Twenty-one recreationally active men (mean ± SD; age = 23.5 ± 2.6, range = 21–30 years; height = 181.3 ± 6.1, range = 168–191 cm; weight = 85.5 ± 10.5 kg, range = 71–115 kg; body mass index, 26.0 ± 2.4, 22–32 kg·m−2) volunteered for this study. The subjects' physical activities included walking or jogging (n = 10), cycling (n = 8), resistance training (n = 11), and recreational sports (n = 2). Specifically, the subjects participated in 1.7 ± 1.5 hours (range = 0–3.5 hours) of physical activity per week, but none of the subjects were competitive athletes. In addition, none of the subjects reported or exhibited (a) a history of medical or surgical events that might have significantly affected the study outcome, including cardiovascular disease or metabolic, renal, hepatic, or musculoskeletal disorders; (b) use of any medication that might have significantly affected the study outcome; (c) use of nutritional supplements (e.g., creatine, protein drinks, amino acids, or vitamins) in the 6 weeks before beginning the study; or (d) participation in another clinical trial or ingestion of another investigational product within 30 days before screening and enrollment. This study was approved by the University Institutional Review Board for Human Subjects, and each subject completed a health history questionnaire and signed a written informed consent document before testing.
After the initial 30-minute resting period, the subjects were fitted with an HR monitor (Polar Electro Inc., Lake Success, NY, USA), and HR was recorded during each of the 4 testing phases and reported as 10-minute mean values (35). In addition, EE, V[Combining Dot Above]O2, and carbon dioxide production rate (V[Combining Dot Above]CO2) were measured continuously during the resting and exercise conditions using a calibrated TrueMax 2400 metabolic cart (Parvo Medics, Sandy, UT, USA). The gas analyzers were calibrated with room air and gases of known concentration before all testing sessions. The temperature was kept between 22 and 24° C, and humidity was maintained at ∼40%. The gas and flow calibration were less than or equal to 2% before each test. For all indirect calorimetry measures, the subjects were fitted with a nose clip and breathed through a 2-way valve (2700 breathing valve; Hans Rudolph Inc., Kansas City, MO, USA). During the resting phases, the subjects were instructed to remain supine and awake, while not talking or fidgeting. Energy expenditure (in kJ·min−1) was derived from the RER data by using the Weir (40) conversion for non-protein RER. The O2, CO2, and EE parameters were recorded breath-by-breath and expressed as 10-minute mean values (35). The subject's arterial blood pressure (i.e., SBP and DBP) was measured every 15 minutes during the resting conditions using a stethoscope (Save Rite Medical, Omron Marshall Nurse Stethoscope, Brooklyn, NY, USA) and an aneroid sphygmomanometer (MDF Instruments Direct, Inc., Agoura Hills, CA, USA) according to the procedures described by Housh et al. (25). Specifically, on arrival to the laboratory, the subjects rested for 30 minutes in a semireclined position. After the initial resting period, a blood pressure measurement was taken. The blood pressure cuff was placed on the subject's upper arm, with the arm at the level of the heart. The brachial artery was palpated on the anterior aspect of the elbow and the middle of the cuff bladder was placed at this location, 2–3 cm above the antecubital fossa. The bell of the stethoscope was placed over the brachial artery with light pressure. The cuff was inflated to 30 mm Hg greater than the estimated systolic value to ensure the artery was completely occluded. The cuff was then deflated at a rate of 2–3 mm Hg per second until pulsatile blood flow occurred. The SBP was determined (within 2 mm Hg) as the pressure where the first Korotkoff sounds were detected. The cuff was continuously deflated at 2–3 mm Hg per second, and DBP was determined when the Korotkoff sounds disappeared. The DBP measure was confirmed by continuing to deflate the cuff for another 10–20 mm Hg to confirm the absence of sounds. The test-retest reliability data from the tester for SBP and DBP indicated that for repeated blood pressures taken 30 minutes apart from the intraclass correlation coefficients (R) were 0.98 and 0.87 for SBP and DBP, respectively, with a standard error of the measurement that ranged from 1 to 2 mm Hg. Ratings of perceived exertion were also recorded every 15 minutes during the exercise trials using the Borg RPE Scale (6). The dependent variables in this study were chosen to determine if the thermogenic supplement had effects on the specific metabolic variables (EE, V[Combining Dot Above]O2, and RER), cardiovascular function (HR, SBP, and DBP), and RPE during postsupplementation rest, exercise, and recovery from exercise.
