Interaction among Skeletal Muscle Metabolic Energy Systems during Intense Exercise

High-intensity exercise can result in up to a 1,000-fold increase in the rate of ATP demand compared to that at rest (Newsholme et al., 1983). To sustain muscle contraction, ATP needs to be regenerated at a rate complementary to ATP demand. Three energy systems function to replenish ATP in muscle: (1) Phosphagen, (2) Glycolytic, and (3) Mitochondrial Respiration. The three systems differ in the substrates used, products, maximal rate of ATP regeneration, capacity of ATP regeneration, and their associated contributions to fatigue. In this exercise context, fatigue is best defined as a decreasing force production during muscle contraction despite constant or increasing effort. The replenishment of ATP during intense exercise is the result of a coordinated metabolic response in which all energy systems contribute to different degrees based on an interaction between the intensity and duration of the exercise, and consequently the proportional contribution of the different skeletal muscle motor units. Such relative contributions also determine to a large extent the involvement of specific metabolic and central nervous system events that contribute to fatigue. The purpose of this paper is to provide a contemporary explanation of the muscle metabolic response to different exercise intensities and durations, with emphasis given to recent improvements in understanding and research methodology

Intra-Arterial Blood Pressure Characteristics during Submaximal Cycling and Recovery

The purpose of this study was to measure intra-arterial (IA) blood pressure from rest to steady-state submaximal exercise and immediately post-exercise. Beat-to-beat blood pressure was compared to breath-by-breath VO2 during steady-state and maximal exercise. Fourteen normotensive subjects volunteered. Systolic (SBP), diastolic (DBP) and mean (mBP) blood pressure was measured from rest to steady state during cycling at 45, 60, and 75% maximal power output (POmax). BP was assessed during recovery from VO2peak through 2 min of cycling at 50 W. During the rest to exercise transition, mBP decreased from 103.41 ± 9.4 to 90.1 ± 8.9 mmHg after 11.6 ± 6.2 s (

Clinical Study Limited Effects of Endurance or Interval Training on Visceral Adipose Tissue and Systemic Inflammation in Sedentary Middle-Aged Men

properly cited. Purpose. Limited data exists for the effects of sprint-interval training (SIT) and endurance training (ET) on total body composition, abdominal visceral adipose tissue, and plasma inflammation. Moreover, whether "active" or "passive" recovery in SIT provides a differential effect on these measures remains uncertain. Methods. Sedentary middle-aged men ( = 62; 49.5±5.8 y; 29.7±3.7 kg⋅m 2 ) underwent abdominal computed tomography, dual-energy X-ray absorptiometry, venepuncture, and exercise testing before and after the interventions, which included the following: 12 wks 3 d⋅wk −1 ET ( = 15; 50-60 min cycling; 80% HR max ), SIT (4-10 × 30 s sprint efforts) with passive (P-SIT; = 15) or active recovery (A-SIT; = 15); or nonexercise control condition (CON; = 14). Changes in cardiorespiratory fitness, whole-body and visceral fat mass, and plasma systemic inflammation were examined. Results. Compared to CON, significant increases in interpolated power output (P-SIT, < 0.001; ET, = 0.012; A-SIT, = 0.041) and test duration (P-SIT, = 0.001; ET, = 0.012; A-SIT, = 0.046) occurred after training. Final VO 2 consumption was increased after P-SIT only ( < 0.001). Despite >90% exercise compliance, there was no change in whole-body or visceral fat mass or plasma inflammation ( > 0.05). Conclusion. In sedentary middle-aged men, SIT was a time-effective alternative to ET in facilitating conditioning responses yet was ineffective in altering body composition and plasma inflammation, and compared to passive recovery, evidenced diminished conditioning responses when employing active recovery

Lactate Regulates Metabolic and Proinflammatory Circuits in Control of T Cell Migration and Effector Functions

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Evidence for the Invalidity of the Wingate Test for the Assessment of Peak Power, Power Decrement and Muscular Fatigue

We hypothesized that the protocol-induced initial cadence of the WAnT is too high to allow high muscle force production and peak power generation. Twenty endurance, strength or power trained subjects (9 male, 11 female) completed two 30 s maximal exertion stationary cycle ergometer tests involving the traditional peak cadence start (TRAD) vs. a stationary start (STAT). Inertia corrected mechanical power, cadence, EMG from the vastus lateralis, and applied force to the pedals were measured continuously throughout both tests. Peak power was higher during TRAD; 11.32 ±1.41 vs. 10.40 ±1.35 Watts/kg (p < 0.0001), as was peak cadence; 171.4 ±16.3 vs. 120.9 ±15.1 rev/min (p < 0.0001). However, during TRAD EMG root mean squared (rms) increased continuously throughout the test, force applied to the pedals increased from 1 to 3 s (0.73 ±0.27 vs. 0.90 ±0.39 N/kg; p = 0.02) and thereafter remained relatively stable. EMG mean frequency also increased from 1 to 3 s, but then decreased throughout the remainder of the test. During TRAD, mechanical power decreased near immediately despite increasing EMG rms, EMGmean frequency and force application to the pedals. The initial 10 s of data from the WAnT is invalid. We recommend that intense cycle ergometer testing should commence with a stationary start

