Low-dose caffeine consumption is a valuable strategy for increasing time to exhaustion, explosive power, and reducing muscle soreness in professional male kickboxers

doi:10.21203/rs.3.rs-4000530/v1

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Low-dose caffeine consumption is a valuable strategy for increasing time to exhaustion, explosive power, and reducing muscle soreness in professional male kickboxers

https://doi.org/10.21203/rs.3.rs-4000530/v1

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Purpose: This study aimed to evaluate the effects of acute caffeine supplementation of varied doses on kickboxing athletes' performance indices and perceived muscle pain.

Methods: Twelve kickboxing athletes participated in 3 exercise sessions and caffeine supplementation comprising doses of 3 mg/kg (C3), 6 mg/kg (C6), or 3- placebo (PLA) with a one-week wash-out period between exercise trials. The supplement was taken 60 minutes before each exercise session. In each session, the subjects first performed the vertical jump, Wingate anaerobic test and after a 45-minute break, performed the Bruce maximal aerobic test and the maximal oxygen consumption (VO2max), oxygen consumption equivalent to ventilation threshold (VT2), Time-to-exhaustion (TTE), Rating of Perceived Exertion (RPE), relative peak power (RPP), relative mean power (RMP), relative lowest power (RLP) and the Wingite Fatigue Index (WFI) after Bruce test were examined.

Results: Consumption of C3 or C6 significantly increased the TTE following treadmill testing (p<0.05), but had no effect on the WFI (p> 0.05). Compared to PLA, the consumption of C3 and C6 significantly increased vertical jump (p<0.05). C3 significantly increases the RPP (p <0.05), whereas C6 did not (p> 0.05) during the Wingate Test. Muscle soreness after two hours (Ms2) showed a significant decrease after C6 supplementation compared to C3 and PLA (p<0.05). In contrast, no significant effect was observed on the VO2max, %VO2max at ventilatory threshold 2, and RPE (p>0.05).

Conclusion: In conclusion, acute consumption of low to moderate doses of caffeine induces relative improvements in anaerobic and lower-body muscular power, muscle soreness, and TTE in male kickboxing athletes.

Aerobic power

Anaerobic power

Caffeine

Kickboxing

Muscle soreness

Kickboxing is a combat sport that involves two competitors attempting to strike each other using forceful blows with the hands, elbows, knees, calves, and legs (1, 2). A typical kickboxing match comprises three to twelve rounds, each lasting two to four minutes, separated by one to two-minute rest periods between rounds. To effectively perform the complex motor tasks and skills required in kickboxing, a high level of aerobic and anaerobic capacity is necessary (1, 2). Competitive athletes in combat-oriented sports consistently seek performance advantages to improve their physical and mental capabilities. Thus, optimizing training techniques and ergogenic strategies for kickboxing athletes is crucial for enhancing their overall performance.

While exercise training certainly plays a prominent role in developing kickboxing athletes' motor skills, a great deal of attention is also given to nutrition and particularly, ergogenic supplements/aids. The ergogenic outcomes resulting from acute or chronic nutritional interventions can prove beneficial during exercise performance, such as during formal competition where small improvements in human performance may have a significant impact on results (3). Specifically, caffeine has garnered much attention in the sports performance literature and is considered one of the most popular ergogenic supplements used by athletes and non-athletes alike to enhance physical and mental capabilities (4).

