Heat Stress, Exercise, and Muscle Injury: Effects on Urate Metabolism and Renal Function

1974 ◽  
Vol 81 (3) ◽  
pp. 321 ◽  
Author(s):  
JAMES P. KNOCHEL
2018 ◽  
Vol 315 (3) ◽  
pp. F726-F733 ◽  
Author(s):  
Carlos A. Roncal-Jimenez ◽  
Yuka Sato ◽  
Tamara Milagres ◽  
Ana Andres Hernando ◽  
Gabriela García ◽  
...  

An epidemic of chronic kidney disease (CKD) has been observed in Central America among workers in the sugarcane fields. One hypothesis is that the CKD may be caused by recurrent heat stress and dehydration, and potentially by hyperuricemia. Accordingly, we developed a murine model of kidney injury associated with recurrent heat stress. In the current experiment, we tested whether treatment with allopurinol (a xanthine oxidase inhibitor that reduces serum urate) provides renal protection against recurrent heat stress and dehydration. Eight-week-old male C57BL/6 mice were subjected to recurrent heat stress (39.5°C for 30 min, 7 times daily, for 5 wk) with or without allopurinol treatment and were compared with control animals with or without allopurinol treatment. Mice were allowed ad libitum access to normal laboratory chow (Harlan Teklad). Kidney histology, liver histology, and renal function were examined. Heat stress conferred both kidney and liver injury. Kidneys showed loss of proximal tubules, infiltration of monocyte/macrophages, and interstitial collagen deposition, while livers of heat-stressed mice displayed an increase in macrophages, collagen deposition, and myofibroblasts. Allopurinol provided significant protection and improved renal function in the heat-stressed mice. The renal protection was associated with reduction in intrarenal uric acid concentration and heat shock protein 70 expression. Heat stress-induced renal and liver injury can be protected with allopurinol treatment. We recommend a clinical trial of allopurinol for individuals developing renal injury in rural areas of Central America where the epidemic of chronic kidney disease is occurring.


1998 ◽  
Vol 30 (Supplement) ◽  
pp. 282
Author(s):  
S. J. Montain ◽  
W. A. Latzka ◽  
K. Spears ◽  
M. N. Sawka
Keyword(s):  

2000 ◽  
Vol 89 (3) ◽  
pp. 1123-1130 ◽  
Author(s):  
Scott J. Montain ◽  
William A. Latzka ◽  
Michael N. Sawka

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 O2 consumption) in a hot room (40°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°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.


2020 ◽  
Vol 2020 (1) ◽  
Author(s):  
T. L. Stallings ◽  
A. Riefkohl Lisci ◽  
N. McCray ◽  
D. E. Weiner ◽  
J. S. Kaufman ◽  
...  
Keyword(s):  

Author(s):  
Tiffany L Stallings ◽  
Alejandro Riefkohl Lisci ◽  
Nathan L McCray ◽  
Daniel E Weiner ◽  
James S Kaufman ◽  
...  

2004 ◽  
Vol 114 (7) ◽  
pp. 1832-1841 ◽  
Author(s):  
Steffen Baumeister ◽  
Nina Ofer ◽  
Christian Kleist ◽  
Peter Terne ◽  
Gerhard Opelz ◽  
...  

2019 ◽  
Vol 127 (1) ◽  
pp. 178-189
Author(s):  
Tsubasa Shibaguchi ◽  
Mizuki Hoshi ◽  
Toshinori Yoshihara ◽  
Hisashi Naito ◽  
Katsumasa Goto ◽  
...  

Limited information exists regarding the impact of different temperature stimuli on myosin heavy chain (MyHC) expression in skeletal muscle during recovery from injury. Therefore, this experiment investigated the impact of both cold and heat exposure on the MyHC isoform profile in the rat soleus during recovery from injury. Male Wistar rats were randomly divided into control, bupivacaine-injected (BPVC), BPVC with icing, and BPVC with heat stress groups. Muscle injury was induced by intramuscular injection of bupivacaine into soleus muscles of male Wistar rats. Icing treatment (0°C for 20 min) was performed immediately after the injury. Intermittent heat stress (42°C for 30 min on alternating days) was carried out during 2–14 days after bupivacaine injection. In response to injury, a transient increase in developmental, IId/x, and IIb MyHC isoforms, as well as various types of hybrid fibers, followed by the recovery of the MyHC profile toward the control level, was noted in the regeneration of the soleus. The restoration of the MyHC profile in the regenerating muscle at whole-muscle and individual myofiber levels was partially delayed by icing but facilitated by heat stress. In addition, the application of repeated heat stress promoted the recovery of soleus muscle mass toward the control level following injury. We conclude that compared with acute and immediate cold (icing) treatment, chronic and repeated heat stress may be a more appropriate treatment for the enhancement of both normalization of the MyHC profile and restoration of muscle mass following injury. NEW & NOTEWORTHY Cold exposure (icing), but not heat exposure, has been well accepted as a first-aid treatment for accidental and/or sports-related injuries. However, recent evidence suggests the negative impact of icing treatment on skeletal muscle regeneration following injury. Here, we demonstrated that acute/immediate icing treatment delayed the restoration of the myosin heavy chain (MyHC) profile, but intermittent hyperthermia, repeated for several days, facilitated the recovery of both muscle mass and the MyHC profile in the regeneration of skeletal muscle following injury.


2007 ◽  
Vol 177 (4S) ◽  
pp. 411-412
Author(s):  
Javier Miller ◽  
Angela Smith ◽  
Kris Gunn ◽  
Erik Kouba ◽  
Eric M. Wallen ◽  
...  

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