The subjects received either the placebo or the thermogenic supplement in a randomized order for the 2 experimental trials. The subjects received the dosage recommended by the manufacturer (General Nutrition, Inc., Pittsburgh, PA, USA). One dose of the nutritional supplement capsules included 200 mg of caffeine, 100 mg of capsicum extract, 2 mg of P. longum, 250 mg of B. serrata extract, 500 mg of dried ginger root, 100 mg of cinnamon bark, 20 mg of niacin, 500 mg of M. pruriens. To maintain the double-blind nature of the experiment, the placebo capsules were matched in size and appearance and contained microcrystalline cellulose (Table 1). In addition, third-party random laboratory testing (Nutra Manufacturing Inc., Greenville, SC, USA) was performed to confirm that the ingredients in the supplement and placebo capsules were ±5% of the manufacturer claims. There were no adverse events reported. Two subjects did report side effects after supplementation. Specifically, 1 subject reported nausea and a headache during the walking portion of the test, and 1 subject reported a tingling sensation in his arms and legs. These side effects were not severe enough to cause the subject to withdraw from the study and all of the symptoms were resolved within the 4-hour testing period.
Separate 2-way analysis of variances (ANOVAs) (condition × time) were used to analyze the EE, V[Combining Dot Above]O2, RER, HR, SBP, DBP, and RPE data. The EE, V[Combining Dot Above]O2, RER, and HR data were analyzed for the presupplementation, postsupplementation, exercise, and postexercise phases using separate 2 (supplement and placebo) × 19 (measurement times) ANOVAs with a Greenhouse-Geisser correction. The SBP and DBP data were analyzed for the presupplementation, postsupplementation, and postexercise phases (2 × 12 ANOVAs), and the RPE data were analyzed for the exercise phase only (2 × 5 ANOVAs). The a priori planned comparisons of the mean differences between the supplement and placebo were examined using paired samples t-tests at an alpha level of p ≤ 0.05. The a priori planned comparisons were also examined using Bonferroni corrected paired samples t-tests (p ≤ 0.05/19 for EE, V[Combining Dot Above]O2, RER, and HR; p ≤ 0.05/12 for SBP and DBP; p ≤ 0.05/5 for RPE). All statistical analyses were performed using SPSS software (version 19.0; IMB SPSS Inc., Chicago, IL, USA).
The results of the 2-way repeated measures ANOVA with a Greenhouse-Geisser correction indicated that there was a significant condition × time interaction (F = 3.23; p = 0.019; partial η 2 = 0.139) for EE. There were no differences in EE between the supplement and placebo during the presupplementation, postsupplementation resting, or postexercise recovery phases. During the exercise phase, however, EE was significantly greater at the Bonferroni corrected alpha (0.05/19 comparisons; p ≤ 0.00263) for the supplement than the placebo at 20 (p = 0.00116), 40 (p = 0.00189), 50 (p = 0.00027), and 60 (p = 0.00011) minutes (Figure 2).
Oxygen Consumption Rate
The results of the 2-way repeated measures ANOVA with a Greenhouse-Geisser correction indicated that there was a significant condition × time interaction (F = 7.345; p < 0.001; partial η 2 = 0.269) for V[Combining Dot Above]O2. During the presupplementation and postsupplementation phases, there were no significant differences in V[Combining Dot Above]O2 between the supplement and placebo. During exercise, however, the V[Combining Dot Above]O2 was significantly greater for the supplement than the placebo at the Bonferroni corrected alpha (0.05/19 comparisons; p ≤ 0.00263) at 20 (p = 0.000517), 30 (p = 0.00205), 40 (p = 0.00219), 50 (p = 0.00016), and 60 (p = 0.00009) minutes. In addition, the postexercise resting V[Combining Dot Above]O2 was significantly greater for the supplement than the placebo at 20 (p = 0.00118) minutes (Figure 3).
