Alterations in plasma volume, electrolytes and protein during incremental exercise at different pedal speeds

We investigated the effects of pedal speed on changes in plasma volume, electrolytes and protein during incremental exercise. Ten adult males participated in two, 30 minute incremental cycle ergometer exercise tests at room temperature (22° C, rh=56%). Exercise load was increased from 20 to 70% of peak . Five minutes were spent at each of six stages which were equally spaced in exercise intensity. Subjects pedaled at 50 (50 RPM) and 90 (90 RPM) rev · min^–1. Venous blood samples were drawn prior to exercise and during the last minute of each stage. Relative plasma volume changes showed a progressive hemoconcentration during the exercise. There were no significant differences due to pedal speed as plasma volume loss averaged –7.3% during exercise. [Na+], [Cl–], and [K+] increased significantly during exercise but were not influenced by pedal speed. Changes in plasma protein and albumin concentrations indicated that there was a loss of globulin from the vascular volume in both conditions and an addition of albumin to the plasma in 50 RPM. The difference in plasma albumin dynamics was possibly related to an effect of pedal speed on movement of fluid in the lymphatic vessels of the legs.This work was supported in part by Grants from the Theresa Monaco Endowment of the University of Houston College of Education and Nautilus Sports/Medical Industries     

Carbohydrate metabolism during intense exercise when hyperglycemic

The effects of hyperglycemia on muscle glycogen use and carbohydrate metabolism were evaluated in eight well-trained cyclists (average maximal O2 consumption 4.5 +/- 0.1 l/min) during 2 h of exercise at 73 +/- 2% of maximal O2 consumption. During the control trial (CT), plasma glucose concentration averaged 4.2 +/- 0.2 mM and plasma insulin remained between 6 and 9 microU/ml. During the hyperglycemic trial (HT), 20 g of glucose were infused intravenously after 8 min of exercise, after which a variable-rate infusion of 18% glucose was used to maintain plasma glucose at 10.8 +/- 0.4 mM throughout exercise. Plasma insulin remained low during the 1st h of HT, yet it increased significantly (to 16-24 microU/ml; P less than 0.05) during the 2nd h. The amount of muscle glycogen utilized in the vastus lateralis during exercise was similar during HT and CT (75 +/- 8 and 76 +/- 7 mmol/kg, respectively). As exercise duration increased, carbohydrate oxidation declined during CT but increased during HT. Consequently, after 2 h of exercise, carbohydrate oxidation was 40% higher during HT than during CT (P less than 0.01). The rate of glucose infusion required to maintain hyperglycemia (10 mM) remained very stable at 1.6 +/- 0.1 g/min during the 1st h. However, during the 2nd h of exercise, the rate of glucose infusion increased (P less than 0.01) to 2.6 +/- 0.1 g/min (37 mg.kg body wt-1.min-1) during the final 20 min of exercise. We conclude that hyperglycemia (i.e., 10 mM) in humans does not alter muscle glycogen use during 2 h of intense cycling.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypohydration effects on skeletal muscle performance and metabolism: a 31P-MRS study

The purpose of this study was to determinewhether hypohydration reduces skeletal muscle endurance and whetherincreased H⁺ andP_i might contribute to performancedegradation. Ten physically active volunteers (age 21-40 yr)performed supine single-leg, knee-extension exercise to exhaustion in a1.5-T whole body magnetic resonance spectroscopy (MRS) system wheneuhydrated and when hypohydrated (4% body wt).³¹P spectra were collected at arate of one per second at rest, exercise, and recovery, and weregrouped and averaged to represent 10-s intervals. The desired hydrationlevel was achieved by having the subjects perform 2-3 h ofexercise in a warm room (40°C dry bulb, 20% relative humidity)with or without fluid replacement 3-8 h before the experiment.Time to fatigue was reduced (P < 0.05) by 15% when the subjects were hypohydrated [213 ± 12 vs. 251 ± 15 (SE) s]. Muscle strength was generally notaffected by hypohydration. Muscle pH andP_i/-ATP ratio were similarduring exercise and at exhaustion, regardless of hydration state. The time constants for phosphocreatine recovery were also similar betweentrials. In summary, moderate hypohydration reduces muscle endurance,and neither H⁺ norP_i concentration appears to berelated to these reductions.

