Massage and Ultrasound as Therapeutic Modalities in Exercise-Induced Muscle Damage

1999 ◽  
Vol 24 (3) ◽  
pp. 267-278 ◽  
Author(s):  
Peter M. Tiidus

Although both massage and ultrasound treatment are used in clinical settings to enhance muscle functional recovery following exercise-induced muscle damage, there is a paucity of experimental evidence for their efficacy. Theoretically both massage and ultrasound could affect some physiological factors associated with enhancement of postexercise muscle recovery. However, the actual physiological mechanisms by which massage or ultrasound could influence postexercise muscle damage and repair are unknown. Most experimental evidence suggests that massage has little influence on muscle blood flow, clearance of "noxious" substances, recovery of postexercise muscle strength, or delayed soreness sensation. However, more data is needed before conclusions can be drawn as to the ability of massage to influence postexercise inflammatory response or various other physiological changes that characterize exercise-induced muscle damage and repair. There is even less information on the ability of ultrasound to influence physiological or functional factors associated with postexercise muscle damage. The few experiments that have been done tend to be contradictory and have yet to consider the range of ultrasound treatment parameters for therapeutic effectiveness in treating postexercise damage and influencing repair processes. Much more research is needed to determine whether either treatment modality can have any therapeutic effect on exercise-induced muscle damage and recovery of postexercise muscle function. Key words: muscle repair, inflammation, muscle soreness, muscle blood flow

2019 ◽  
Vol 126 (3) ◽  
pp. 658-667 ◽  
Author(s):  
Jonathon W. Senefeld ◽  
Jacqueline K. Limberg ◽  
Kathleen M. Lukaszewicz ◽  
Sandra K. Hunter

The aim of this study was to compare fatigability, contractile function, and blood flow to the knee extensor muscles after dynamic exercise in patients with type 2 diabetes mellitus (T2DM) and controls. The hypotheses were that patients with T2DM would demonstrate greater fatigability than controls, and greater fatigability would be associated with a lower exercise-induced increase in blood flow and greater impairments in contractile function. Patients with T2DM ( n = 15; 8 men; 62.4 ± 9.0 yr; 30.4 ± 7.7 kg/m2; 7,144 ± 3,294 steps/day) and 15 healthy control subjects (8 men, 58.4 ± 6.9 yr; 28.4 ± 4.6 kg/m2; 7,893 ± 2,323 steps/day) were matched for age, sex, body mass index, and physical activity. Fatigability was quantified as the reduction in knee extensor power during a 6-min dynamic exercise. Before and after exercise, vascular ultrasonography and electrical stimulation were used to assess skeletal muscle blood flow and contractile properties, respectively. Patients with T2DM had greater fatigability (30.0 ± 20.1% vs. 14.6 ± 19.0%, P < 0.001) and lower exercise-induced hyperemia (177 ± 90% vs. 194 ± 79%, P = 0.04) than controls but similar reductions in the electrically evoked twitch amplitude (37.6 ± 24.8% vs. 31.6 ± 30.1%, P = 0.98). Greater fatigability of the knee extensor muscles was associated with postexercise reductions in twitch amplitude ( r = 0.64, P = 0.001) and lesser exercise-induced hyperemia ( r = −0.56, P = 0.009). Patients with T2DM had greater lower-limb fatigability during dynamic exercise, which was associated with reduced contractile function and lower skeletal muscle blood flow. Thus, treatments focused on enhancing perfusion and reversing impairments in contractile function in patients with T2DM may offset lower-limb fatigability and aid in increasing exercise capacity. NEW & NOTEWORTHY Although prior studies compare patients with type 2 diabetes mellitus (T2DM) with lean controls, our study includes controls matched for age, body mass, and physical activity to more closely assess the effects of T2DM. Patients with T2DM demonstrated no impairment in macrovascular endothelial function, evidenced by similar flow-mediated dilation to controls. However, patients with T2DM had greater fatigability and reduced exercise-induced increase in blood flow (hyperemia) after a lower-limb dynamic fatiguing exercise compared with controls.


