Factors contributing to increased muscle fatigue with β-blockers

1991 ◽  
Vol 69 (2) ◽  
pp. 254-261 ◽  
Author(s):  
R. S. McKelvie ◽  
N. L. Jones ◽  
G. I. F. Heigenhauser

β-Adrenoceptor blockers are widely used clinically and can be classified as nonselective (β1 and β2) or selective (β1). Impairment of exercise performance is a well-known side effect of this group of drugs. This paper reviews mechanisms that could potentially be responsible for this impairment. In addition to cardiovascular and metabolic effects, β -blockade inhibits Na+–K+ ATPase pumps controlling ion movement between muscle and plasma and thus may contribute to muscle fatigue through this mechanism. To investigate the relationship between the change in plasma [K+] and exercise performance, we studied healthy male subjects taking propranolol. Eight subjects performed maximal incremental cycle ergometer exercise tests during control (no drug), low dose (LD) (40 mg daily), and high dose (HD) (265 ± 4.3 (SE) mg daily) of propranolol. The control plasma [K+] (5.8 ± 0.12 mequiv./L) during exercise was significantly lower than either the LD (6.4 ± 0.05 mequiv./L) or HD (6.1 ± 0.16 mequiv./L) values. There was no significant difference between plasma [K+] for the LD and HD of propranolol. However, maximum oxygen uptake was reduced only while taking the HD of propranolol. Six of the subjects also performed three 30-s bouts of high intensity exercise on an isokinetic cycle ergometer while taking the LD and HD of propranolol. There was no significant difference between doses for the increase in plasma [K+] (LD, 7.8 ± 0.35 mequiv./L vs. HD, 7.6 ± 0.36 mequiv./L) during exercise. However, exercise performance was significantly reduced during HD compared with LD. These results suggest that the increases in plasma [K+] with propranolol did not play a direct significant role in the reduced performance observed during the HD.Key words: exercise, potassium, performance, lactate.

1998 ◽  
Vol 85 (3) ◽  
pp. 921-926 ◽  
Author(s):  
Manabu Shibasaki ◽  
Narihiko Kondo ◽  
Hirotaka Tominaga ◽  
Ken Aoki ◽  
Eiichi Hasegawa ◽  
...  

The purpose of this study was to investigate the utility of an infrared tympanic thermometry by using an optical fiber for measuring tympanic temperature (Tty). In the head cooling and facial fanning tests during normothermia, right Tty measured by this method (infrared-Tty) and esophageal temperature (Tes) were not affected by decreased temple and forehead skin temperatures, suggesting that the infrared sensor in this system measured the infrared radiation from the tympanic membrane selectively. Eight male subjects took part in passive-heat-stress and progressive-exercise tests. No significant differences among infrared-Tty, the left Tty measured by thermistor (contact-Tty), and Tes were observed at rest or at the end of each experiment, and there was no significant difference in the increase in these core temperatures from rest to the end. Furthermore, there were no significant differences in the core temperature threshold at the onset of sweating and slope (the relationship of sweating rate vs. infrared-Tty and vs. contact-Tty). These results suggest that this method makes it possible to measure Tty accurately, continuously, and more safely.


1991 ◽  
Vol 80 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones

1. This study was designed to examine whether normal subjects could differentiate between the ‘intensity’ of their breathlessness and the amount of ‘distress’ it evoked, by specific wording of the instructions. 2. A preliminary study showed no significant difference between ‘distress’ score during exercise measured on two separate occasions (P = 0.3). 3. Ten subjects each performed two identical incremental cycle-ergometer exercise tests on separate occasions during which they were asked to quantify either ‘intensity’ or ‘distress’ by using modified Borg scales. 4. In all subjects there was a significant correlation (P <0.001) between ‘intensity’ and minute ventilation. In eight subjects there was a significant correlation (P <0.05) between ‘distress’ and minute ventilation. One subject displayed no significant correlation and one registered no distress. 5. Mean ‘intensity’ was greater than the mean ‘distress’ (P = 0.0001). The slope of ‘intensity’/minute ventilation was greater than the slope of ‘distress’/minute ventilation (P = 0.0001). 6. Within individuals there was a significant correlation beween ‘intensity’ and ‘distress’ (P <0.05). There was a wide scatter in the slope of this relationship between subjects and maximum ‘intensity’ and ‘distress’ did not correlate. 7. Different elements of the breathlessness sensation could be identified and selectively measured depending on the wording of the instructions given to the subject. 8. There was a wide intersubject variation in the magnitude of both breathlessness ‘intensity’ and ‘distress’ estimates, but the differences between subjects in these two components of the sensation did not appear to follow a common pattern.


