. Medbø J, Sejersted O. Plasma potassium
changes with high intensity exercise. J Physiol 421: 105–122, 1990.
23. Morgan R, Patterson M, Nimmo M. Acute effects of dehydration on sweat composition in men during prolonged exercise in the heat. Acta Physiol Scand 182: 37–43, 2004.
24. Nicholson G, Mcloughlin G, Bissas A, Ispoglou T. Do the acute biochemical and neuromuscular responses justify the classification of strength-and hypertrophy-type resistance exercise? J Strength Cond Res 28: 3188–3199, 2014.
25. Perrault H, Cantin M, Thibault G, Brisson G, Brisson G, Beland M. Plasma atrial natriuretic peptide during brief upright and supine exercise in humans. J Appl Physiol (1985) 66: 2159–2167, 1989.
26. Ploutz-Snyder L, Convertino V, Dudley G. Resistance exercise-induced fluid shifts: Change in active muscle size and plasma volume. Am J Physiol 269: R536–R543, 1995.
27. Ratamess N, Alvar B, Evetoch T, Housh T, Kibler W, Kraemer W. Progression models in resistance training for healthy adults [ACSM position stand]. Med Sci Sports Exerc 41: 687–708, 2009.
28. Rehrer NJ. Fluid and electrolyte balance in ultra-endurance sport. Sports Med 31: 701–715, 2001.
29. Smilios I, Pilianidis T, Karamouzis M, Tokmakidis SP. Hormonal responses after various resistance exercise protocols. Med Sci Sports Exerc 35: 644–654, 2003.
30. Uchida MC, Crewther BT, Ugrinowitsch C, Bacurau RFP, Moriscot AS, Aoki MS. Hormonal responses to different resistance exercise schemes of similar total volume. J Strength Cond Res 23: 2003–2008, 2009.
31. Wallace MB, Moffatt RJ, Hancock LA. The Delayed effects of heavy resistance exercise on plasma volume shifts. J Strength Cond Res 4: 154–159, 1990.
32. Wasserman K, Stringer WW, Casaburi R, Zhang YY. Mechanism of the exercise hyperkalemia: An alternate hypothesis. J Appl Physiol (1985) 83: 631–643, 1997.