While several studies have demonstrated the ergogenic effects of caffeine consumption on physical performance, questions remain about the timing, dose, and type (e.g., pill, coffee, liquid, etc.) of supplementation by athletes and coaches alike in various sports, including kickboxing (5–7). More specifically, several factors may play a role in the effectiveness of caffeine as an ergogenic aid, such as dose/dosage, volume of exercise training, timing of caffeine intake during the day in reference to training/competition, habitual caffeine consumption, and type of exercise performed (5, 6). It has been demonstrated that caffeine directly affects the central nervous system (CNS), thus improving cognitive function and reaction time as well as reducing perceived exertion (5, 6). A recent investigation examined the effects of low (3 mg/kg), medium (6 mg/kg), and high (9 mg/kg) doses of caffeine on cognitive function and brain activation in healthy male participants (8). Perhaps counterintuitively, findings indicated that consuming a lower dose of caffeine compared to medium and higher doses (6 or 9 mg/kg) had a greater effect on cognitive function and brain activity as measured by reaction time to stimuli (8). It was concluded that low-dose caffeine ingestion (≤ 3 mg/kg) may more effectively saturate the CNS which facilitated an increase in cerebral blood flow and volume (6, 8). In addition, the use of medium or high doses of caffeine has been suggested to increase the likelihood of peripheral ergogenic effects (e.g., directing improved muscle strength and power) as opposed to the aforementioned central effects of lower caffeine doses (6). Such conclusions nevertheless remain contradictory and further research should address the apparent dichotomy between low vs. higher caffeine doses on human performance (6). To this, recent review articles indicate that despite rather robust data, a decisive position concerning the possible ergogenic effects of caffeine on physical activities requiring power or strength remains ambiguous at best (6). In part, this may owe to specific individual differences in the ability to tolerate higher doses of caffeine or be related to the type of performance tests utilized in the literature (e.g., higher caffeine doses may trigger a beneficial increase in lipid utilization during endurance activity compared to lower doses) (6, 9).

As suggested recently, high doses of caffeine (above 6 mg/kg) may be associated with increased strength and power compared to moderate doses by stimulating greater calcium release of the sarcoplasmic reticulum which in turn may promote cross-bridge cycling during contraction (6, 10). However, this hypothesis should be confirmed since a recent study indicated that lower caffeine doses (3 mg/kg) produced similar improvements in muscle strength (e.g., chest, shoulder, and biceps exercises) compared to medium doses (6, 11). Based on the inconsistency of these findings, determining an ideal caffeine dose for athletic pursuits requiring both aerobic (endurance) and anaerobic (strength and power) metabolic and physical contributions, such as combat sports, remains inconclusive and yet essential.

The vast majority of investigations analyzing the role of caffeine on exercise performance have focused their efforts on its effects on metabolism, hormones, and/or the central nervous system. However, the influence of caffeine on ventilatory and pulmonary function is often neglected (12) despite research indicating its role as a powerful stimulant of the ventilatory drive. It has been suggested that caffeine promotes increased sensitivity of peripheral chemoreceptors in untrained subjects and exercise ventilation across workloads in well-trained endurance athletes (12). It was additionally reported that a 3 mg/kg caffeine dose given daily over 20 days increased the intensity of exercise at the second ventilatory threshold (VT2) in healthy active adults. Certainly, these results suggest an important and potential advantage for training and competition since VT2 is defined as the point of change in the predominant energy system; aerobic to anaerobic, and is an important indicator of endurance exercise tolerance (13). Since endurance exercise, particularly in athletes, is often performed at intensities equivalent to the VT2, any factor that may delay the onset of VT2 would prove advantageous during high-intensity training and competition (14). However, as noted by the authors of this study, no investigation has yet examined the effects of varied caffeine doses on VT2 in athletes, let alone kickboxers. Considering the important implications of delaying VT2 on human performance, it seems that further research on caffeine’s effects on cardiopulmonary function and related parameters, such as maximal oxygen consumption (VO2max) and VT2, is warranted.