1989 ◽  
Vol 66 (6) ◽  
pp. 2710-2716 ◽  
Author(s):  
J. Chwalbinska-Moneta ◽  
R. A. Robergs ◽  
D. L. Costill ◽  
W. J. Fink

The purpose of this study was to investigate the relationship between muscle and blood lactate concentrations during progressive exercise. Seven endurance-trained male college students performed three incremental bicycle ergometer exercise tests. The first two tests (tests I and II) were identical and consisted of 3-min stage durations with 2-min rest intervals and increased by 50-W increments until exhaustion. During these tests, blood was sampled from a hyperemized earlobe for lactate and pH measurement (and from an antecubital vein during test I), and the exercise intensities corresponding to the lactate threshold (LT), individual anaerobic threshold (IAT), and onset of blood lactate accumulation (OBLA) were determined. The test III was performed at predetermined work loads (50 W below OBLA, at OBLA, and 50 W above OBLA), with the same stage and rest interval durations of tests I and II. Muscle biopsies for lactate and pH determination were taken at rest and immediately after the completion of the three exercise intensities. Blood samples were drawn simultaneously with each biopsy. Muscle lactate concentrations increased abruptly at exercise intensities greater than the “below-OBLA” stage [50.5% maximal O2 uptake (VO2 max)] and resembled a threshold. An increase in blood lactate and [H+] also occurred at the below-OBLA stage; however, no significant change in muscle [H+] was observed. Muscle lactate concentrations were highly correlated to blood lactate (r = 0.91), and muscle-to-blood lactate ratios at below-OBLA, at-OBLA, and above-OBLA stages were 0.74, 0.63, 0.96, and 0.95, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)


2002 ◽  
Vol 92 (2) ◽  
pp. 602-608 ◽  
Author(s):  
K. A. Stokes ◽  
M. E. Nevill ◽  
G. M. Hall ◽  
H. K. A. Lakomy

The present study examined the growth hormone (GH) response to repeated bouts of maximal sprint cycling and the effect of cycling at different pedaling rates on postexercise serum GH concentrations. Ten male subjects completed two 30-s sprints, separated by 1 h of passive recovery on two occasions, against an applied resistance equal to 7.5% (fast trial) and 10% (slow trial) of their body mass, respectively. Blood samples were obtained at rest, between the two sprints, and for 1 h after the second sprint. Peak and mean pedal revolutions were greater in the fast than the slow trial, but there were no differences in peak or mean power output. Blood lactate and blood pH responses did not differ between trials or sprints. The first sprint in each trial elicited a serum GH response (fast: 40.8 ± 8.2 mU/l, slow: 20.8 ± 6.1 mU/l), and serum GH was still elevated 60 min after the first sprint. The second sprint in each trial did not elicit a serum GH response ( sprint 1 vs. sprint 2, P < 0.05). There was a trend for serum GH concentrations to be greater in the fast trial (mean GH area under the curve after sprint 1vs. after sprint 2: 1,697 ± 367 vs. 933 ± 306 min · mU−1 · l−1; P = 0.05). Repeated sprint cycling results in an attenuation of the GH response.


Author(s):  
Wenqian Yang ◽  
Yuqian Liu ◽  
Guang Yang ◽  
Binglin Meng ◽  
Zhicheng Yi ◽  
...  

