Blood ammonium and lactate accumulation response to different training protocols using the parallel squat exercise.

Three parallel squat protocols with equal total work volume were used to determine the metabolic response of resistance exercise with different practical training protocols combining program variables in the way that they are typically prescribed in field. Sixteen men able to back squat 1.5 times their body weight participated in the study. Individualized muscular endurance (ME), strength (STR), and hypertrophy (HYP) squat workouts were developed based on a 1 repetition maximum back squat. Each protocol was performed 3-7 days apart in random order. Venous blood was obtained after 5 minutes of seated rest both before and after each workout for ammonium and lactate analysis. The ME protocol (79.8 µM [SD = 45.4], 95% confidence interval [CI]: 55.7-104.0) produced a greater change of plasma ammonium than both the HYP (45.3 µM [SD = 34.5], 95% CI: 26.9-63.6, p = 0.017) and STR (31.7 µM [SD = 52.3], 95% CI: 3.9-59.6, p = 0.006) protocols. Change of blood lactate concentration from resting levels to postexercise levels was significantly different (p = 0.005) between ME (6.1 mM [SD = 2.9], 95% CI: 4.6-7.7) and STR (3.9 mM [SD = 2.5], 95% CI: 2.6-5.2) protocols. The main finding of this study is that blood ammonium and lactate seem to accumulate in response to an increasing number of repetitions with decreasing rest time between sets. As consequence, a greater number of repetitions should be added to a resistance workout, along with a shorter rest time between sets when training for events that induce a large metabolic load. The metabolic accumulation associated with high repetition exercise may represent the need for longer recovery time between these types of workouts compared with workouts using a low number of repetitions.

Effects of beta-alanine supplementation on sprint endurance.

Recent research has shown that beta-alanine (BA) supplementation can increase intramuscular carnosine levels. Carnosine is an intramuscular buffer, and it has been linked to improvements in performance, specifically during bouts of high-intensity exercise that are likely limited by muscle acidosis. Therefore, the purpose of this study was to examine the effect of BA supplementation on sprint endurance at 2 different supramaximal intensities. Twenty-one anaerobically trained (rugby players [n = 4], wrestlers [n = 11], and recreationally strength trained athletes [n = 6]) college-aged men participated in a double-blind, placebo controlled study. The subjects performed an incremental VO2max test and 2 sprint to exhaustion tests set at 115 and 140% of their VO2max on a motorized treadmill before (PRE) and after (POST) a 5-week supplementation period. During this time, the subjects ingested either a BA supplement or placebo (PLA) with meals. The subjects ingested 4 g·d(-1) of BA or PLA during the first week and 6 g·d(-1) the following 4 weeks. Capillary blood samples were taken before and after each sprint to determine blood lactate response to the sprint exercise. No significant group (BA, PLA) × intensity (115%, 140%; p = 0.60), group by time (PRE, POST; p = 0.72), or group × intensity × time (p = 0.74) interactions were observed for time to exhaustion. In addition, similar nonsignificant observations were made for lactate response to the sprints (group × intensity, p = 0.43; group × time, p = 0.33, group × intensity × time, p = 0.56). From the results of this study, it was concluded that beta-alanine supplementation did not have a significant effect on sprint endurance at supramaximal intensities.

Cardiorespiratory effects of inelastic chest wall restriction.

We examined the effects of chest wall restriction (CWR) on cardiorespiratory function at rest and during exercise in healthy subjects in an attempt to approximate the cardiorespiratory interactions observed in clinical conditions that result in restrictive lung and/or chest wall changes and a reduced intrathoracic space. Canvas straps were applied around the thorax and abdomen so that vital capacity was reduced by >35%. Data were acquired at rest and during cycle ergometry at 25 and 45% of peak workloads. CWR elicited significant increases in the flow-resistive work performed on the lung (160%) and the gastric pressure-time integral (>400%) at the higher workload, but it resulted in a decrease in the elastic work performed on the lung (56%) compared with control conditions. With CWR, heart rate increased and stroke volume (SV) fell, resulting in >10% fall in cardiac output at rest and during exercise at matched workloads (P < 0.05). Blood pressure and catecholamines were significantly elevated during CWR exercise conditions (P < 0.05). We conclude that CWR significantly impairs SV during exercise and that a compensatory increase in heart rate does not prevent a significant reduction in cardiac output. O(2) consumption appears to be maintained via increased extraction and a redistribution of blood flow via sympathetic activation.