Notwithstanding the functional improvements in reaction time and muscle strength and power, caffeine also seems to influence the speed of muscle recovery. Caffeine consumption has been shown to reduce the perception of pain in several investigations, including following repetitive and prolonged contractions as documented in the quadriceps muscles following moderate- and high-intensity cycling (15, 16); during physical activity under conditions that promote exercise-induced muscle damage (17–19); and by facilitating more rapid recovery after performing maximal voluntary isometric contractions (MVIC) of the knee extensors (19). Yet, the role varied caffeine doses may play on the perception of muscle pain following exhausting exercises, such as the severity and duration of acute muscle soreness, has been less studied. Given the significance of enhancing both aerobic and anaerobic performance, facilitating muscle recovery, and prolonging resistance to fatigue in combat sports athletes like kickboxers, and considering the conflicting evidence concerning the central and peripheral ergogenic effects of caffeine, the present study was undertaken with the aim of examining the acute effects of varied caffeine consumption on aerobic and anaerobic performance, as well as fatigue and muscular pain of kickboxing athletes.

Subjects and Study Design

The present study was a randomized, double-blind, placebo-controlled, and cross-over design (Fig. 1) which was approved by the Ethics Committee of the Faculty of Rehabilitation Sciences, Shiraz University of Medical Sciences, Shiraz, Iran and carried out in accordance with the Declaration of Helsinki. Twelve kickboxing athletes with three years of competitive experience voluntarily participated in this study. Participant demographic and anthropometric characteristics are displayed in Table 1. Prior to data collection, study participants attended an introductory session to familiarize them with the exercise intervention and methods of data collection. Each participant completed an informed consent and health status form, with specific questions on the existence of prior caffeine allergies if any. After height and weight were recorded and following one week of controlled caffeine consumption and nutritional patterns, participants engaged in 3 separate sessions of exercise testing (lower-body power, anaerobic and aerobic fitness) and caffeine (C) or placebo (PLA) consumption with one week separating each session (Fig. 1). Throughout the testing protocol, one week before the exercise test participants were instructed to avoid food and beverage containing caffeine. Food recall was obtained from participants the day prior to each intervention session to ensure compliance with caffeine abstinence.

Table 1

Participant Demographic and Anthropometric Characteristics (mean ± SD)
Index	Value
Age (years)	24 ± 2.0
Weight (kg)	70.31 ± 8.80
Height (cm)	178.31 ± 6.20
BMI (kg/m²)	22.13 ± 2.63

Exercise Tests

Each exercise session consisted of having participants initially undertake the Sergeant Vertical Jump (VJ) to assess the jumping ability of participants, and all assessments in the Sargent jump test were performed three times consecutively (1 min passive rest between them), with the best score recorded as the final result (20), followed by a 5-minute rest period after the last jump, and then perform the Wingate anaerobic test on the Monark Ergomedic 894E cycle ergometer (Monark, Sweden). After a 45-minute recovery period, participants performed the maximal Bruce treadmill test (cosmos Germany) (20). During the rest interval between each exercise test (vertical jump, Wingate, Bruce tests), participants were given access to only water (no food or caffeine). During the Bruce treadmill test, participants were monitored for changes in respiratory gases (O2 and CO2) and maximum oxygen consumption (VO2max) by indirect calorimetry (Cortex Biophysik Germany). Subsequently, each participant’s VO2max, oxygen consumption value at VT2, and time-to-exhaustion (TTE) were determined and recorded where TTE was equal to the time interval between the beginning and end of the Bruce incremental treadmill test (e.g., participant reached exhaustion and the test was terminated). Prior to the Wingate anaerobic test, athletes initially performed a warm-up for 5 minutes at a speed of (60 to 70 rpm) with a light resistance equivalent to 20% of actual test resistance. Several short instances of speed pedaling were also introduced as part of the warm-up according to standard protocol (21–23). After warming up, the participants were given the "Go" command, pedaled with zero resistance at the maximum possible speed to overcome inertia, at which point 75 grams per kilogram of body weight was applied as the resistance to the cycle ergometer (24). From this point forward, athletes pedaled at the maximum possible speed (revolutions per minute; rpm) for 30 seconds and the test was concluded. The pedaling technique was controlled and standing pedaling was avoided (21, 22, 25). Following the Wingate test, the relative anaerobic peak power (RPP), relative anaerobic average power (RAP), relative anaerobic minimum power (RMP), and fatigue index (WFI) were determined for each participant.