The gut microbiota is closely associated with the health of the host and is affected by many factors, including exercise. In this study, we compared the gut microbial changes and exercise performance over a 14-week period in mice that performed exercise (NE; n = 15) and mice that did not perform exercise (NC; n = 15). Mice were subjected to stool collection and exercise tests one week prior to adaptive training and after 2, 6, 10, and 14 weeks of exercise. Bacteria associated with the stool samples were assessed via Illumina-based 16S rRNA gene sequencing. While there was no significant difference in body weight between the groups (p &gt; 0.05), the NE group had a significantly higher exercise performance from weeks 2–14 (p &lt; 0.01) and lower fat coefficient (p &lt; 0.01) compared with the NC group. The Shannon index of the gut microbiota in the NC group was higher than that in the NE group at weeks 6 and 10, and the Chao1 index was higher than that in the NE group at week 14. Exercise performance positively correlated with the relative abundance of Phascolarctobacterium. Grouped time series data analysis demonstrated that Bifidobacteria, Coprococcus, and one unnamed genus in the Clostridiales order were significantly increased in the NE group, which correlated with increased glucose, flavonoid, arginine, and proline metabolism. In conclusion, moderate-intensity treadmill exercise significantly increased the exercise performance of mice and changed the core bacteria and bacterial metabolic activity. These results provide a reference for studying the effects of exercise intervention and exercise performance on the gut microbiota of mice.


2009 ◽  
Vol 38 ◽  
pp. 709-718
Author(s):  
Dong Yup Han ◽  
Tae Beom Seo ◽  
Dong Hee Lee ◽  
Kwang Sub Byun ◽  
Il Gue Jeong ◽  
...  

1990 ◽  
Vol 69 (1) ◽  
pp. 104-111 ◽  
Author(s):  
E. C. Johnson ◽  
T. L. Hudson ◽  
E. R. Greene

The directional response of human left ventricular stroke volume during exercise recovery is unclear. Stroke volume has been reported to increase and decrease over exercise values during early recovery. The confounding variable may be posture. With the use of pulsed Doppler ultrasound, we tested the hypothesis that there is a significant difference between seated and supine stroke index (SI) during passive recovery from seated ergometer exercise. Thirteen subjects aged 26 +/- 2 yr performed two seated cycle ergometer exercise tests to 70% of predicted maximum heart rate (HR). Recovery was supine on one test and seated on the other. Cardiac index (CI), HR, and SI were calculated during rest, exercise, and 10 min of recovery. At rest, SI and CI were significantly (P less than 0.01) less and HR significantly (P less than 0.01) greater when the subjects were seated than when they were supine. At the last exercise work load, no significant differences were found in any measured variable between tests. During recovery, supine SI was maximal 180 s postexercise (99 +/- 14 ml/m2) and exceeded (P less than 0.01) resting supine (81 +/- 14 ml/m2) and peak exercise (77 +/- 14 ml/m2) SI by 22 and 29%, respectively. Seated SI was constant at peak exercise levels for 2 min. Seated and supine recovery CI never exceeded exercise values. Systolic and diastolic blood pressure recovery curves were similar in the two postures. We conclude that posture significantly affects SI during recovery from submaximal seated exercise. These results have implications for choice of recovery posture after stress testing in cardiac patients where it is desirable to minimize ventricular loading.


1997 ◽  
Vol 29 (6) ◽  
pp. 762-768 ◽  
Author(s):  
PETER HOFMANN ◽  
ROCHUS POKAN ◽  
SERGE P. VON DUVILLARD ◽  
&NA; J. SEIBERT ◽  
ROBERT ZWEIKER ◽  
...  

1994 ◽  
Vol 76 (4) ◽  
pp. 1462-1467 ◽  
Author(s):  
W. Stringer ◽  
K. Wasserman ◽  
R. Casaburi ◽  
J. Porszasz ◽  
K. Maehara ◽  
...  

