Junctophilins (JP1 and JP2) are expressed in skeletal muscle and are the primary proteins involved in transverse (T)-tubule and sarcoplasmic reticulum (SR) membrane apposition. During the performance of eccentric contractions, the apposition of T-tubule and SR membranes may be disrupted, resulting in excitation-contraction (EC) coupling failure and thus reduced force-producing capacity. In this study, we made three primary observations: 1) through the first 3 days after the performance of 50 eccentric contractions in vivo by the left hindlimb anterior crural muscles of female mice, both JP1 and JP2 were significantly reduced by approximately 50% and 35%, respectively, while no reductions were observed after the performance of nonfatiguing concentric contractions; 2) following the performance of a repeated bout of 50 eccentric contractions in vivo, only JP1 was immediately reduced ( approximately 30%) but recovered by 3-day postinjury in tandem with the recovery of strength and EC coupling; and 3) following the performance of 10 eccentric contractions at either 15 degrees or 35 degrees C by isolated mouse extensor digitorum longus (EDL) muscle, isometric force, EC coupling, and JP1 and JP2 were only reduced after the eccentric contractions performed at 35 degrees C. Regression analysis of JP1 and JP2 content in tibialis anterior and EDL muscles from each set of experiments indicated that JP damage is significantly associated with early (0-3 days) strength deficits after performance of eccentric contractions (R = 0.49; P < 0.001). As a whole, the results of this study indicate that JP damage plays a role in early force deficits due to EC coupling failure following the performance of eccentric contractions.

A number of recent research studies have demonstrated that providing glucose and fructose together in a beverage consumed during exercise results in significantly higher oxidation rates of exogenous carbohydrate (CHO) than consuming glucose alone. However, there is insufficient evidence to determine whether the increased exogenous CHO oxidation improves endurance performance. The purpose of this study was to determine whether consuming a beverage containing glucose and fructose (GF) would result in improved cycling performance compared with an isocaloric glucose-only beverage (G). Nine male competitive cyclists (32.6 +/- 5.8 years, peak oxygen uptake 61.5 +/- 7.9 ml x kg(-1) x min(-1)) completed a familiarization trial and then 2 simulated 100-km cycling time trials on an electronically braked Lode cycle ergometer separated by 5-7 d. During the randomly ordered experimental trials, participants received 36 g of CHO of either G or GF in 250 ml of water every 15 min. All 9 participants completed the 100-km time trial significantly faster when they received the GF beverage than with G (204.0 +/- 23.7 vs. 220.6 +/- 36.6 min; p = .023). There was no difference at any time point between trials for blood glucose or for blood lactate. Total CHO oxidation increased significantly from rest during exercise but was not statistically significant between the GF and G trials, although there was a trend for CHO oxidation to be higher with GF in the latter stages of the time trial. Consumption of a CHO beverage containing glucose and fructose results in improved 100-km cycling performance compared with an isocaloric glucose-only beverage.

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Our data show for the first time that skeletal muscle protein-HNE adducts are related to the severity of insulin resistance in sedentary adults. These results suggest that muscle lipid peroxidation could be involved in the development of insulin resistance.

Brandenberger, KJ, Ingalls, CP, Rupp, JC, and Doyle, JA. Consumption of a 5-mg melatonin supplement does not affect 32.2-km cycling time trial performance. J Strength Cond Res 32(10): 2872-2877, 2018-Some studies suggest that exogenous melatonin supplementation may improve athletic performance in hot humid environments because of its precooling effect. However, melatonin is also consumed as a sleep aid for its depressive effects on the central nervous system (CNS), which may hinder performance. Therefore, this study was conducted to determine whether consuming a 5-mg supplement of melatonin would affect performance in a laboratory-simulated 32.2-km cycling time trial. The time trial was conducted in a thermoneutral environment to separate CNS depressive effects of the melatonin from the cooling effects. Trained male subjects (n = 10; V[Combining Dot Above]O2max = 62.7 ± 6.3 ml·kg·min; age = 25.1 ± 4.0 years; mass = 69.9 ± 9.1 kg; height = 176.0 ± 7.1 cm) performed three 32.2-km time trials on an electronically braked cycle ergometer. The first trial was a familiarization. During the 2 experimental trials, subjects received in a random order either a placebo or a 5-mg melatonin supplement 15 minutes before exercise in a double-blind, crossover design. Variables were measured before exercise and at 8-km intervals. The mean 32.2-km time trial completion times for the melatonin (64.94 ± 5.95 minutes) and placebo (65.26 ± 6.85 minutes) trials were not different (p = 0.682). The mean time trial power output for the melatonin (190.4 ± 40.4 watts) and placebo (190.0 ± 45.7 watts) trials was not different (p = 0.927). Rectal temperature was not significantly different for melatonin compared with placebo (p = 0.827). These results suggest that a 5-mg melatonin supplement administered 15 minutes before exercise does not measurably impact the performance of a 32.2-km cycling time trial in a thermoneutral environment.