Caffeine supplementation

At 60 minutes prior to each exercise session, participants randomly ingested placebo-containing tablets (PLA; starch) or caffeine supplements of 3 (C3) or 6 milligrams (C6) per kilogram (mg/kg) of body mass. The selected dosage and ingestion times were based on previous research that demonstrated the performance-enhancing advantages of low and moderate caffeine doses (26). A treatment washout period of one week was implemented following each exercise test session, after which the identical exercise session and caffeine protocol was repeated (Fig. 1) for a total of 3 exercise/caffeine or placebo interventions. It should be noted that caffeine consumption of participants was controlled (e.g., participants were instructed to abstain from caffeine ingestion and through food and beverage recall) during washout periods.

Assessment of rating of perceived exertion and muscle soreness

The Borg rating of perceived exertion (RPE, 0–10 scale) questionnaire was used to measure each participant’s perception of exertion immediately after Bruce test (27, 28). The Visual Analogue Scale (VAS) was used to measure the level of muscle soreness (MS) after the exercise test (27). The scale consists of a 10-centimeter line printed on paper and representing a continuum of MS between "minimal MS" and "maximal MS". Participants were instructed to place a mark («×») on the scale representing their perception of the severity of MS (29). The mark was then measured for each participant in mm along the continuum and averaged for each group (placebo vs. C3 vs. C6). MS was measured immediately (MS0), 2 hours (MS2), and 12 hours (MS12) after the end of each exercise test session.

Statistical Analysis

All data were analyzed using SPSS software (version 26, IBM-SPSS Inc., Chicago, IL, USA). The data distribution normality was determined using the Shapiro–Wilk test. For parametric data (including TTE, VO2max, VT2, RPE, RPP, RAP, RMP, WFI, and VJ), one-way repeated measure ANOVA and Bonferroni's post hoc tests were used (the effect size calculated via the partial eta squared). Friedman and Wilcoxon's tests were also used for nonparametric data (including MS, and the effect size calculated via Kendall's W value). The statistical significance level was considered at p < 0.05.

All data and statistical analysis results across interventions for each variable are presented in Table 2. Data analysis indicated that the main effect for TTE was significant [F (2, 22) = 8.37, P = 0.002]. The TTE (during the Bruce treadmill test (after C3 (MD = 31.91, P = 0.027) and C6 (MD = 45.50, P = 0.019) significantly increased compared to the PLA. No significant difference was noted between C3 and C6 for TTE (MD = 13.58, P = 0.64; Fig. 2). The main effect for VO2max [F (1.37, 15.09) = 0.91, P = 0.41], VT2 [F (2, 22) = 1.08, P = 0.35], oxygen consumption equivalent to VT2 [F (2, 22) = 2.22, P = 0.13] was not significant. Additionally, the main effect for RPE was not significant [F (2, 22) = 1.44, P = 0.25].

