Function Of Exercise Intensity Research Articles

Control of nasal dilator muscle activities during exercise: role of nasopharyngeal afferents

Our primary aim was to determine whether reducing the activity of nasal airway receptors would influence drive to the nasal dilator muscles (NDMs) during exercise. We used lidocaine (2%) or nasal splints to diminish afferent airway receptor activity and measured the electromyogram (EMG) activity of the NDMs during incremental bicycle exercise in subjects who breathed nasally. NDM EMG activities increased as a function of exercise intensity but were not changed by lidocaine and were only slightly reduced by splinting. Similarly, neither intervention altered the normal decrease in NDM EMG activity associated with reductions in airway resistance evoked by He-O2 breathing. We also compared the NDM EMG response to exercise with that evoked by CO2 rebreathing at rest to determine whether the nature of the ventilatory stimulus influences drive to the NDMs; comparisons were made at constant levels of nasal inspired ventilation and, therefore, constant total ventilatory output. The increase in EMG activity was much higher during exercise compared with hyperoxic hypercapnia. In conclusion, 1) desensitizing the nasal airway does not alter NDM activity significantly during exercise and 2) exercise results in much greater increases in NDM activity compared with hypercapnia, indicating that different ventilatory stimuli can evoke more or less activation of upper airway motoneurons, even when comparisons are made at constant levels of total ventilatory output.

EXERCISE INTENSITY AFFECTS BREAST MILK COMPOSITION IN LACTATING WOMEN357

This study examined the relationship between breast milk composition and exercise intensity in lactating women. Milk and blood samples from nine lactating women were collected before and after one resting session (rest) and 3 bouts of exercise (50%, 75% and 100% VO2max). Blood was collected via finger stick 30 min pre-, and 0, 30, 60, and 90 min post-rest or exercise and analyzed for lactic acid (LA). Milk was collected via breast pump 30 and 0 min pre-, and 0, 30, 60 and 90 min post-rest or exercise, and analyzed for LA, urea, ammonium, fat and pH. LA in milk was significantly elevated 0 min post-exercise at 100% VO2max when compared to rest (0.94±0.31 vs. 0.12±0.09) but not 0 min after the 75% or 50% VO2max bouts(0.26±0.13 and 0.08±0.03, respectively, vs. 0.12±0.09). There were no changes in milk pH, urea, ammonium or fat 0 min post-exercise at any of the exercise intensities compared to rest but there were changes as a function of collection time post-exercise. The significant increase in milk LA after 100%VO2max persisted to the 90 post-exercise collection; LA in blood mirrored these changes. These data suggest that (1) breast milk pH, urea, ammonium and fat do not change with exercise intensity, (2) LA appearance in breast milk is a function of exercise intensity, and (3) moderate intensity exercise will not increase breast milk LA levels.

Effect of the slow-component rise in oxygen uptake on VO2max.

During constant-rate high-intensity (CRHI) exercise lasting longer than 3 min, VO2 has been reported to exceed VO2max measured with a traditional graded exercise test (GXT). This could be because VO2max was not achieved on the GXT or because the factors responsible for the slow-component rise in VO2 alter VO2max. The objective of this study was to test the hypothesis that the slow-component rise in VO2 measured during CRHI running leads to a total VO2 that exceeds VO2max measured during a running GXT. VO2max was determined in eight highly trained individuals using data collected from five grade-incremented, treadmill-running GXT. Each subject demonstrated a definitive plateau of VO2 as a function of exercise intensity. Three VO2max values based on different approaches for representing the VO2max plateau were obtained. Subjects also completed two exhaustive CRHI bouts of treadmill running lasting 7-13 min at speeds estimated from the ACSM equation to elicit an average of 99 +/- 5% VO2max. The mean (+/- SD) VO2peak determined during the CRHI runs (4.17 +/- 0.9 l.min-1) was not different form or less than the three VO2max values (4.19-4.32 +/- 0.09 l.min-1). We conclude that in highly trained individuals, the slow-component rise in VO2 during CRHI treadmill running does not lead to a total VO2 that exceeds the VO2max measured during a running graded exercise test.