Respiratory Exchange Ratio
The results of the 2-way repeated measures ANOVA with a Greenhouse-Geisser correction indicated that there was indicated a significant condition × time interaction (F = 2.758; p = 0.021; partial η 2 = 0.121) for RER. There were no significant differences in RER between the supplement and placebo during the presupplementation, postsupplementation, exercise, or postexercise recovery phases (Figure 4).
The results of the 2-way repeated measures ANOVA with a Greenhouse-Geisser correction indicated that there was no significant condition × time interaction (F = 1.865; p = 0.122; partial η 2 = 0.085) for HR. There were no significant differences in HR between the supplement and placebo during the presupplementation, postsupplementation, exercise, or postexercise recovery phases (Figure 5).
Systolic Blood Pressure
The results of the 2-way repeated measures ANOVA with a Greenhouse-Geisser correction indicated that there was no condition × time interaction (F = 0.976; p = 0.434; partial η 2 = 0.047) for SBP. In addition, during the resting and recovery phases, there were no significant differences in SBP between the supplement and placebo (Figure 6).
Diastolic Blood Pressure
The results of the 2-way repeated measures ANOVA with a Greenhouse-Geisser correction indicated that there was no significant condition × time interaction (F = 0.874; p = 0.499; partial η 2 = 0.042) for DBP. In addition, during the resting and recovery, there were no significant differences in DBP between the supplement and placebo (Figure 7).
Ratings of Perceived Exertion
The results of the 2-way repeated measures ANOVA with a Greenhouse-Geisser correction indicated there was no condition × time interaction (F = 0.677; p = 0.547; partial η 2 = 0.033) for RPE during the exercise phase and there were no significant differences in RPE between the supplement and placebo at any time period.
The purpose of the present study was to examine the acute physiological effects (EE, V[Combining Dot Above]O2, RER, HR, SBP, DBP, and RPE) of supplementation with a thermogenic nutritional blend at rest, during low-intensity exercise, and recovery from exercise in men. There were no significant differences between the supplement and placebo for any of the metabolic (EE, V[Combining Dot Above]O2, RER) or cardiovascular (HR, SBP, DBP) measures taken for 30 minutes before supplementation. In addition, the resting values for EE, V[Combining Dot Above]O2, RER, HR, SBP, and DBP in this study were similar to those typically reported after a 12-hour overnight fast (7,12,17,24,31,34). Specifically, the mean (±SD) presupplementation EE for the supplement (6.10 ± 0.92 kJ·min−1) was not different from the placebo (6.13 ± 0.79 kJ·min−1) and was similar to the resting EE values (5.39–5.95 kJ·min−1) previously reported (17,31). The V[Combining Dot Above]O2 values for the supplement (3.6 ± 0.36 ml·kg−1·min−1) and the placebo (3.6 ± 0.26 ml·kg−1·min−1) were within the range of V[Combining Dot Above]O2 values reported (3.5–3.7 ml·kg−1·min−1) at rest (7,17). In addition, the RER values in this study for the supplement and placebo (0.77 ± 0.05 and 0.79 ± 0.05, respectively) were not significantly different and were consistent with resting RER values previously reported (0.76–0.81) (31,34). Furthermore, the HR (supplement = 58 ± 7.9 b·min−1; placebo = 58 ± 7.4 b·min−1), SBP (supplement = 115 ± 8 mm Hg; placebo = 116 ± 8 mm Hg), and DBP (supplement = 72 ± 5 mm Hg; placebo = 71 ± 6 mm Hg) presupplementation resting values were not different for the supplement and placebo and were similar to the HR (58 ± 3 b·min−1), SBP (110 ± 3 mm Hg), and DBP (75 ± 2 mm Hg), values were reported at rest (24,31).
During the 50-minute postsupplementation resting phase, there were no significant differences between the supplement and placebo for any of the metabolic or cardiovascular measures. Although no previous studies have examined the physiological responses to the specific blend of thermogenic ingredients (caffeine, capsaicin, P. longum, ginger, niacin, B. serrata extract, cinnamon, and M. pruriens) used in this study, a number of studies (8,24,35,38,41) have examined the effects of caffeine and various caffeine-containing thermogenic blends on resting EE, V[Combining Dot Above]O2, RER, HR, SBP, and DBP. In contrast to the current findings, significant increases in resting EE (6–29%) and V[Combining Dot Above]O2 (4–15%) have been reported after supplementation with thermogenic ingredients. In addition, some studies have reported that thermogenic supplements resulted in increases (24,38) or decreases (24,38) in RER. Furthermore, several studies (24,35,41) have shown that various thermogenic blends alter hemodynamic function, reflected by increases or decreases in HR and blood pressure.