Table 2

Describing the mean and standard deviation of the measured variables in each condition
variable	PLA	C3	C6	Main effect
variable	mean ± SD			Sig (eta² or Kendall's W)
TTE (min)	12.04 ± 1.24	12.58 ± 1.21	12.80 ± 1.15	0.002 (0.4)
VO2max (ml/kg.min)	50.50 ± 5.61	49.41 ± 6.00	49.75 ± 6.07	0.38 (0.1)
Oxygen consumption at VT₂ (ml/kg.min)	42.75 ± 5.32	41.25 ± 5.25	41.91 ± 4.96	0.13 (0.1)
VT₂ (%VO2max)	84.56 ± 2.17	83.43 ± 2.48	84.32 ± 3.15	0.35 (0.1)
RPE (unit)	7.91 ± 1.56	8.50 ± 0.79	8.58 ± 0.90	0.25 (0.1)
Relative Peak power output (watt/kg)	9.15 ± 1.25	9.87 ± 1.43	9.63 ± 2.10	0.03 (0.3)
Relative average power output (watt/kg)	7.00 ± 0.86	7.04 ± 0.77	7.26 ± 1.18	0.32 (0.1)
Relative minimum power output (watt/kg)	4.05 ± 1.01	4.15 ± 0.56	4.16 ± 0.95	0.80 (0.01)
WFI (%)	58.2 ± 6.68	57.8 ± 5.44	57.8 ± 11.61	0.93 (0.02)
VJ (cm)	50.00 ± 6.70	51.75 ± 5.11	52.91 ± 4.66	0.002 (0.5)
MS0 (mm)	78.75 ± 25.68	75.00 ± 29.38	78.33 ± 26.91	0.69 (0.03)
MS2 (mm)	37.91 ± 29.80	34.58 ± 29.95	22.08 ± 19.36	0.004 (0.45)
MS12 (mm)	20.83 ± 22.24	18.33 ± 24.52	10.00 ± 12.24	0.16 (0.15)
TTE: Time to exhaustion, VO_2max: Maximum oxygen consumption, VT₂: Secondary ventilatory threshold, RPE: Rate of perceived exertion,VJ: Vertical jump (cm) ، WFI: Wingate fatigue index, MS0: muscle soreness immediately post-exercise session, MS2: muscle soreness at 2 hours post exercise session, MS12: muscle soreness at 12 hours post exercise session, PLA: Placebo, C3: 3 mg/kg Caffeine, C6: 6 mg/kg Caffeine.

The main effect for relative peak power output was significant [F (2.22) = 4.00, P = 0.03]. The post hoc test showed that, compared to PLA, C3 significantly increased the relative peak power output (MD = 0.071, P = 0.015), however in the C6 condition no significant changes were observed compared to PLA (MD = 0.48, P = 0.51). Also, the relative peak power output of kickboxing athletes was not significantly different between C3 and C6 (MD = 0.23, P = 0.94). No significant main effect was observed for relative average power output [F (1.13, 12.44) = 1.1, P = 0.32], relative minimum power output [F (1.31, 14.48) = 0.11, P = 0.8] and WFI [F (1.27, 22) = 0.018, P = 0.93] in the Wingate test (Fig. 3).

The main effect was significant for vertical jump height [F (1.27,13.98) = 11.95, P = 0.002]. The post hoc test showed that the vertical jump height was significantly increased after C3 (MD = 1.75, P = 0.02) and C6 (MD = 2.91, P = 0.01) compared to PLA. However, vertical jump height after C6 did not show significant changes compared to C3 (MD = 1.16, P = 0.06).

The results of the Friedman test showed that there was no significant difference in muscle soreness between C3, C6, and PLA at MS0 (X2 = 0.74, P = 0.7) and MS12 (X2 = 3.7, P = 0.16) (Fig. 4). However, a significant main effect was observed for MS2 (X2 = 10.88, P = 0.004). Wilcoxon post-hoc test showed that MS2 values were significantly lower than PLA after the C6 (Z = 2.37, P = 0.018). When comparing caffeine doses, C6 promoted a significant reduction in MS2 compared to the C3 condition (Z = 2.21, P = 0.03), however, no significant difference was observed between C3 and PLA in MS2 values (Z = 1.16, P = 0.24).

In summary, the findings of the present study showed that acute caffeine consumption in low to medium doses caused a relative improvement in lower-body power and endurance performance as well as muscle soreness in male kickboxers.