The slow rise in O2 uptake (VO2), which has been shown to be linearly correlated with the increase in lactate concentration during heavy constant work rate exercise, led us to investigate the role of H+ from lactic acid in facilitating oxyhemoglobin (O2Hb) dissociation. We measured femoral venous PO2, O2Hb saturation, pH, PCO2, lactate, and standard HCO3- during increasing work rate and two constant work rate cycle ergometer exercise tests [below and above the lactic acidosis threshold (LAT)] in two groups of five healthy subjects. Mean end-exercise femoral vein blood and VO2 values for the below- and above-LAT square waves and the increasing work rate protocol were, respectively, PO2 of 19.8 +/- 2.1 (SD), 18.8 +/- 4.7, and 19.8 +/- 3.3 Torr; O2 saturation of 22.5 +/- 4.1, 13.8 +/- 4.2, and 18.5 +/- 6.3%; pH of 7.26 +/- 0.01, 7.02 +/- 0.11, and 7.09 +/- 0.07; lactate of 1.9 +/- 0.9, 11.0 +/- 3.8, and 8.3 +/- 2.9 mmol/l; and VO2 of 1.77 +/- 0.24, 3.36 +/- 0.4, and 3.91 +/- 0.68 l/min. End-exercise femoral vein PO2 did not differ statistically for the three protocols, whereas O2Hb saturation continued to decrease for work rates above LAT. We conclude that decreasing capillary PO2 accounted for most of the O2Hb dissociation during below-LAT exercise and that acidification of muscle capillary blood due to lactic acidosis accounted for virtually all of the O2Hb dissociation above LAT.


1992 ◽  
Vol 70 (1) ◽  
pp. 100-105 ◽  
Author(s):  
Savio W. T. Cheng ◽  
William G. North

Peripheral administration of vasopressin (VP) was previously shown to exert a negative feedback influence on its own release and on the release of oxytocin (OT). In this study we examined the possible influence that OT has on the function of hypothalamic magnocellular neurones. Oxytocin was administered intraperitoneally and its effects on release from VP neurones and from OT neurones were determined as indexed by plasma concentrations of vasopressin-associated neurophysin ([VP-RNP]) and oxytocin-associated neurophysin ([OT-RNP]) under basal conditions and conditions of high plasma osmolality (Posm) induced by acute salt loading. Studies were performed on conscious, chronically instrumented Long-Evans rats. Oxytocin (1 nmol or 10 nmol) dissolved in 1 mL of 0.9% saline was administered intraperitoneally to animals 1 h before they received an intravenous infusion of hypertonic saline over 60 min at a rate designed to raise Posm by approximately 0.75 mosmol∙min−1. Intraperitoneal injection of vehicle or 1 nmol of OT did not significantly alter [VP-RNP], [OT-RNP], or basal Posm. Administration of 10 nmol OT also had no effect on [VP-RNP] or [OT-RNP], but this dose of peptide significantly lowered basal Posm (299 ± 2 to 290 ± 2 mosmol/kg H2O, p < 0.001). Both doses of OT did not significantly alter the responsiveness of VP neurones to hyperosmotic stimulation. The slopes of the relationship between the rise in [VP-RNP] (A[VP-RNP]) and the rise in Posm (ΔPosm) for the groups receiving pretreatment of 1 nmol OT (n = 5), 10 nmol OT (n = 7), and vehicle (n = 7) were similar (6.1 ± 1.4, r = 0.86; 5.1 ± 0.9, r = 0.91; and 6.6 ± 0.9 fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93, respectively). For the 1-nmol dose of OT that generated plasma OT levels in the physiological range, the slopes of the relationship between the rise in [OT-RNP] (Δ[OT-RNP]) and ΔPosm over the period of salt loading for peptide-treated animals and control animals (39.5 ± 8.9, r = 0.89 vs. 23.4 ± 5.9, fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93) indicated an increased responsiveness of OT neurones, but this difference was not significant (p < 0.1426). Higher plasma levels of OT were generated by administering the 10 nmol dose of OT, and the slopes of the relationship between Δ[OT-RNP] and ΔPosm for peptide-treated animals and control animals (13.9 ± 1.6, r = 0.96 vs. 23.4 ± 8.9 fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93) suggested a decreased responsiveness of OT neurones, but again this difference was not significant (p < 0.1637). However, there was a significant difference in the rise in OT-RNP with plasma osmolality for rats receiving high versus low dose of peptide (p < 0.0475). Our data indicate that peripherally administered OT, unlike VP, does not exert a negative feedback influence on osmotically stimulated release from VP neurones and most probably OT neurones. However, it cannot be ruled out that the lack of modulation of magnocellular neurones by the high dose of OT could be due to the summation of a positive OT effect (since the 1-nmol group appeared to exhibit an enhancing effect) and of a negative VP effect as indicated by blood pressure increases and plasma dilution. OT also does not appear to have an influence on basal release from magnocellular neurones.Key words: neurophysins, oxytocin neurones, vasopressin neurones.


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