     

Impact of muscle injury and accompanying inflammatory response on thermoregulation during exercise in the heat.

This study examined whether muscle injury and the accompanying inflammatory responses alter thermoregulation during subsequent exercise-heat stress. Sixteen subjects performed 50 min of treadmill exercise (45-50% maximal O(2) consumption) in a hot room (40 degrees C, 20% relative humidity) before and at select times after eccentric upper body (UBE) and/or eccentric lower body (LBE) exercise. In experiment 1, eight subjects performed treadmill exercise before and 6, 25, and 30 h after UBE and then 6, 25, and 30 h after LBE. In experiment 2, eight subjects performed treadmill exercise before and 2, 7, and 26 h after LBE only. UBE and LBE produced marked soreness and significantly elevated creatine kinase levels (P < 0.05), but only LBE increased (P < 0.05) interleukin-6 levels. In experiment 1, core temperatures before and during exercise-heat stress were similar for control and after UBE, but some evidence for higher core temperatures was found after LBE. In experiment 2, core temperatures during exercise-heat stress were 0.2-0.3 degrees C (P < 0.05) above control values at 2 and 7 h after LBE. The added thermal strain after LBE (P < 0.05) was associated with higher metabolic rate (r = 0.70 and 0.68 at 2 and 6-7 h, respectively) but was not related (P > 0.05) to muscle soreness (r = 0.47 at 6-7 h), plasma interleukin-6 (r = 0.35 at 6-7 h), or peak creatine kinase levels (r = 0.22). Local sweating responses (threshold core temperature and slope) were not altered by UBE or LBE. The results suggest that profuse muscle injury can increase body core temperature during exercise-heat stress and that the added heat storage cannot be attributed solely to increased heat production.     

Effects of dietary protein content on IGF-I, testosterone, and body composition during 8 days of severe energy deficit and arduous physical activity.

Energy restriction coupled with high energy expenditure from arduous work is associated with an altered insulin-like growth factor-I (IGF-I) system and androgens that are coincident with losses of fat-free mass. The aim of this study was to determine the effects of two levels of dietary protein content and its effects on IGF-I, androgens, and losses of fat-free mass accompanying energy deficit. We hypothesized that higher dietary protein content would attenuate the decline of anabolic hormones and, thus, prevent losses of fat-free mass. Thirty-four men [24 (SD 0.3) yr, 180.1 (SD 1.1) cm, and 83.0 (SD 1.4) kg] participated in an 8-day military exercise characterized by high energy expenditure (16.5 MJ/day), low energy intake (6.5 MJ/day), and sleep deprivation (4 h/24 h) and were randomly divided into two dietary groups: 0.9 and 0.5 g/kg dietary protein intake. IGF-I system analytes, androgens, and body composition were assessed before and on days 4 and 8 of the intervention. Total, free, and nonternary IGF-I and testosterone declined 50%, 64%, 55%, and 45%, respectively, with similar reductions in both groups. There was, however, a diet x time interaction on day 8 for total IGF-I and sex hormone-binding globulin. Decreases in body mass (3.2 kg), fat-free mass (1.2 kg), fat mass (2.0 kg), and percent body fat (1.5%) were similar in both groups (P = 0.01). Dietary protein content of 0.5 and 0.9 g/kg minimally attenuated the decline of IGF-I, the androgenic system, and fat-free mass during 8 days of negative energy balance associated with high energy expenditure and low energy intake.     

Use of phosphocreatine kinetics to determine the influence of creatine on muscle mitochondrial respiration: an in vivo 31P-MRS study of oral creatine ingestion.