Compared to the literature, our findings appear to be in agreement with those studies indicating that endurance indices such as VO2max (30–35) remained unaffected by acute medium dose caffeine ingestion compared to others that did (36–40). Differences in sample size (e.g., statistical power) and the mode of exercise protocol, as well as supplementation type (e.g., pill, food, liquid), may partly explain this inconsistency in findings across the literature. More specifically, Usman et al. (37) indicated a relative improvement in the VO2max of athletes after caffeine consumption by indirect determination of the VO2max (beep test), whereas in the present study, the Bruce treadmill test and indirect calorimetry were employed which perhaps offered a more sensitive evaluation of aerobic capacity. Contrary to our results, Powers et al. demonstrated that caffeine consumption did not have a significant effect on the TTE in the cycle ergometer test (38) however, others have shown positive benefits of caffeine to improve TTE (31–33). A meta-analysis also suggested that TTE was increased following caffeine ingestion compared to placebo, yet a dose-response relationship failed to materialize (41). Therefore, our results indicated that acute caffeine ingestion at medium dosing strategies appears to increase TTE during treadmill testing to a similar extent.

Multiple mechanisms have been proposed to explain the increase in TTE after caffeine supplementation. Several investigations indicate caffeine increases beta-endorphin release, mobilization of free fatty acids, and plasma epinephrine (42–44) thus promoting substrate availability and utilization during exercise (42, 45). In addition, caffeine concurrently reduces reliance on glycogen and increases the availability and utilization of free fatty acids during endurance exercise, ultimately promoting a glycogen-sparing effect to reduce fatigue (41, 42, 44, 46). However, concerning incremental exercise to maximum exertion, evidence suggests that the ergogenic benefits of caffeine of any increased epinephrine release, glycogen-sparing effect, or fatty acid utilization may have lesser or no effect (41) as observed in the present study. Since caffeine crosses nerve and muscle cell membranes, supplementation at lower doses may induce more neurological than muscular effects (43, 47). Nevertheless, if the primary effect of caffeine supplementation is to directly impact muscle function, it may more profoundly stimulate muscle via contractile rather than metabolic properties (42, 47). Accordingly, a primary action of caffeine is its role as adenosine A1 and A2a receptor antagonists in the central nervous system (5, 6, 41–43). Adenosine suppresses neurophysiological excitability by inhibiting excitatory neurotransmitters in the brain (42), thus blocking adenosine receptors via caffeine ingestion may lead to increased activity of D1 and D2 dopamine receptors, resulting in increased psychomotor activity and exercise tolerance (42, 48). Also, caffeine has been suggested to modify muscle physiology and thus sports performance through mechanisms of motor unit activation, muscle contractile function, and sodium/potassium ATPase pump activity (10, 42, 43, 47). Moderate caffeine doses of 6 mg/kg have been shown to augment calcium release from the sarcoplasmic reticulum which enhances muscle contractility and resistance to fatigue (26, 41). Similar to our results, after C6 supplementation the mean TTE increased by 13.58 seconds compared to C3, which in part may be explained by the stimulatory effects of caffeine on intracellular calcium release and/or ryanodine receptors (49). Such modification of central and peripheral mechanisms by caffeine may also be explained through the reduced perception of MS (42, 43, 48) and improved endurance and power performance (10, 42), as noted in the present study.

Although numerous investigations have shown improvement in RPE after caffeine consumption (40, 50), the lack of any significant RPE alterations in the present study may be explained in several ways. For example, unlike physiological outcomes, differences in individual psychological responses may show greater variability and help to explain such rather unexpected findings (30). Further, any caffeine effects on RPE may also be affected by the type and intensity of exercise. Research indicates that exercise at an intensity below the anaerobic threshold (by as little as 10%), significantly lowered RPE response after caffeine consumption while concurrently increasing TTE compared to placebo. However, as intensity increased, no effect of caffeine consumption on RPE and TTE was observed when exercise exceeded the anaerobic threshold (51). Therefore, since RPE was measured following the Bruce maximal aerobic test in the present study, it is reasonable to conclude that RPE may not be affected in this situation as participants simply reached their relative maximal level of exertion, regardless of the absolute exercise intensity achieved. In line with this argument, Doherty and Smith (2005) as well indicated that following caffeine intake, RPE was lower compared to placebo during submaximal exercise at constant loads. Similarly, there was no significant difference in RPE between caffeine supplementation and placebo immediately following exhaustive (maximal) exercise where VO2max and/or maximal heart rate were reached (40). Future investigations would do well to monitor RPE following caffeine supplementation at various submaximal intensities as exercise intensity ramps up to maximal voluntary efforts.