It is possible that, in this study, the lack of effect of the thermogenic blend on any of the metabolic or cardiovascular measures during the initial 50 minutes of postsupplementation resting was related to the length of measurement at rest, the relative dose of caffeine, or the specific blend of thermogenic ingredients. Specifically, most studies (8,24,38,41) have examined the metabolic and cardiovascular responses to various caffeine-containing blends over 3 or more hours of rest. In this study, however, resting measurements were only taken for 50 minutes after supplementation. It has been shown (18) that caffeine concentration peaks in the blood between 15 and 120 minutes. Thus, the metabolic and cardiovascular changes associated with caffeine may not fully manifest for several hours after ingestion. For example, Hoffman et al. (24) reported that the greatest increase in EE appeared 2 and 3 hours after supplementation with a caffeine-containing thermogenic blend, and no change in HR or RER was observed until hour 2. Although no significant changes in EE, V[Combining Dot Above]O2, RER, HR, SBP, or DBP were reported during the resting phase of this study, it is possible that responses typically observed after thermogenic supplementation would have been observed if the resting measures were continued for 2 or more hours.
Previous studies have found that the effects of caffeine are dose dependent (3,9), and the magnitude of responses differ with various combinations of thermogenic ingredients (24,35,38). For example, a relative dose of 4.1 mg·kg−1 of caffeine contained in a thermogenic blend (caffeine, green tea extract, G. cambogia, and niacin) resulted in significant increases in EE (12.1%), V[Combining Dot Above]O2 (15.1%), RER (2.3%), and SBP (1.3%), while at a lower relative dose of caffeine (2.1 mg·kg−1) not contained in a thermogenic blend, there was no significant change in EE and significant decreases in V[Combining Dot Above]O2 (5.6%), RER (6.2%), as well as SBP (2.9%) (38). Differences in the magnitude of the metabolic responses have also been observed with blends containing the same relative dose (2.4 mg·kg−1) of caffeine. Specifically, a thermogenic blend containing caffeine and epigallocatechin gallate resulted in a 10.5% increase in EE (8), while only a 6% increase in EE was reported after supplementation with a blend containing caffeine, capsaicin, bioperine, and niacin (35). In the present study, a mean relative dose of 2.4 ± 0.3 mg·kg−1 combined with capsaicin, P. longum, ginger, niacin, B. serrata extract, cinnamon, and M. pruriens did not result in any significant metabolic or cardiovascular changes at rest. These findings suggested that thermogenic blends that contain a relatively lower dose (2.4 mg·kg−1) of caffeine may have less effect on metabolic and cardiovascular responses at rest than those that contain a relatively greater dose (4.1 mg·kg−1). It is also possible, however, that the combination of ingredients used in the present study (Table 1) were less effective at rest than the combination of ingredients used in other thermogenic blends (e.g., caffeine, green tea extract, G. cambogia, and niacin).