Effect of unweighting on skeletal muscle use during exercise

Exercise-induced spin-spin relaxation time (T2) shifts in magnetic resonance (MR) images were used to test the hypothesis that more muscle would be used to perform a given submaximal task after 5 wk of unweighting. Before and after unilateral lower limb suspension (ULLS), 7 subjects performed 5 sets of 10 unilateral concentric actions with the quadriceps femoris muscle group (QF) at each of 4 loads: 25, 40, 55, and 70% of maximum. T2-weighted MR images of the thigh were collected at rest and after each relative load. ULLS elicited a 20% decrease in strength of the left unweighted QF and a 14% decrease in average cross-sectional area (CSA) with no changes in the right weight-bearing QF. Average CSA of the left or right QF showing exercise-induced T2 shift increased as a function of exercise intensity both before and after ULLS. On average, 12 +/- 1, 15 +/- 2, 18 +/- 2, and 22 +/- 1 cm2 of either QF showed elevated T2 for the 25, 40, 55, and 70% loads, respectively, before ULLS. Average CSA of the left but not the right QF, showing elevated T2 after ULLS, was increased to 16 +/- 2, 23 +/- 3, 31 +/- 7, and 39 +/- 5 cm2, respectively. The results indicated that unweighting increased exercise-induced T2 shift in MR images, presumably due to greater muscle mass involvement in exercise after than before unweighting, suggesting a change in motor control.

Relationship of middle cerebral artery blood flow velocity to intensity during dynamic exercise in normal subjects.

Cerebral blood flow has been reported to increase during dynamic exercise, but whether this occurs in proportion to the intensity remains unsettled. We measured middle cerebral artery blood flow velocity (vm) by transcranial Doppler ultrasound in 14 healthy young adults, at rest and during dynamic exercise performed on a cycle ergometer at a intensity progressively increasing, by 50 W every 4 min until exhaustion. Arterial blood pressure, heart rate, end-tidal, partial pressure of carbon dioxide (PETCO2), oxygen uptake (VO2) and carbon dioxide output were determined at exercise intensity. Mean vM increased from 53 (SEM 2) cm.s-1 at rest to a maximum of 75 (SEM 4) cm.s-1 at 57% of the maximal attained VO2 (VO2max), and thereafter progressively decreased to 59 (SEM 4) cm.s-1 at VO2max. The respiratory exchange ratio (R) was 0.97 (SEM 0.01) at 57% of VO2max and 1.10 (SEM 0.01) at VO2max. The PETCO2 increased from 5.9 (SEM 0.2) kPa at rest to 7.4 (SEM 0.2) kPa at 57% of VO2max, and thereafter decreased to 5.9 (SEM 0.2) kPa at VO2max. Mean arterial pressure increased from 98 (SEM 1) mmHg (13.1 kPa) at rest to 116 (SEM 1) mmHg (15.5 kPa) at 90% of VO2max, and decreased slightly to 108 (SEM 1) mmHg (14.4 kPa) at VO2max. In all the subjects, the maximal value of vm was recorded at the highest attained exercise intensity below the anaerobic threshold (defined by R greater than 1). We concluded that cerebral blood flow as evaluated by middle cerebral artery flow velocity increased during dynamic exercise as a function of exercise intensity below the anaerobic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Body position affects the power spectrum of heart rate variability during dynamic exercise.