Recent human isolated muscle fiber studies suggest that phosphocreatine (PCr) and creatine (Cr) concentrations play a role in the regulation of mitochondrial respiration rate. To determine whether similar regulatory mechanisms are present in vivo, this study examined the relationship between skeletal muscle mitochondrial respiration rate and end-exercise PCr, Cr, PCr-to-Cr ratio (PCr/Cr), ADP, and pH by using (31)P-magnetic resonance spectroscopy in 16 men and women (36.9 +/- 4.6 yr). The initial PCr resynthesis rate and time constant (T(c)) were used as indicators of mitochondrial respiration after brief (10-12 s) and exhaustive (1-4 min) dynamic knee extension exercise performed in placebo and creatine-supplemented conditions. The results show that the initial PCr resynthesis rate has a strong relationship with end-exercise PCr, Cr, and PCr/Cr (r > 0.80, P < 0.001), a moderate relationship with end-exercise ADP (r = 0.77, P < 0.001), and no relationship with end-exercise pH (r = -0.14, P = 0.34). The PCr T(c) was not as strongly related to PCr, Cr, PCr/Cr, and ADP (r < 0.77, P < 0.001-0.18) and was significantly influenced by end-exercise pH (r = -0.43, P < 0.01). These findings suggest that end-exercise PCr and Cr should be taken into consideration when PCr recovery kinetics is used as an indicator of mitochondrial respiration and that the initial PCr resynthesis rate is a more reliable indicator of mitochondrial respiration compared with the PCr T(c).     

Surface contamination artificially elevates initial sweat mineral concentrations

Several sweat mineral element concentrations decline with serial sampling. Possible causes include reduced dermal mineral concentrations or flushing of surface contamination. The purpose of this study was to simultaneously sample mineral concentrations in transdermal fluid (TDF), sweat, and serum during extended exercise-heat stress to determine if these compartments show the same serial changes during repeat sampling. Sixteen heat-acclimated individuals walked on a treadmill (1.56 m/s, 3.0% grade) in a 35°C, 20% relative humidity (RH), 1 m/s wind environment 50 min each hour for 3 h. Mineral concentrations of Ca, Cu, Fe, K, Mg, Na, and Zn were measured each hour from serum, sweat from upper back (sweat pouch) and arm (bag), and TDF from the upper back. Sites were meticulously cleaned to minimize surface contamination. Mineral concentrations were determined by spectrometry. TDF remained stable over time, with exception of a modest increase in TDF [Fe] (15%) and decrease in TDF [Zn] (-18%). Likewise, serum and pouch sweat samples were stable over time. In contrast, the initial arm bag sweat mineral concentrations were greater than those in the sweat pouch, and [Ca], [Cu], [Mg], and [Zn] declined 26-76% from initial to the subsequent samples, becoming similar to sweat pouch. Nominal TDF mineral shifts do not affect sweat mineral concentrations. Arm bag sweat mineral concentrations are initially elevated due to skin surface contaminants that are not removed despite meticulous cleaning (e.g., under fingernails, on arm hair), then decrease with extended sweating and approach those measured from the scapular region.     

Blood pressure and hemodynamic responses after exercise in older hypertensives

Recently, systolic and diastolic blood pressure have been reported to be significantly lower for several hours after exercise than when measured at rest before exercise in individuals with essential hypertension. We sought to determine the hemodynamic mechanism underlying this reduction in blood pressure. Twenty-four men and women 60-69 yr of age with persistent essential hypertension completed one of the following protocols: exercise at 50% of maximum O2 consumption (VO2 max) followed by 1 h of recovery, exercise at 70% of VO2 max followed by 3 h of recovery, or a 4-h control study. Systolic pressure was significantly lower during recovery after both intensities of exercise, but diastolic pressure was unchanged. The lower blood pressure was primarily due to a reduction in cardiac output, since total peripheral resistance was increased throughout both recovery periods. Cardiac output was reduced in recovery because of a reduction in stroke volume. Heart rate was above, or no different from, that at rest before exercise. Changes in plasma volume could not entirely account for the reduction in stroke volume. Therefore, other mechanisms altering venous return and/or myocardial contractility appear to be responsible for the reduction in systolic blood pressure evident after a single bout of submaximal exercise in individuals with essential hypertension.