In this study, a caffeine-containing thermogenic blend (caffeine, capsaicin, P. longum, ginger, niacin, B. serrata extract, cinnamon, and M. pruriens), at a relative dose of 2.4 ± 0.3 mg·kg−1 resulted in EE and V[Combining Dot Above]O2 (Figure 3) values that were 3–4% greater for the supplement than the placebo, with no change in HR during 60 minutes of walking (3.2–4.8 km·hr−1) . It has been shown (17) that caffeine supplementation, at a relative dose of 5 mg·kg−1, increased the metabolic rate (EE and V[Combining Dot Above]O2) and blood pressure but did not change HR or RER during low-intensity (30% V[Combining Dot Above]O2max) exercise. During walking, caffeine supplementation at a lower relative dose (∼3 mg·kg−1), however, did not result in significant metabolic (V[Combining Dot Above]O2 or RER) changes, although blood pressure was increased and HR decreased (37). It has been suggested (35) that a relatively lower dose (2–4 mg·kg−1) of caffeine combined with other thermogenic ingredients may work synergistically to increase the metabolic rate, with limited cardiovascular effects. The metabolic and cardiovascular responses to various thermogenic blends, however, have been shown to differ depending on the specific blend of ingredients (31,35). For example, Ryan et al. (35) reported that during 60 minutes of walking there were no changes in EE or RER, significant increases in V[Combining Dot Above]O2, and a transient increase in HR after supplementation with 1.9–4.1 mg·kg−1 of caffeine contained in a blend (caffeine, capsaicin, niacin, and bioperine). Different combinations of thermogenic ingredients that contained a lower relative dose of caffeine (2 mg·kg−1) have been shown to have less of an effect on metabolic and cardiovascular responses. Specifically, supplementation with various thermogenic blends (e.g., caffeine, taurine, guarana, yerba mate, etc.) containing approximately 2 mg·kg−1 of caffeine did not have any significant effect on EE, V[Combining Dot Above]O2, HR, or RER during treadmill exercise at 50% V[Combining Dot Above]O2max (31). Thus, the current findings suggested that the specific blend of thermogenic ingredients used in this study was more effective for increasing the metabolic rate during exercise than those previously reported (31), despite using a similar (2.4 mg·kg−1 vs. 2 mg·kg−1) relative dose of caffeine. In addition, these findings indicated that, during exercise, the specific combination of thermogenic ingredients used in this study may work synergistically to increase the metabolic rate with fewer cardiovascular changes at a lower relative dose of caffeine (2.4 ± 0.3 mg·kg−1) than caffeine alone (5 mg·kg−1) (17).
Increases in the metabolic rate after thermogenic supplementation have been attributed to caffeine's role as an adenosine receptor antagonist and/or β-adrenergic receptor agonist (1,20). Specifically, caffeine's effects on β-adrenergic receptors prolong the actions of cAMP and increase lipolysis resulting in an increase in the metabolic rate and a potential shift in substrate utilization (1). In addition, it has been suggested (5) that the actions of caffeine may be enhanced when combined with other thermogenic ingredients such as capsaicin. Thus, in this study, the greater EE and V[Combining Dot Above]O2 values for the supplement than the placebo during exercise were likely related to the synergistic effects of caffeine and other thermogenic ingredients on β-adrenergic receptors.
Previous studies (11,26,30,32) have suggested that caffeine ingestion may decrease the perception of effort during exercise. For example, caffeine has been shown to alter the central drive (26), have an analgesia effect (30,32), and/or improve cardiorespiratory dynamics (11). These effects have been reported during heavy to supramaximal exercise. In this study, however, the caffeine-containing thermogenic blend had no effect on RPE during low-intensity walking exercise (Figure 8). These findings were similar to those of Ryan et al. (35) who reported that thermogenic supplementation did not change the perception of effort during exercise. Thus, caffeine-containing thermogenic blends may have no effect on RPE during low-intensity exercise.
In contrast to the findings of Ryan et al. (35), the caffeine-containing thermogenic blend used in this study resulted no significant change in EE during recovery from exercise (Figure 2). Although EE was 10–11% greater, V[Combining Dot Above]O2 was 5–6% greater, and RER was 4–6% lower for the supplement than placebo, these difference were not significant using a Bonferroni correction for the type 1 error rate. In addition, in this study, the supplement had no effect on HR (Figure 5), SBP (Figure 6), or DBP (Figure 7) during recovery from low-intensity walking. Previous studies (22,35) have shown that both HR and blood pressure were increased after supplementation with caffeine or caffeine-containing thermogenic blends. For example, Ryan et al. (35) reported significant increases in HR, SBP, and DBP after supplementation with a caffeine-containing thermogenic blend (caffeine, capsaicin, niacin, bioperine) during postexercise recovery. In addition, it has been suggested (22) that the increased blood pressure and HR responses after caffeine supplementation (3.3 mg·kg−1) in men were because of increased vascular resistance mediated through caffeine's actions as an adenosine receptor antagonist that blocked the vasodilation actions of adenosine. It is possible that the differences in cardiovascular responses in this study and those that have examined a different thermogenic blend (35) or caffeine alone (22) were related to differences in the specific blend of thermogenic ingredients or the relative amount of caffeine. Although the thermogenic blend used in this study and that of Ryan et al. (35) contained some similar ingredients (caffeine, capsaicin, niacin, and P. longum), the addition of ginger, which has been shown to have a depressor effect on arterial blood pressure, to the blend used in this study may have had potential cardiovascular effects (19,36,43). Thus, it is possible that HR, SBP, and DBP did not change in this study as a result of the interaction between caffeine, which can increase blood pressure, and ginger, which has the potential to decrease blood pressure. It is also possible that the lack of any significant changes in EE, RER, blood pressure changes, or HR during postexercise recovery were related to the relatively lower mean dose of caffeine (2.4 ± 0.3 mg·kg−1) when compared with caffeine supplementation alone (3.3 mg·kg−1) (22). It has been shown (1,22) that higher doses of caffeine (3.3–5.7 mg·kg−1) are associated with greater metabolic and cardiovascular changes than lower doses (1.4–2.9 mg·kg−1). Future studies should examine the metabolic and cardiovascular responses to various thermogenic blends during recovery from exercise to determine if these blends have the potential to increase the metabolic rate and minimize the changes in blood pressure and HR responses typically associated with caffeine ingestion.