The power spectrum analysis of R-R interval variability (RRV) has been estimated by means of an autoregressive method in six men in supine (S) and sitting (C) postures at rest and during steady-state cycle exercise at about 14%, 28%, 45%, 67% of the maximal oxygen consumption (% VO2max). The total power of RRV decreased exponentially as a function of exercise intensity in a similar way in both postures. Three components were recognized in the power spectra: firstly, a high frequency peak (HF), an expression of respiratory arrhythmia, the central frequency (fcentral) of which increased in both S and C from a resting value of about 0.26 Hz to 0.42 Hz at 67% VO2max; secondly, a low frequency peak (LF) related to arterial pressure control, the fcentral of which remained constant at 0.1 Hz in C, whereas in S above 28% VO2max decreased to 0.07 Hz; and thirdly, a very low frequency component (VLF; less than 0.05 Hz, no fcentral). The power of the three components (as a percentage of the total power) depended on the body posture and the metabolic demand. HF% at rest was 30.3 (SEM 6.6) % in S and 5.0 (SEM 0.8) % in C. During exercise HF% decreased by about 30% in S and increased to 19.7 (SEM 5.5) % at 28% VO2max in C. LF% was lower in S than in C at rest [31.6 (SEM 5.7) % vs 44.9 (SEM 6.4) %; P < 0.05], remaining constant up to 28% VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in insulation of body tissue and wet suits during underwater exercise at various atmospheric pressures

To clarify the independent changes of insulations of body tissues (Itissue) and wet suit (Isuit) in the wet-suited subject during underwater exercise, overall heat flow from the skin (Htissue) and wet suit (Hsuit) and esophageal (Tes), skin (Tsk), and wet suit temperatures were measured at 1, 2, and 2.5 atmospheres absolute (ATA) at critical water temperature (Tcw). The average Tcw in nine wet-suited men (23-38 yr) was 22.3 +/- 0.2, 26.3 +/- 0.2, and 28.0 +/- 0.4 degrees C (SE) at 1, 2, and 2.5 ATA, respectively. At Tcw of each pressure male volunteers wearing 5-mm neoprene wet suits completed three 2-h experiments while immersed up to the neck. During one experiment the subjects remained at rest, and in the other two they exercised on an underwater ergometer at two different intensities (2 and 3 met). Tes significantly declined (P less than 0.05) over 2 h from 37.1 to 36.5 degrees C during rest in each pressure. The 2-met exercise prevented Tes from falling in all pressures, and the 3-met exercise elevated Tes by 0.2-0.3 degrees C. There was no exercise-dependent difference in Isuit, but a pressure-dependent difference was remarkable. The Itissue at rest was identical for all pressures; however, it progressively decreased as a function of exercise intensity. It is concluded that overall Itissue is entirely determined by work intensity at Tcw, but not by atmospheric pressure. On the contrary, Isuit at Tcw is solely dependent on the pressure, but not on the work intensity.

Oxygen consumption and distribution of blood flow in rats climbing a laddermill

The purpose of this study was threefold: 1) to determine whether untrained rats that refused to run on treadmill would climb on a laddermill (75 degrees incline); 2) to determine O2 consumption (VO2) in untrained rats as a function of laddermill climbing speed; and 3) to determine whether the circulatory response of untrained rats to laddermill climbing is similar to that previously reported for treadmill running at an equivalent VO2. Eighteen female Sprague-Dawley rats that would not perform on a treadmill as part of another study were used to measure VO2 as a function of laddermill speed (5-17 m/min). Data were obtained from all 18 rats; VO2 increased linearly as a function of laddermill speed (r = 0.83, y = 3.0 x + 63.2). Twenty-four female Sprague-Dawley rats that also refused to run on a treadmill were used to measure mean arterial pressure, heart rate, and blood flow distribution (with microspheres) during climbing at 5 and 10 m/min. These exercise intensities were metabolically equivalent to level treadmill running at 45 and 60 m/min (VO2 approximately 78 and 93 ml.min-1.kg-1, respectively). Of the 24 animals, 23 were willing to climb. Mean arterial pressures were higher (approximately 10%) during laddermill climbing than during equivalent treadmill running, but heart rates were the same. General blood flow distribution among muscles as a function of fiber type (with red muscles receiving higher flows) and between muscles and visceral tissues (muscle blood flow increased as a function of exercise intensity while visceral blood flows decreased) were similar to data for rats running on the level.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood gas measurements during exercise: errors due to temperature correction