1985 ◽  
Vol 58 (3) ◽  
pp. 698-701 ◽  
Author(s):  
R. B. Armstrong ◽  
C. B. Vandenakker ◽  
M. H. Laughlin

We studied the distribution of blood flow within and among muscles of partially curarized (40–100 micrograms/kg body wt) rats during preexercise and at 1 min of low-speed treadmill exercise (15 m/min). Glycogen loss in the deep red muscles and parts of muscles was significantly reduced in the curarized animals during exercise, indicating the fibers in these muscles were recruited to a lesser extent and/or had lower metabolisms than fibers in the same muscles of control rats. However, elevations in blood flow in the red muscles of the curarized rats were as great or greater than those in the control rats. Thus reduced recruitment and/or metabolism of the deep red muscle fibers of the curarized animals was not accompanied by reduced blood flow. These findings suggest a dissociation between red fiber metabolism and blood flow in the curarized rats during the 1st min of slow treadmill exercise and indicate that release of vasodilator substances or local physical factors associated with muscle fiber activity are not solely responsible for the initial hyperemia during exercise.


1998 ◽  
Vol 30 (Supplement) ◽  
pp. 2
Author(s):  
M P McHugh ◽  
D AJ Connolly ◽  
R G Eston ◽  
I J Kremenic ◽  
G W Gleim

2013 ◽  
Vol 38 (12) ◽  
pp. 1181-1186 ◽  
Author(s):  
Mitchel R. Stacy ◽  
Kallie J. Bladon ◽  
Jennifer L. Lawrence ◽  
Sarah A. McGlinchy ◽  
Barry W. Scheuermann

Muscle damage is a common response to unaccustomed eccentric exercise; however, the effects of skeletal muscle damage on local vascular function and blood flow are poorly understood. This study examined serial local vascular responses to flow-mediated (endothelial-dependent) and nitroglycerin-mediated (endothelial-independent) dilation in the brachial artery after strenuous eccentric exercise and serially assessed resting blood flow. Ten healthy males performed 50 maximal eccentric unilateral arm contractions to induce muscle damage to the biceps brachii. Changes in maximal isometric strength and vascular responses were assessed 1, 24, 48, and 96 h after exercise. Mean blood velocities and arterial diameters, measured with Doppler ultrasound, were used to calculate blood flow and shear stress (expressed as area under the curve). Eccentric exercise resulted in impaired maximal isometric strength for up to 96 h (p < 0.001). Reductions in flow-mediated dilation (before exercise, 9.4% ± 2.6%; 1 h after exercise, 5.1% ± 2.2%) and nitroglycerin responses (before exercise, 26.3% ± 6.5%; 1 h after exercise, 20.7% ± 4.7%) were observed in the 1 h after exercise and remained lower for 96 h (p < 0.05). The shear stress response was attenuated immediately after exercise and remained impaired for 48 h (p < 0.05). Resting blood pressure and muscle blood flow remained similar throughout the study. Results suggest that muscle damage from eccentric exercise leads to impaired local endothelial and vascular smooth muscle function. Lower shear stress after exercise might contribute to the observed reduction in flow-mediated dilation responses, but the mechanism responsible for the attenuated endothelial-independent vasodilation remains unclear.


2009 ◽  
Vol 41 ◽  
pp. 8-9
Author(s):  
Jordan A. Guenette ◽  
Ioannis Vogiatzis ◽  
Spyros Zakynthinos ◽  
Robert Boushel ◽  
Peter D. Wagner ◽  
...  

2008 ◽  
Vol 586 (22) ◽  
pp. 5575-5587 ◽  
Author(s):  
Ioannis Vogiatzis ◽  
Dimitris Athanasopoulos ◽  
Robert Boushel ◽  
Jordan A. Guenette ◽  
Maria Koskolou ◽  
...  

2005 ◽  
Vol 22 (3) ◽  
pp. 405-412 ◽  
Author(s):  
Pierre Jean Ferr� ◽  
Eckart Thein ◽  
Isabelle Raymond-Letron ◽  
Pierre-Louis Toutain ◽  
Herv� Pierre Lefebvre

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