Abstract
Hyperthermia and dehydration can occur during exercise in hot environments. Nevertheless, whether elevations in extracellular osmolality contributes to the increased skeletal muscle tension, sarcolemmal injury, and oxidative stress reported in warm climates remains unknown. We simulated osmotic and heat stress, in vitro, in mouse limb muscles with different fiber compositions. Extensor digitorum longus (EDL) and soleus (SOL) were dissected from 36 male C57BL6J and mounted at optimal length in tissue baths containing oxygenated buffer. Muscles were stimulated with non-fatiguing twitches for 30 min. Four experimental conditions were tested: isotonic-normothermia (285 mOsm•kg-1 and 35°C), hypertonic-normothermia (300 mOsm•kg-1 and 35°C), isotonic-hyperthermia (285 mOsm•kg-1 and 41°C), and hypertonic-hyperthermia (300 mOsm•kg-1 and 41°C). Passive tension was recorded continuously. The integrity of the sarcolemma was determined using a cell-impermeable fluorescent dye and immunoblots were used for detection of protein carbonyls. In EDL muscles, isotonic and hypertonic-hyperthermia increased resting tension (P < 0.001). Whereas isotonic-hyperthermia increased sarcolemmal injury in EDL (P < 0.001), this effect was absent in hypertonic-hyperthermia. Similarly, isotonic-hyperthermia elevated protein carbonyls (P = 0.018), a response not observed with hypertonic-hyperthermia. In SOL muscles, isotonic-hyperthermia also increases resting tension (P < 0.001); however, these effects were eliminated in hypertonic-hyperthermia. Unlike EDL, there were no effects of hyperthermia and/or hyperosmolality on sarcolemmal injury or protein carbonyls. Osmolality selectively modifies skeletal muscle response to hyperthermia in this model. Fast-glycolytic muscle appears particularly vulnerable to isotonic-hyperthermia, resulting in elevated muscle tension, sarcolemmal injury and protein oxidation; whereas slow-oxidative muscle exhibits increased tension but no injury or protein oxidation under the conditions and duration tested.
Highlights
Hyperthermia is a common feature of exercise in hot environments and is accompanied by sweatinduced dehydration when fluid losses are not adequately matched by fluid replacement
Thereafter, we switched the connectors of the water circulation unit to 41◦C for hyperthermia conditions or maintained at 35◦C for control conditions and we switched the buffer to fresh hypertonic or isotonic depending on the condition studied
In SOL muscles, hyperthermia had no effects on protein carbonyls regardless of the osmolality employed
Summary
Hyperthermia is a common feature of exercise in hot environments and is accompanied by sweatinduced dehydration when fluid losses are not adequately matched by fluid replacement. Several secondary factors related to both hyperthermia and dehydration may Skeletal Muscle, Heat and Osmolality contribute to muscle injury in the heat. Hyperthermia per se can induce increases in passive tension (Oliver et al, 2008), a response often attributed to elevations in intracellular calcium (Ca2+) release from the sarcoplasmic reticulum (SR) (Hill, 1972; van der Poel and Stephenson, 2002, 2007). Increases in extracellular osmolality associated with dehydration can induce increases in muscle tension (Clausen et al, 1979; Farhat et al, 2018) by affecting muscle lattice structure and Ca2+ release (Clausen et al, 1979; Millman, 1998; Cleary et al, 2005). The extent of osmotic and heat stress involvement and the mechanisms behind their influences are not well understood
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