This study assessed the degree to which correcting blood gas measurements to rectal temperature (Tre) rather than to the temperatures at which gas exchange occurs [pulmonary arterial (Tpa) or intramuscular (Tm)] introduces errors into blood gas analysis of exercising mammals. Horses and steers weighing 450 kg were run on a treadmill at speeds up to those eliciting maximal rates of O2 consumption (VO2max), and temperatures were measured in various body compartments. In both species Tpa rose faster than Tre during the run, the degree of dissociation being a function of exercise intensity and duration. Tm was measured only in horses, and it rose faster than Tpa during the run and decreased more slowly postrun. Correcting blood gas values measured at an analyzer temperature of 37 degrees C to Tre without accounting for transient increases during the run of Tpa and Tm that were never reflected in Tre significantly biased estimates of blood gases. The biased estimates erroneously indicated that both species experienced more severe hypoxemia than they actually did at VO2max and masked the hypercapnia experienced by the horses at VO2max.

Bench Press Metabolic Rate as a Function of Exercise Intensity

Bench Press Metabolic Rate as a Function of Exercise Intensity

Bench Press Metabolic Rate as a Function of Exercise Intensity

Bench Press Metabolic Rate as a Function of Exercise Intensity

Distribution of blood flow in muscles of miniature swine during exercise.

The purpose of this study was to determine how the distribution of blood flow within and among the skeletal muscles of miniature swine (22 +/- 1 kg body wt) varies as a function of treadmill speed. Radiolabeled microspheres were used to measure cardiac output (Q) and tissue blood flows in preexercise and at 3-5 min of treadmill exercise at 4.8, 8.0, 11.3, 14.5, and 17.7 km/h. All pigs (n = 8) attained maximal O2 consumption (VO2max) (60 +/- 4 ml X min-1 X kg-1) by the time they ran at 17.7 km/h. At VO2max, 87% of Q (9.9 +/- 0.5 l/min) was to skeletal muscle, which constituted 36 +/- 1% of body mass. Average total muscle blood flow at VO2max was 127 +/- 14 ml X min-1 X 100 g-1; average limb muscle flow was 135 +/- 17 ml X min-1 X 100 g-1. Within the limb muscles, blood flow was distributed so that the deep red parts of extensor muscles had flows about two times higher than the more superficial white portions of the same muscles; the highest muscle blood flows occurred in the elbow flexors (brachialis: 290 +/- 44 ml X min-1 X 100 g-1). Peak exercise blood flows in the limb muscles were proportional (P less than 0.05) to the succinate dehydrogenase activities (r = 0.84), capillary densities (r = 0.78), and populations of oxidative (slow-twitch oxidative + fast-twitch oxidative-glycolytic) fiber types (r = 0.93) in the muscles. Total muscle blood flow plotted as a function of exercise intensity did not peak until the pigs attained VO2max, although flows in some individual muscles showed a plateau in this relationship at submaximal exercise intensities. The data demonstrate that blood flow in skeletal muscles of miniature swine is distributed heterogeneously and varies in relation to fiber type composition and exercise intensity.

Effect of exercise intensity and starvation on activation of branched-chain keto acid dehydrogenase by exercise.

Branched-chain keto acid (BCKA) dehydrogenase activity was examined in rat skeletal muscle as a function of exercise intensity and nutritional status. The activity of BCKA dehydrogenase increased with increasing exercise intensity, showing increases over resting values of 76, 172, and 245% at 10, 20, and 30 m X min-1. The exercise-induced increase in BCKA dehydrogenase activity was the same in the gastrocnemius and in the quadriceps muscles. Rapid removal of the muscle after death is essential because the activity of BCKA dehydrogenase decreased rapidly after death. Thus the likely reasons Wagenmakers et al. (Biochem. J. 223: 815-821, 1984) found exercise caused a much smaller increase in BCKA dehydrogenase activity than Kasperek et al. [Am. J. Physiol. 248 (Regulatory Integrative Comp. Physiol. 17): R166-R171, 1985] are differences in muscle removal time and the duration of exercise. Starvation for 24 h before exercise increased the exercise-induced activation of BCKA dehydrogenase by 160%, which suggests that the increased BCKA dehydrogenase activity is in response to an increased requirement for citric acid cycle intermediates.