The findings of this study indicated no significant short-term caffeine consumption effect on the percentage of oxygen consumption equivalent to VT2 compared to placebo. In contrast, several studies have demonstrated both short- and long-term effects of caffeine consumption on ventilatory and anaerobic thresholds (52, 53). For example, Quesada and Gillum (53) found that acute caffeine consumption increased the anaerobic ventilatory threshold in moderately active males. However, care should be taken when interpreting the results of these and other studies due to methodological limitations (e.g., smaller sample size) as well as an overall dearth of investigations on the acute effects of caffeine supplementation. In addition, research by Ruiz-Moreno et al. (2020) utilized absolute oxygen consumption as the criterion index equivalent to ventilatory threshold, while in the present study, relative oxygen consumption (e.g., adjusted for body mass and expressed as mL-kg-min rather than L-min) was used to express VT2 (52). As such, absolute VO2 reflects the amount of bodily oxygen consumption regardless of size, age, and gender, whereas the relative expression of VO2 adjusts for body mass, as noted, and may provide more meaningful results, particularly for weight-bearing activities. Further, the findings of Ruiz-Moreno et al. (2020) followed 20 days of repeated caffeine consumption as opposed to a one-time dose prior to exercise making direct comparisons between their and our own study difficult. Due to limitations in any precise control of participant caffeine ingestion prior to our and others' research may also factor into such discrepancies in VT2 outcomes (e.g., heavy caffeine users would likely see a reduction in their caffeine intake during data collection thus potentially influencing results). Therefore, future investigations should attempt to control or elucidate on the prior history of participant’s caffeine consumption to more accurately determine any true effects of caffeine on anaerobic or other metabolic thresholds. Despite our lack of significant VT2 results, short-term caffeine consumption at higher doses than those used in the present study (e.g., 7 mg/kg) may increase oxygen consumption at the respiratory threshold (54) or decrease blood lactate accumulation at the same exercise intensity (55). High-dose caffeine (650 mg) has also been observed to increase respiratory response as CO2 production increases during moderate exercise, which in turn may have an influence on anaerobic and ventilatory thresholds as exercise intensity increases (56). In summary, moderate caffeine doses (as utilized in the present study) do not seem to have an effect on oxygen consumption equivalent to VT2. However, it is important to acknowledge several methodological limitations that may have influenced exercise performance outcomes, including the lack of prospective research, variability in the units used to express VO2, and the prior history of caffeine ingestion among participants in this and other related studies. Therefore, further investigation is warranted to fully elucidate the potential effects of moderate caffeine doses on oxygen consumption and to account for these methodological limitations.

The present study demonstrated that lower-body muscular power, as measured through the vertical jump and Wingate Test (RPP), improves after acute caffeine consumption. However, other indices of muscular power including WFI, RLP, and RMP remained unchanged between caffeine and placebo interventions. The literature appears divided on similar outcomes for muscular power as a number of investigations have demonstrated improved performance (49, 57–60) while others have not (35, 61–63). Since RPP and RLP play an important role in the calculation of WFI, a lack of any significant changes in WFI may have been due to minimal differences or changes (e.g., statistical power) between these two outcomes. In addition, Grgic et al. (2020) showed that although caffeine and placebo consumption both improved vertical jump height, no significant effect was observed on maximal power output in recreationally trained males (64). Therefore, improvements in the vertical jump may not be entirely accompanied by an increase in measures of power output in part due to sample sizes, the method used to assess power output (e.g., the Wingate test measures power over 5 second time period vs. the vertical jump which applies force over a much shorter time span), subject motivation, and timing of caffeine supplementation. As demonstrated by Duncan et al. (2019), the upper-body Wingate test to determine the effects of caffeine on anaerobic power may produce different responses compared to the lower-body Wingate test (62). Nevertheless, certain mechanisms may justify an increase in RPP and VJ seen in the present study such that caffeine may directly enhance contractile properties of skeletal muscle during excitation-contraction coupling (65). Improved RPP may also be related to a CNS response where an antagonistic effect of caffeine on adenosine receptors, leads to increased neurotransmitter release, motor unit firing rate, and dopaminergic transmission (6, 66). Subsequent literature has corroborated a potential for this CNS hypothesis where caffeine was reported to increase maximal voluntary contraction and facilitate motor pool recruitment when compared to placebo (26).

