Alexander R. Gonglach

Caffeine’s Ergogenic Effects on Cycling: Neuromuscular and Perceptual Factors

UNLABELLED Caffeine improves endurance exercise performance, but its ergogenic mechanism(s) remain unclear. PURPOSE This investigation sought to examine the effects of caffeine on perceptual and physiological responses to endurance exercise. METHODS Two experiments were performed. In study A, 14 participants were tested. Maximal voluntary strength (MVC) and motor-unit recruitment (%ACT) of the knee extensors and elbow flexors were tested before and 60 min after ingestion of a 5-mg·kg⁻¹ dose of caffeine or placebo and after completion of 40 min of exercise (30 min of submaximal leg or arm cycling followed by a 10-min time-trial performance). Muscle pain, RPE, and cardiorespiratory variables were assessed throughout. To determine the effects of caffeine on muscle pain and RPE during high-intensity exercise, a second study (study B) was performed. Twelve participants exercised at 95% of their gas exchange threshold (GET) and at 70% of the difference between their GET and VO(2peak) (70%Δ) after caffeine and placebo ingestion. RESULTS Compared to placebo, caffeine improved MVC (6.3%, P = 0.014) and %ACT (5.5%, P = 0.013) in the knee extensors, but not the elbow flexors, and reduced muscle pain (P < 0.05) and RPE (P < 0.05) during both submaximal cycling modalities. Caffeine ingestion improved time-trial performance during leg cycling (4.9% ± 6.5%, P = 0.03), but not arm crank cycling (2.1% ± 8.2%, P = 0.28), but the effect on pain and RPE was eliminated. Caffeine ingestion had no effect on pain or RPE during cycling at 95% GET and 70%Δ. CONCLUSIONS Our results suggest that augmented strength and motor-unit recruitment, rather than reductions in pain and effort, may underlie caffeines ergogenic effect on endurance exercise.

Time-course of recovery of peak oxygen uptake after exercise-induced muscle damage.

V̇O2 peak has been shown to be reduced 48 h following exercise-induced muscle damage (EIMD), but it is unclear how long this reduction may persist. In this study eight endurance trained participants (21.5 ± 1.1 years old) performed a maximal exercise tests over 10-days followings EIMD. Cardiorespiratory variables were collected via open-circuit spirometry and soreness, maximal strength (MVC), motor-unit recruitment, and contractile properties were assessed prior to each test. MVC was reduced for up to 4-days (p ≤ 0.05) and soreness was evident for 10-days in the quadriceps (p < 0.05). V̇O2peak was reduced 7.4% 2-days post EIMD (55.5 ± 6.0 vs. 51.3 ± 5.8; p = 0.006) and remained reduced in 6 of 8 participants at 10-days post (p = 0.005). No relationship was found between changes in MVC, soreness, motor-unit recruitment, and contractile properties and changes in V̇O2peak (p > 0.05). EIMD resulted in small, but prolonged reductions in V̇O2peak. Our findings suggest mechanisms aside from force loss and soreness are primarily responsible for the reductions in V̇O2peak after EIMD.

Local and Generalized Endogenous Pain Modulation in Healthy Men: Effects of Exercise and Exercise-Induced Muscle Damage.

Isometric exercise has been shown to activate endogenous pain inhibitory pathways in healthy adults, but not in some clinical pain populations. OBJECTIVE Exercise-induced muscle damage (EIMD) and the associated delayed-onset muscle soreness (DOMS) are a model for studying clinical pain; thus, our purpose was to examine the effects of isometric exercise on pressure pain threshold (PPT) in the presence and absence of DOMS. METHODS Data were collected on 23 males (22.8 ± 2.5 yrs). PPT was assessed in the right (exercising) and left (resting) quadriceps prior to, every 30 seconds during, and 2 and 15 minutes following an isometric contraction of the right quadriceps at 25% of maximal voluntary contraction (MVC) held until fatigue. Unilateral eccentric exercise was performed to induce DOMS in the exercising leg and testing was repeated 48 hours later. RESULTS DOMS increased (P < 0.001) and resting PPT decreased (P = 0.03) following EIMD. PPTs were elevated during exercise in the exercising (P ≤ 0.002) and resting (P ≤ 0.002) quadriceps but did not differ between the control and EIMD conditions in either leg (P ≤ 0.61). PPT remained elevated 2 and 15 minutes postexercise (P < 0.05) in the exercised quadriceps in both conditions, but values returned to baseline at 2 (P = 0.91) and 15 minutes (P = 0.28) postisometric exercise in the resting quadriceps. CONCLUSIONS Unlike clinical pain, DOMS had no effect on the PPT response during exercise in either the exercising or resting quadriceps. The fact that exercise altered PPT in both quadriceps during exercise suggests a generalized pain inhibitory mechanism was activated. However, the restriction of postexercise effects to the exercised limb suggests localized inhibitory mechanism(s) were activated after exercise.

The effects of caffeine ingestion on exercise-induced hypoalgesia: A pilot study

Exercise acutely reduces pain sensitivity, termed exercise-induced hypoalgesia (EIH). The mechanisms underlying EIH remain unclear. Caffeine, a non-specific adenosine receptor antagonist has been shown to attenuate EIH in animals-suggesting the involvement of the adenosinergic system. This pilot study investigated the effects of caffeine on pain sensitivity following cycling exercise in college-aged men. Pressure pain threshold (PPT) and thermal pain threshold (TPT) were assessed in thirteen low caffeine consuming men prior to ingestion of a counter-balanced 5mg·kg(-1) dose of caffeine or a placebo (Pre), 60min following ingestion (Post-In), and then following a 15min bout of cycling exercise (Post-Ex) at an intensity eliciting a quadriceps muscle pain rating of 3 out of 10. Nine of the men completed follow-up testing which was identical except that the exercise consisted of 10min of cycling eliciting a pain rating of 5 out of 10. Caffeine had no effect compared to placebo on PPT (p≥0.15) or TPT (p≥0.41) 60min following ingestion and following exercise. PPT increased from 599±176kPa to 648±202kPa (p=0.009) and from 578±217kPa to 666±278kPa (p=0.01) following 15 and 10min of cycling, respectively. TPT increased from 46.2±2.9°C to 46.8±2.6°C (p=0.008) following the 15min exercise bout, but did not change (46.4±3.6°C vs. 46.8±3.3°C; p=0.24) following the shorter, higher intensity exercise bout. The results from this study indicate cycling exercise reduces pain sensitivity, especially to pressure stimuli. Caffeine ingestion did not alter the EIH response-suggesting adenosine may not play a prominent role in the EIH response in humans.