Among this population, both HI and LO improve the VO2 at VT and peak, but the improvement is greater with HI. The VT can be a useful adjunct to heart rate and peak oxygen uptake when prescribing exercise.

Contraction-induced muscle injury may reduce running economy (RE) by altering motor unit recruitment, lowering contraction economy, and disturbing running mechanics, any of which may have a deleterious effect on endurance performance. The purpose of this study was to determine if RE is reduced 2 days after performing injurious, low-intensity exercise in 11 healthy active men (27.5 ± 5.7 years; 50.05 ± 1.67 VO2peak). Running economy was determined at treadmill speeds eliciting 65 and 75% of the individual's peak rate of oxygen uptake (VO2peak) 1 day before and 2 days after injury induction. Lower extremity muscle injury was induced with a 30-minute downhill treadmill run (6 × 5 minutes runs, 2 minutes rest, -12% grade, and 12.9 km·h(-1)) that elicited 55% VO2peak. Maximal quadriceps isometric torque was reduced immediately and 2 days after the downhill run by 18 and 10%, and a moderate degree of muscle soreness was present. Two days after the injury, steady-state VO2 and metabolic work (VO2 L·km(-1)) were significantly greater (4-6%) during the 65% VO2peak run. Additionally, postinjury VCO2, VE and rating of perceived exertion were greater at 65% but not at 75% VO2peak, whereas whole blood-lactate concentrations did not change pre-injury to postinjury at either intensity. In conclusion, low-intensity downhill running reduces RE at 65% but not 75% VO2peak. The results of this study and other studies indicate the magnitude to which RE is altered after downhill running is dependent on the severity of the injury and intensity of the RE test.

This study determined whether disrupted glucose and insulin responses to an oral glucose-tolerance test (OGTT) induced by eccentric exercise were attenuated after a repeated bout. Female participants (n = 10, age 24.7 +/- 3.0 yr, body mass 64.9 +/- 7.4 kg, height 1.67 +/- 0.02 m, body fat 29% +/- 2%) performed 2 bouts of downhill running (DTR 1 and DTR 2) separated by 14 d. OGTTs were administered at baseline and 48 hr after DTR 1 and DTR 2. Maximum voluntary isometric quadriceps torque (MVC), subjective soreness (100-mm visual analog scale), and serum creatine kinase (CK) were assessed pre-, post-, and 48 hr post-DTR 1 and DTR 2. Insulin and glucose area under the curve (38% +/- 8% and 21% +/- 5% increase, respectively) and peak insulin (44.1 +/- 5.1 vs. 31.6 +/- 4.0 muU/ml) and glucose (6.5 +/- 0.4 vs. 5.5 +/- 0.4 mmol/L) were elevated after DTR 1, with no increase above baseline 48 hr after DTR 2. MVC remained reduced by 9% +/- 3% 48 hr after DTR 1, recovering back to baseline 48 hr after DTR 2. Soreness was elevated to a greater degree 48 hr after DTR 1 (48 +/- 6 vs. 13 +/- 3 mm), with a tendency for greater CK responses 48 hr after DTR 1 (813 +/- 365 vs. 163 +/- 43 U/L, p = .08). A novel bout of eccentric exercise confers protective effects, with subsequent bouts failing to elicit disruptions in glucose and insulin homeostasis.