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p -Synephrine is deemed a safe and effective substance to increase fat utilization during exercise of low-to-moderate intensity in men but not in women. Additionally, the existence of a diurnal variation in substrate utilization has been documented during exercise with enhanced fat oxidation in the evening compared with early morning. However, it remains unknown whether there is an interaction between the effect of p -synephrine and the time of the day on fat oxidation during exercise. This study aimed to evaluate the effect of the acute ingestion of 3 milligram of p -synephrine per kilogram of body mass (mg/kg) on fat oxidation during exercise of increasing intensity when the exercise is performed in the morning vs. the evening. Using a randomized, double-blind, placebo-controlled experimental design, 16 healthy and active women performed four identical exercise trials after the ingestion of 3 mg/kg of p -synephrine and 3 mg/kg of a placebo (cellulose) both in the morning (8-10 am) and in the evening (5-7 pm). In the exercise trials, the substances were ingested 60 min before an incremental test on a cycle ergometer with 3 min stages at workloads from 30 to 80% of maximal oxygen uptake (VO 2 max). Substrate oxidation rates were measured by indirect calorimetry. In each trial, the maximum rate of fat oxidation (MFO) and the intensity that elicited MFO (Fatmax) were measured. A two-way analysis of variance (time-of-the day × substance) was used to detect differences among the trials. With the placebo, MFO was 0.25 ± 0.11 g/min in the morning and 0.24 ± 0.07 g/min in the evening. With p -synephrine, MFO was 0.26 ± 0.09 g/min in the morning and 0.21 ± 0.07 g/min in the evening. There was no main effect of substance ( p = 0.349), time of day ( p = 0.186) and the substance × time of day ( p = 0.365) on MFO. Additionally, Fatmax was reached at a similar exercise intensity with the placebo (41.33 ± 8.34% VO 2 max in the morning and 44.38 ± 7.37% VO 2 max in the evening) and with p -synephrine (43.33 ± 7.24% VO 2 max in the morning and 45.00 ± 7.43% VO 2 max in the evening), irrespective of the time of day with no main effect of substance ( p = 0.633), time of day ( p = 0.191), or interaction ( p = 0.580). In summary, the acute intake of 3 mg/kg of p -synephrine before exercise did not increase MFO and Fatmax, independently of the time of day, in female athletes. This indicates that the time of day is not a factor explaining the lack of effectiveness of this substance to enhance fat oxidation during aerobic exercise in women.

p -Synephrine is the principal alkaloid of bitter orange ( Citrus aurantium ). Several recent investigations have found that the intake of 2-3 mg/kg of p -synephrine raises fat oxidation rate during exercise of low-to-moderate intensity. However, these investigations have been carried out only with samples of male participants or mixed men/women samples. Therefore, the aim of this investigation was to study the effect of p -synephrine intake on fat oxidation during exercise of increasing intensity in healthy women. Using a double-blind, randomized experiment, 18 healthy recreationally active women performed two identical exercise trials after the ingestion of (a) 3 mg/kg of p -synephrine and (b) 3 mg/kg of a placebo (cellulose). The exercise trials consisted of a ramp test (from 30 to 80% of maximal oxygen uptake; VO 2 max) on a cycle ergometer while substrate oxidation rates were measured at each workload by indirect calorimetry. In comparison to the placebo, the intake of p -synephrine increased resting tympanic temperature (36.1 ± 0.5 vs. 36.4 ± 0.4 °C p = 0.033, d = 0.87) with no effect on resting heart rate ( p = 0.111) and systolic ( p = 0.994) and diastolic blood pressure ( p = 0.751). During exercise, there was no significant effect of p -synephrine on fat oxidation rate (F = 0.517; p = 0.484), carbohydrate oxidation rate (F = 0.730; p = 0.795), energy expenditure rate (F = 0.480; p = 0.833), heart rate (F = 4.269; p = 0.068) and participant's perceived exertion (F = 0.337; p = 0.580). The maximal rate of fat oxidation with placebo was 0.26 ± 0.10 g/min and it was similar with p -synephrine (0.28 ± 0.08 g/min, p = 0.449, d = 0.21). An acute intake of 3 mg/kg of p -synephrine before exercise did not modify energy expenditure and substrate oxidation during submaximal aerobic exercise in healthy active women. It is likely that the increase in resting tympanic temperature induced by p -synephrine hindered the effect of this substance on fat utilization during exercise in healthy active women.