Muscle glycogenolysis during weight-resistance exercise

Skeletal muscle glycogenolysis was investigated in eight subjects during both high (HI) (70% 1 RM) and low (LO) intensity (35% 1 RM) leg extension weight-resistance exercise. Total force application to the machine lever arm was determined and equated between trials via a strain gauge and computer interfaced system. After the sixth set, muscle glycogen degradation was similar in the HI and LO trials (46.9 ± 6.6 and 46.6 ± 6.0 mmol•kg-1 wet wt, respectively), with the LO trial characterized by almost double the repetitions (6.0 and 12.7 ± 1.1) and half the peak concentric torque per repetition (24.2 ± 1.0 and 12.4 ± 0.5). After the sixth set, muscle lactate accumulation was also similar (13.8 ± 0.7 and 16.7 ± 4.2 mmol•kg-1 wet wt for HI and LO trials, respectively). After two hours of passive recovery with no feedings, muscle glycogen storage during the HI and LO trials was 22.2 (±6.8) and 14.2 (±2.5) mmol•kg-1 wet wt, respectively These values represented glycogen synthesis rates of 11.1 (±3.4) and 7.1 (±1.3) mmol•kg-1 •hr-1 , and occurred without significant increases in blood glucose relative to resting concentrations. Optical absorbance measurement of PAS stained muscle sections revealed no differences in the glycogen content of fast (FT) and slow twitch (ST) fibers between trials. When data from each trial were combined, declines in absorbance were larger in FT than ST fibers after the sixth set (0.356 ± 0.048) than in slow twitch fibers (0.222 ± 0.039, p < 0.05). The increase in absorbanceduring the two hour recovery was also larger in FT than ST fibers (0.119 ± 0.024 and 0.055 ± 0.024, p < 0.05). When total force application was constant, muscle glycogenolysis was the same regardless of the intensity of resistance exercise. Glycogenolysis was greater in fast twitch fibers, as was glycogen storage during the immediate post-exercise recovery. The relatively high rate of glycogen synthesis after exercise may be evidence of glycogenesis from intramuscular metabolites.Thesis (Ph. D.)Human Performance Laborator

Editorial: A critical review of peer review: The need to scrutinize the"gatekeepers" of research in exercise physiology

I have developed as an educator and researcher accepting the premise that any system of peer review was unquestionably good. An explanation for this belief can be based, in part, on the mentor system within academia. After all, we can be molded as students to reflect the attitudes and professional interpretations of those we hold in high esteem. In addition, a summary of the historical development of peer review (see latter section) reveals that the process flourished relatively recently. Consequently, the more senior scientists of today who have and continue to function as mentors to many of our "younger" researchers, can recognize and remember the time of the transition in science towards an organized editorial peer review system for research manuscripts and grant submission ..

Nutrition and exercise determinants of postexercise glycogen synthesis

During the initial hours of recovery from prolonged exhaustive lower body exercise, muscle glycogen synthesis occurs at rates approximating 1-2 mmol.kg^-1 wet wt.hr^-1 if no carbohydrate is consumed. When carbohydrate is consumed during the recovery, the maximal rate of glycogen synthesis approximates 7-10 mmol.kg^-1 wet wt.hr^-1. The rate of post-exercise glycogen synthesis is lower if the magnitude of glycogen degradation is small, if less than 0.7 gm glucose.kg^-1 body wt.hr^-1 is ingested, when the recovery is active, and when the carbohydrate feeding is delayed. The rate of postexercise glycogen synthesis is not reduced during the initial hours (< 4) after eccentric exercise. For studies evaluating muscle glycogen synthesis in excess of 12 hours of recovery, average rates of glycogen synthesis are below 4 mmol.kg^-1 wet wt.hr^-1. Glycogen synthesis is known to be impaired for time periods in excess of 24 hours following exercise causing eccentric muscle damage. Following intense exercise resulting in high concentrations of muscle lactate, muscle glycogen synthesis occurs at between 15-25 mmol.kg^-1 wet wt.hr^-1. These synthesis rates occur without ingested carbohydrate during the recovery period and are maintained when a low intensity active recovery is performed