In conclusion, a thermogenic blend containing caffeine, capsaicin, piperine, ginger, niacin, Platycodi grandiflorus, cinnamon, and M. pruriens resulted in no metabolic (EE, V[Combining Dot Above]O2, and RER) or cardiovascular (HR, SBP, and DBP) changes during the 50-minute postsupplementation resting or postexercise recovery phase. During exercise, however, the thermogenic blend resulted in a greater metabolic rate and may have the potential to increase EE. Furthermore, there were no significant changes in HR, SBP, DBP, or RPE. These findings suggested that the specific blend of ingredients in the thermogenic nutritional supplement, when combined with exercise, increased the metabolic rate with no changes in cardiovascular function and no effect on the perception of effort in aerobically untrained younger men (19–29 years).
Thermogenic blends are marketed as weight loss and/or weight management supplements. It has been suggested (5,42) that the various ingredients contained in these blends work synergistically to increase the metabolic rate, increase lipid oxidation, and alter cardiovascular function. Thus, it is possible that thermogenic supplements, used in conjunction with exercise, may increase weight loss and improve body composition. Few studies (31,35), however, have examined effects of various thermogenic blends during low-intensity exercise. It is important to examine the efficacy of the purported metabolic and cardiovascular responses to these supplements during various activities of daily living (e.g., at rest, during exercise, and recovery from exercise). The present findings suggested that, when taken with sufficient time (∼50 minutes) before exercise, a thermogenic blend containing caffeine, capsaicin, P. longum, ginger, niacin, B. serrata extract, cinnamon, and M. pruriens has the potential to increase the metabolic rate without significant changes in the perception of effort or cardiovascular function. Therefore, it is possible that the thermogenic supplement used in this study would help athletes and nonathletes to achieve a negative caloric balance, increase weight loss, and improve body composition when combined with long duration, low-intensity exercise.
This study was funded by a research Grant from General Nutrition Corporation. The results of this study do not constitute endorsement of the product by the authors or the National Strength and Conditioning Association.
1. Acheson KJ, Gremaud G, Meirim I, Montigon F, Krebs Y, Fay LB, Gay L-J, Schneiter P, Schindler C, Tappy L. Metabolic effects of caffeine in humans: Lipid oxidation or futile cycling? Am J Clin Nutr 79: 40–46, 2004.
2. Akilen R, Tsiami A, Devendra D, Robinson N. Glycated haemoglobin and blood pressure-lowering effect of cinnamon in multi-ethnic Type 2 diabetic patients in the UK: A randomized, placebo-controlled, double-blind clinical trial. Diabet Med 27: 1159–1167, 2010.
3. Astrup A, Toubro S, Cannon S, Hein P, Breum L, Madsen J. Caffeine: A double-blind, placebo-controlled study of its thermogenic metabolic, and cardiovascular effects in healthy volunteers. Am J Clin Nutr 51: 759–767, 1990.