The aim of this study was to investigate the acute effects of p -synephrine ingestion on substrate oxidation during exercise in elite cyclists. Fifteen elite cyclists volunteered to participate in a double blind, crossover, randomized and placebo-controlled experimental trial. During two different trials, participants either ingested a placebo (cellulose) or 3 mg/kg of p -synephrine. After 60 min for substances absorption, participants performed an incremental maximal cycle ergometer test until volitional fatigue (25 W/min). Breath-by-breath gas exchange data was continuously recorded during the entire test to estimate energy expenditure, carbohydrate oxidation, and fat oxidation rates by stoichiometric equations. Heart rate was continuously measured by using a heart rate monitor. The ingestion of p -synephrine had no significant effects on energy expenditure (F = 0.71, P   =  0.40) or heart rate (F = 0.66, P   =  0.43) during exercise. However, there was a main effect of p -synephrine to increase the rate of fat oxidation over the placebo (F = 5.1, P   =  0.04) and the rate of fat oxidation was higher with p -synephrine in the following loads: 45 ± 2%, 51 ± 3%, 62 ± 3%, 67 ± 4%, 79 ± 5% and 85 ± 5% of the maximum wattage obtained in the test (all P  < 0.05). The ingestion of p -synephrine did not modify the maximal rate of fat oxidation during the ramp test (mean value; 95%CI =  0.91; 0.79-1.03 vs 1.01; 0.91-1.11 g/min, respectively, P  = 0.06) nor the exercise intensity at which maximal fat oxidation was achieved (i.e. Fatmax =  49; 48-53 vs 50; 47-51% Wmax, P  = 0.52). Acute p -synephrine ingestion moved the fat oxidation-exercise intensity curve upwards during an incremental cycling test without affecting Fatmax.

The p -synephrine is the principal phytochemical found in bitter orange ( Citrus aurantium ). This substance is widely included in dietary supplements for weight loss/body fat reduction due to its potential benefits of increasing fat oxidation. For years, p -synephrine-containing dietary supplements have been marketed without proper knowledge of their true effectiveness to enhance fat utilization, especially when combined with exercise. However, the effects of p -synephrine on fat oxidation during exercise have been investigated in the last few years. The aim of the current discussion is to summarize the evidence on the effects of p -synephrine intake on fat oxidation and performance during exercise. Previous investigations have demonstrated that the acute intake of p -synephrine does not modify running sprint performance, jumping capacity, or aerobic capacity. However, the acute intake of p -synephrine, in a dose of 2-3 mg/kg of body mass, has been effective to enhance the rate of fat oxidation during incremental and continuous exercise. This effect has been observed in a range of exercise workloads between 30% and 80% of peak oxygen uptake (VO 2peak ). The p -synephrine has the ability to increase the maximal rate of fat oxidation during exercise of increasing intensity without affecting the workload at which maximal fat oxidation is obtained (Fatmax). The effect of p -synephrine on fat oxidation is normally accompanied by a concomitant reduction of carbohydrate utilization during exercise, without modifying the energy expended during exercise. The shifting in substrate oxidation is obtained without any effect on heart rate during exercise and the prevalence of adverse effects is negligible. Thus, the acute use of p -synephrine, or p -synephrine-containing products, might offer some benefits for those individuals seeking higher fat utilization during exercise at low to moderate intensities. However, more research is still necessary to determine if the effect of p -synephrine on fat oxidation during exercise is maintained with chronic ingestion, in order to ascertain the utility of this substance in conjunction with exercise programs to produce an effective body fat/weight loss reduction.

Purpose: p-Synephrine, the principal alkaloid of bitter orange (Citrus aurantium), is widely used in dietary supplements for weight loss due to its purported effect of increasing fat oxidation. However, there is a paucity of scientific information about its effectiveness in enhancing fat oxidation during exercise. The aim of this investigation was to determine the effect of an acute dose of p-synephrine on substrate oxidation during prolonged and constant intensity exercise., Methods: In a double-blind and randomized experiment, 14 healthy subjects performed two acute experimental trials after ingesting either p-synephrine (3 mg kg -1 ) or a placebo (cellulose). Energy expenditure and fat oxidation rates were continuously measured by indirect calorimetry during 1 h of continuous cycling at Fatmax, the intensity that induces maximal fat oxidation rate., Results: In comparison to the placebo, energy expenditure during 1 h of cycling remained unchanged with p-synephrine (698 ± 129 vs. 686 ± 123 kcal, P = 0.08). However, p-synephrine increased whole-body fat oxidation (33.6 ± 10.4 vs. 37.3 ± 9.8 g, P < 0.01) while also reducing carbohydrate oxidation (99.5 ± 30.4 vs. 85.0 ± 28.4 g, P < 0.01). However, the magnitude of the shift on substrate oxidation induced by p-synephrine was small., Conclusion: Acute ingestion of p-synephrine augments fat oxidation during prolonged and constant-intensity exercise.