Muscle soreness in the time following high-intensity exercise is an important consideration in human performance and participants in the present study indicated less MS following C6 compared to C3 and placebo at 2 hours post-exercise (MS2). Similarly, caffeine consumption of between 5–6 mg/kg led to a considerable reduction in muscle pain, albeit more so in males than females, following high-intensity activity (17, 67). Even lower doses of caffeine (3 mg/kg) seem to be capable of reducing muscle pain which persists for several days following exhaustive exercise (68). The rate of bodily caffeine metabolism may partly explain the findings of the present study such that its effectiveness to reduce MS may be correlated to peak plasma caffeine levels seen 30 to 180 minutes post consumption (6). However, this process occurs with wide variation among individuals due to environmental and/or genetic differences (e.g., caffeine half-life varies from 3 to 7 hours in the general population) (40). Thus, a potential explanation for the decrease in MS2 after C6 may be the result of optimal caffeine availability at this time interval. Since the time course of blood caffeine levels was not measured in the present study, future investigations would do well to analyze the relationship between caffeine dose and timing of post-exercise blood concentrations and muscle soreness. Exactly how caffeine ingestion reduces post-exercise muscle soreness remains to be fully elucidated, however, one such explanation may be related to enhanced dopamine release and its role as a CNS analgesic (50).

It is important to acknowledge the limitations of our investigation. Firstly, our study design could have been strengthened by including a group with high caffeine dosage. Additionally, since our subjects were exclusively male kickboxers, caution should be taken when generalizing our findings to other athletes. Therefore, future studies should include the evaluation of these variables to expand on our findings.

In summary, the present study suggests that consuming low to medium doses of caffeine can improve various performance aspects in male kickboxers. Specifically, acute caffeine intake resulted in a relative improvement in power (RPP), endurance performance (TTE), vertical jump (VJ), and muscle soreness (at 2 hours post-exercise). Notably, the observed changes in muscle soreness were only significant when consuming higher caffeine doses (6 mg/kg), compared to a placebo or lower doses of caffeine (3 mg/kg). As a result, kickboxing athletes may benefit from acute caffeine consumption at both low (3 mg/kg) and moderate (6 mg/kg) doses, leading to improved power and endurance performance.

Author Contributions: Conceptualization, M.S., R.R. and M.H.; methodology, M.S., M.N., R.B., A.W.; software, F.SH., A.N., M.N.; formal analysis, F.SH., R.B., A.W., K.S.; writing—original draft preparation, A.N., A.W., R.R., M.H. and F.SH.; visualization, M.S., M.N., R.B., K.S.; writing—review and editing, M.S., R.R., F.SH., M.H. and A.N.; supervision, M.H. and R.R. All authors have read and agreed to the published version of the manuscript.

Funding: This research investigation received no external funding.

Data Availability: Additional data can on request be made available

Ethics approval and consent to participate: The study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of the Faculty of Rehabilitation Sciences, Shiraz University of Medical Sciences, Shiraz, Iran (ethics approval code: IR.SUMS.REHAB.REC.1399.10). Informed consent was obtained from all individual participants included in the study.

Consent for publication: Not applicable.

Competing of interests: The authors declare no competing interests

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No competing interests reported.

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Low-dose caffeine consumption is a valuable strategy for increasing time to exhaustion, explosive power, and reducing muscle soreness in professional male kickboxers

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