4. Bellet S, Kershbaum A, Finck ME. Response of free fatty acids to coffee and caffeine. Metabolism 17: 702–707, 1968.
5. Belza A, Jessen AB. Bioactive food stimulants of sympathetic activity: Effect on 24-hr energy expenditure and fat oxidation. Eur J Clin Nutr 59: 733–741, 2005.
6. Borg G. Borg's Rating of Perceived Exertion and Pain Scale. Champaign, IL: Human Kinetics, 1998.
7. Chad K, Quigley B. Effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur J Appl Physiol 59: 48–54, 1989.
8. Dalbo VJ, Roberts MD, Stout JR, Kerksick CM. Acute effects of ingesting a commercial thermogenic drink on changes in energy expenditure and markers of lipolysis. J Int Soc Sports Nutr 5: 1–7, 2008.
9. Denaro CP, Brown CR, Wilson M, Jacob P, Benowitz NL. Does-dependency of caffeine metabolism with repeated dosing. Clin Pharmacol Ther 48: 277–285, 1990.
10. Depeint F, Bruce WR, Shangari N, Mehta R, O'Brien PJ. Mitochondrial function and toxicity: Role of the B vitamin family on mitochondrial energy metabolism. Chem Biol Interact 163: 94–112, 2006.
11. Doherty M, Smith PM. Effects of caffeine ingestion on rating of perceived exertion during and after exercise: A meta-analysis. Scand J Med Sci Sports 15: 69–78, 2005.
12. Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, Vandermander J. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. Am J Clin Nutr 70: 1040–1047, 1999.
13. Dulloo AG, Geissler CA, Horton T, Collins A, Miller DS. Normal caffeine consumption: Influence on thermogenesis and daily energy expenditure in lean and post obese human volunteers. Am J Clin Nutr 49: 44–50, 1989.
14. Dulloo AG, Seydoux J, Girardier L. Potentiation of the thermogenic antiobesity effects of ephedrine by dietary methylxanthines: Adenosine antagonism or phosphodiesterase inhibition? Metabolism 41: 1233–1241, 1992.
15. Eldershaw TP, Colquhoun EQ, Bennet KL, Dora KA, Clark MG. Resiniferatoxin and piperine: Capsaicin-like stimulators of oxygen uptake in the perfused rat hindlimb. Life Sci 55: 389–397, 1994.
16. Eldershaw TP, Colquhoun EQ, Bennet KL, Dora KA, Peng ZC, Clark MG. Pungent principles of ginger (Zingiber officinale) are thermogenic in the perfused rat hindlimb. Int J Obes Relat Metab Disord 16: 755–763, 1992.
17. Engels HJ, Wirth JC, Celik S, Dorsey JL. Influence of caffeine on metabolic and cardiovascular functions during sustained light intensity cycling and at rest. Int J Sport Nutr 9: 361–370, 1999.
18. Fredholm BB, Battig K, Holmen J, Nehlig A, Zvartau EE. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev 51: 83–133, 1999.
19. Ghayur MN, Gilani AH. Ginger lowers blood pressure through blockade of voltage-dependent calcium channels. J Cardiovasc Pharmacol 45: 74–80, 2005.
20. Graham TE. Caffeine and exercise metabolism, endurance and performance. Sports Med 31: 785–807, 2001.
21. Gulati V, Harding IH, Palombo EA. Enzyme inhibitory and antioxidant activities of traditional medicinal plants: Potential application in the management of hyperglycemia. BMC Complement Altern Med 12: 2–9, 2012.
22. Hartley TR, Lovallo WR, Whitsett TL. Cardiovascular effects of caffeine in men and women. Am J Cardiol 93: 1022–1026, 2004.
23. Hassapidou M, Fotiadou E, Maglara E, Papadopoulou SK. Energy intake, diet composition, energy expenditure, and body fatness of adolescents in northern Greece. Obesity (Silver Spring) 14: 855–862, 2006.
24. Hoffman JR, Kang J, Ratamess NA, Rashti SL, Tranchina CP, Faigenbaum AD. Thermogenic effect of an acute ingestion of a weight loss supplement. J Int Soc Sports Nutr 6: 1–9, 2009.
25. Housh TJ, Cramer JT, Weir JP, Beck TW, Johnson GO. Physical Fitness Laboratories on a Budget. Scottsdale, AZ: Holcomb Hathaway Publishers, 2009.
26. Kalmar JM, Cafarelli E. Caffeine: A valuable tool to study central fatigue in humans. Exerc Sport Sci Rev 32: 143–147, 2004.
27. Kawada T, Sakabe S, Watanabe T, Yamamoto M, Iwai K. Some pungent principles of spices cause the adrenal medulla to secrete catecholamine in anesthetized rats. Proc Soc Exp Biol Med 188: 229–233, 1988.
28. Keppel G, Wickens TD. Design and Analysis. Upper Saddle River, NJ: Pearson, 2004.
29. Liu L, Simon S. Similarities and differences in the currents activated by capsaicin, piperine, and zingerone in rat trigeminal ganglion cells. J Neurophysiol 76: 1858–1869, 1996.
30. Myers DE, Shaikh Z, Zullo TG. Hypoalgesic effect of caffeine in experimental ischemic muscle contraction pain. Headache 37: 654–658, 1997.
31. Nienhueser J, Brown GA, Shaw BA, Shaw I. Effects of energy drinks on metabolism at rest and during submaximal treadmill exercise in college age males. Int J Exerc Sci 4: 65–76, 2011.
32. O'Connor PJ, Motl RW, Broglio SP, Ely MR. Dose-dependent effect of caffeine on reducing leg pain during cycling exercise is unrelated to systolic blood pressure. Pain 109: 291–298, 2004.
33. Pandey RS, Singh BK, Tripathi YB. Extract of gum resins of Boswellia serrate L. inhibits lipopolysaccharide induced nitric oxide production in rat macrophages along with hypolipidemic property. Indian J Exp Biol 43: 509–516, 2005.
34. Poehlman ET, LaChance PL, Tremblay A, Nadeau A, Dussault J, Thériault G, Després J-P, Bouchard C. The effect of prior exercise caffeine ingestion on metabolic rate
and hormones in young adult males. Can J Physiol Pharmacol 67: 10–16, 1988.
35. Ryan ER, Beck TW, Herda TJ, Smith AE, Walter AA, Stout JR. Acute effects of a thermogenic nutritional supplement on energy expenditure and cardiovascular function at rest, during low-intensity exercise, and recovery from exercise. J Strength Cond Res 23: 807–817, 2009.
36. Suekawa M, Ishige A, Yuasa K, Sudo K, Masaki A, Hosoya E. Pharmacological studies on ginger. I. pharmacological actions of pungent constituents, (6)-gingerol and (6)-shagaol. J Pharmacobiodyn 7: 836–848, 1984.
37. Sullivan JJ, Knowlton RG, Brown DD. Caffeine affects heart rate and blood pressure response to prolonged walking. J Cardiopulm Rehabil 12: 418–422, 1992.
38. Taylor LW, Wilborn CD, Harvey T, Wismann J, Wiloughby DS. Acute effects of ingesting Java Fit™ energy extreme functional coffee on resting energy expenditure and hemodynamic responses in male and female coffee drinkers. J Int Soc Sports Nutr 4: 1–9, 2007.
39. Watanabe T, Kawada T, Kurosawa M, Sato A, Iwai K. Thermogenic action of capsaicin and its analogs. Jpn Sci Soc Press 67–77, 1991.
40. Weir JB. New methods for calculating metabolic rate
with special reference to protein metabolism. J Physiol 109: 1–9, 1949.
41. Wilborn C, Taylor L, Poole C, Bushey B, Williams L, Foster C, Campbell B. Effects of ingesting a commercial thermogenic product on hemodynamic function and energy expenditure at rest in males and females. Appl Physiol Nutr Metab 34: 1073–1078, 2009.
42. Yoshioka M, Doucet E, Drapeau V, Dionne I, Tremblay A. Combined effects of red pepper and caffeine consumption on 24 h energy balance in subjects given free access to foods. Br J Nutr 85: 203–211, 2001.
43. Ziegenfuss TN, Hofheins JE, Mendel RW, Landis J, Anderson RA. Body composition and features of the metabolic syndrome in pre-diabetic men and women. J Int Soc Sports Nutr 3: 45–53, 2006.
Keywords:Copyright © 2014 by the National Strength & Conditioning Association.
physical activity; thermogenic aids; metabolic rate